CLIN - Pécsi Tudományegyetem
PÉCSI TUDOMÁNYEGYETEM
Orvostudományi és Egészségtudományi Centrum
Szak- és Továbbképző Központ
H-7624 Pécs, Szigeti út 12.
Tel.: (72) 512-643
Fax: (72) 512-683
IGAZGATÓ: PROF. DR. ERTL TIBOR
SZAKORVOSI TOVÁBBKÉPZÉS
TÉMA: CLINICAL NEPHROLOGY
Szerkesztette: DR. NÉMETH LÁSZLÓ
Cím: Petz Aladár Megyei Oktató Kórház – Rendelőintézet
I.sz. Belgyógyászati Szakrendelés
9024 Győr, Szent Imre u. 41. Tel.: (96) 418-244/1494
IRODALOM: 2006. JÚLIUS 1. – SZEPTEMBER 30.
GYŐR, 2006. OKTÓBER 6.
C O N T E N T S
Part One
SECTIONS
I. EPIDEMILOGY
II. ETIOPATHOGENESIS
III. CLINICAL PRESENTATION
IV. TREATMENT
V. TRANSPLANTATION
TITLE OF PUBLICATIONS – AUTHORS – PUBLICATIONS
Part One
I. EPIDEMIOLOGY
1. DNA polymorphisms and renal disease: a critical appraisal of studies presented at the annual ERA/EDTA and ASN conferences in 2004 and 2005.
Mondry A, Loh M, Laurence KB, Low N.
Nephrol Dial Transplant. 2006 Jul 4; [Epub ahead of print]
2. Lessons in ethnonephrology.
Hoy WE.
Kidney Int. 2006 70 (2): 251-7.
3. Racial disparities in the association between birth weight in the term infant and blood presure at age 7 years: Results from Collaborative Perinatal Project.
Hemachandra AH, Klebanoff MA, Furth SL.
J Am Soc Nephrol. 2006 Jul 26; [Epub ahead of print]
4. The enigma of hypertensive ESRD: Observation on incidence and trends in 18 European, Canadian, and Asian-Pacific populations, 1998 to 2002.
Stewart JH, McCredie MR, Williams SM; Canadian Organ Replacement Register; Fenton SS, Trepski L; Australia and New Zealand Dialysis and Transplant Registry; McDonald SP; European Renal Association-European Dialysis and Transplant Association Registry; Jager KJ, van Dijk PC; Finnish Registry for Kidney Diseases; Finne P; Swedish Registry for Active Treatment of Uremia; Schon S; Norwegian Renal Registry; Leivestad T; Danish National Registry on Regular Dialysis and Transplantation; Lokkegaard H; Dutch-speaking Belgian Society of Nephrology; Billiouw JM; Austrian Dialysis and Transplant Registry; Kramer R; Basque Renal Patients’ Registry; Magaz A; Catalan Renal Registry; Vela E; Valencian Renal Registry; Garcia-Blasco MJ; Hellenic Renal Registry; Ioannidis GA; Malaysian National Renal Registry; Lim YN.
Am J Kidney Dis. 2006 48 (2): 183-91.
5. Glomerular hyperfiltration predicts the development of microalbuminuria in stage 1 hypertension: The HARVEST.
Palatini P, Mormino P, Dorigatti F, Santonastaso M, Mos L, De Toni R, Winnicki M, Follo MD, Biasion T, Garavelli G, Pessina AC.
Kidney Int. 2006 Jun 21; [Epub ahead of print]
6. Prevalence and risk factor analysis of microalbuminuria in Japanese general population: The Takahata study.
Konta T, Hao Z, Abiko H, Ishikawa M, Takahashi T, Ikeda A, Ichikawa H, Takasaki S, Kubota I.
Kidney Int. 2006 Jun 28; [Epub ahead of print]
7. Traditional and emerging cardiovascular and renal risk factors: An epidemiologic perspective.
Zoccali C.
Kidney Int. 2006 70 (1): 26-33.
8. Cardiovascular disease in early stages of chronic kidney disease in a Chinese population.
Zhang L, Zuo L, Wang F, Wang M, Wang S, Lv J, Liu L, Wang H.
J Am Soc Nephrol. 2006 Aug 2; [Epub ahead of print]
9. Identifying genetic susceptibilities to diabetes-related complications among individuals at low risk of complications: An application of tree-structured survival analysis.
Costacou T, Chang Y, Ferrell RE, Orchard TJ.
Am J Epidemiol. 2006 Aug 23; [Epub ahead of print]
10. A cohort analysis of type 1 diabetes mortality in Havana and Allegheny County, Pittsburgh, PA.
Barcelo A, Bornyak Z, Orchard T.
Diabetes Res Clin Pract. 2006 Jul 27; [Epub ahead of print]
11. Diabetic microvascular complications -- can the presence of one predict the development of another?
Girach A, Vignati L.
J Diabetes Complications. 2006 20 (4): 228-37.
12. Relationship between common functional polymorphisms of the p22phox gene (-930A > G and +242 > T) and nephropathy as a result of type 2 diabetes in a Chinese population.
Lim SC, Goh SK, Lai YR, Tee WW, Koh A, Xu XH, WuYS, Yap E, Subramaniam T, Sum CF.
Diabet Med. 2006 23 (9): 1037-41.
13. Metabolic syndrome and CKD in a general Japanese population: The Hisayama Study.
Ninomiya T, Kiyohara Y, Kubo M, Yonemoto K, Tanizaki Y, Doi Y, Hirakata H, Iida M.
Am J Kidney Dis. 2006 48 (3): 383-91.
14. The relationship of microalbuminuria with metabolic syndrome.
Choi HS, Ryu SH, Lee KB.
Nephron Clin Pract. 2006 104 (2): c85-93.
15. Racial differences in the prevalence of chronic kidney disease among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort study.
McClellan W, Warnock DG, McClure L, Campbell RC, Newsome BB, Howard V, Cushman M, Howard G.
J Am Soc Nephrol. 2006 17 (6): 1710-5.
16. International comparison of the relationship of chronic kidney disease prevalence and ESRD risk.
Hallan SI, Coresh J, Astor BC, Asberg A, Romundstad S, Hallan HA, Lydersen S, Holmen J.
J Am Soc Nephrol. 2006 Jun 21; [Epub ahead of print]
17. Ethnic disparities in cardiovascular risk factors and coronary disease prevalence among individuals with chronic kidney disease: Findings from the Third National Health and Nutrition Examination Survey.
Nguyen HT, Stack AG.
J Am Soc Nephrol. 2006 17 (6): 1716-23.
18. Trends in treatment and outcomes of survival of adolescents initiating end-stage renal disease care in the United States of America.
Ferris ME, Gipson DS, Kimmel PL, Eggers PW.
Pediatr Nephrol. 2006 21 (7): 1020-6.
19. Chronic kidney disease and mortality risk: A systematic review.
Tonelli M, Wiebe N, Culleton B, House A, Rabbat C, Fok M, McAlister F, Garg AX.
J Am Soc Nephrol. 2006 17 (7): 2034-47.
20. Stabilized incidence of diabetic patients referred for renal replacement therapy in Denmark.
Sorensen VR, Hansen PM, Heaf J, Feldt-Rasmussen B.
Kidney Int. 2006 70 (1): 187-91.
21. Paulista registry of glomerulonephritis: 5-year data report.
Malafronte P, Mastroianni-Kirsztajn G, Betonico GN, Romao JE, Alves MA, Carvalho MF, Neto OM, Cadaval RA, Bergamo RR, Woronik V, Sens YA, Marrocos MS, Barros RT.
Nephrol Dial Transplant. 2006 Sep 12; [Epub ahead of print]
22. A scoring system to predict renal outcome in IgA nephropathy: From a nationwide prospective study.
Wakai K, Kawamura T, Endoh M, Kojima M, Tomino Y, Tamakoshi A, Ohno Y, Inaba Y, Sakai H.
Nephrol Dial Transplant. 2006 Jul 5; [Epub ahead of print]
23. Membranous nephropathy and cancer: Epidemiologic evidence and determinants of high-risk cancer association.
Lefaucheur C, Stengel B, Nochy D, Martel P, Hill GS, Jacquot C, Rossert J.
Kidney Int. 2006 Aug 30; [Epub ahead of print]
24. Genetic kidney diseases in the pediatric population of southern Israel.
Finer G, Shalev H, Landau D.
Pediatr Nephrol. 2006 21 (7): 910-6.
25. Spectrum of clinical features and type IV collagen {alpha}-chain distribution in Chinese patients with Alport syndrome.
Wei G, Zhihong L, Huiping C, Caihong Z, Zhaohong C, Leishi L.
Nephrol Dial Transplant. 2006 Aug 29; [Epub ahead of print]
26. Viral hepatitis and proteinuria in an area endemic for hepatitis B and C infections: Another chain of link?
Huang JF, Chuang WL, Dai CY, Ho CK, Hwang SJ, Chen SC, Lin ZY, Wang LY, Chang WY, Yu ML.
J Intern Med. 2006 260 (3): 255-62.
27. Reduced nephron number and glomerulomegaly in Australian Aborigines: A group at high risk for renal disease and hypertension.
Hoy WE, Hughson MD, Singh GR, Douglas-Denton R, Bertram JF.
Kidney Int. 2006 70 (1): 104-10.
28. Epidemiology and prognostic implications of contrast-induced nephropathy.
McCullough PA, Adam A, Becker CR, Davidson C, Lameire N, Stacul F, Tumlin J; CIN Consensus Working Panel.
Am J Cardiol. 2006 98 (6 Suppl 1): 5-13.
II. ETIOPATHOGENESIS
1. Cis and trans regulatory elements in NPHS2 promoter: Implictions in proteinuria and progression of renal diseases.
Di Duca M, Olegginin R, Sanna-Cherchi S, Pasquali L, Di Donato A, Parodi S, Bertelli R, Caridi G, Frasca G, Cerullo G, Amoroso A, Schena FP, Scolari F, Ghiggeri GM.
Kidney Int. 2006 Aug 9; [Epub ahead of print]
2. Collapsing glomerulopathy.
Albaqumi M, Soos TJ, Barisoni L, Nelson PJ.
J Am Soc Nephrol. 2006 Aug 16; [Epub ahead of print]
3. The molecular biology of thrombotic microangiopathy.
Tsai HM.
Kidney Int. 2006 70 (1): 16-23.
4. Renal vascular sclerosis is associated with inherited thrombophilias.
Goforth RL, Rennke H, Sethi S.
Kidney Int. 2006 Jun 7; [Epub ahead of print]
5. Polycystic kidney disease: Cell division without a c(l)ue?
Simons M, Walz G.
Kidney Int. 2006 Jun 28; [Epub ahead of print]
6. Renal cystic diseases: Diverse phenotypes converge on the cilium/centrosome complex.
Guay-Woodford LM.
Pediatr Nephrol. 2006 Jul 6; [Epub ahead of print]
7. Understanding pathogenic mechanisms in polycystic kidney disease provides clues for therapy.
Harris PC, Torres VE.
Curr Opin Nephrol Hypertens. 2006 15 (4): 456-63.
8. mRNA translation: Unexplored territory in renal science.
Kasinath BS, Mariappan MM, Sataranatarajan K, Lee MJ, Feliers D.
J Am Soc Nephrol. 2006 Sep 7; [Epub ahead of print]
9. Further insights into the role of angiotensin II in kidney development.
Lasaitiene D, Chen Y, Adams MA, Friberg P.
Clin Physiol Funct Imaging. 2006 (26): 197-204.
10. Physiology of local renin-angiotensin systems.
Paul M, Poyan Mehr A, Kreutz R.
Physiol Rev. 2006 86 (3): 747-803.
11. The podocyte’s response to injury: Role in proteinuria and glomerulosclerosis.
Shankland SJ.
Kidney Int. 2006 69 (12): 2131-47.
12. Erythropoietin and the cardiorenal syndrome: Cellular mechanisms on the cardiorenal connectors.
Jie KE, Verhaar M, Cramer MJ, Van Der Putten K, Gaillard C, Doevendans P, Koomans HA, Joles J, Braam B.
Am J Physiol Renal Physiol. 2006 Aug 1; [Epub ahead of print]
13. Common mechanisms in nephropathy induced by toxic metals.
Sabolic I.
Nephron Physiol. 2006 104 (3): p107-14.
14. Meeting report: ISN forefronts in nephrology on endothelial biology and renal disease: From bench to prevention.
Goligorsky MS, Rabelink T.
Kidney Int. 2006 70 (2): 258-64.
15. Role of endothelin and endothelin receptor antagonists in renal disease.
Neuhofer W, Pittrow D.
Eur J Clin Invest. 2006 36 (Suppl 3): 78-88.
16. Cross-talk between the kidney and the cardiovascular system.
Amann K, Wanner C, Ritz E.
J Am Soc Nephrol. 2006 17 (8): 2112-9.
17. Heme oxygenase-1: A provenance for cytoprotective pathways in the kidney and other tissues.
Nath KA.
Kidney Int. 2006 70 (1): 432-43.
18. Oxidants and iron in progressive kidney disease.
Shah SV.
J Ren Nutr. 2006 16 (3): 185-9.
19. The role of urotensin II in cardiovascular and renal physiology and diseases.
Zhu YC, Zhu YZ, Moore PK.
Br J Pharmacol. 2006 (148): 834-901.
20. Eicosanoids and renal vascular function in diseases.
Imig JD.
Clin Sci (Lond). 2006 111 (1): 21-34.
21. TGF-beta1 induces COX-2 expression and PGE (2) synthesis through MAPK and PI3K pathways in human mesangial cells.
Rodriguez-Barbero A, Dorado F, Velasco S, Pandiella A, Banas B, Lopez-Novoa JM.
Kidney Int. 2006 Jul 5; [Epub ahead of print]
22. Interferon-gamma enhances superoxide production in human mesangial cells via the JAK-STAT pathway.
Moriwaki K, Kiyomoto H, Hitomi H, Ihara G, Kaifu K, Matsubara K, Hara T, Kondo N, Ohmori K, Nishiyama A, Fukui T, Kohno M.
Kidney Int. 2006 70 (4): 788-93.
23. A critical look at growth factors and epithelial-to-mesenchymal transition in the adult kidney. Interrelationships between growth factors that regulate EMT in the adult kidney.
Wahab NA, Mason RM.
Nephron Exp Nephrol. 2006 104 (4): e129-34.
24. Consequences of intrauterine growth restriction for the kidney.
Schreuder M, Delemarre-van de Waal H, van Wijk A.
Kidney Blood Press Res. 2006 29 (2): 108-25.
25. Matrix metalloproteinase 2 and basement membrane integrity: A unifying mechansims for progressive renal injury.
Cheng S, Pollock AS, Mahimkar R, Olson JL, Lovett DH.
FASEB J. 2006 20 (11): 1898-900.
26. Mechanisms of development and progression of cyanotic nephropathy.
Inatomi J, Matsuoka K, Fujimaru R, Nakagawa A, Iijima K.
Pediatr Nephrol. 2006 Aug 11; [Epub ahead of print]
27. Genetic and functional analyses of membrane cofactor protein (CD46) mutations in atypical hemolytic uremic syndrome.
Fremeaux-Bacchi V, Moulton EA, Kavanagh D, Dragon-Durey MA, Blouin J, Caudy A, Arzouk N, Cleper R, Francois M, Guest G, Pourrat J, Seligman R, Fridman WH, Loirat C, Atkinson JP.
J Am Soc Nephrol. 2006 17 (7): 2017-25.
28. Microbial nucleic acids pay a toll in kidney disease.
Pawar RD, Patole PS, Wornle M, Anders HJ.
Am J Physiol Renal Physiol. 2006 291 (3): F509-16.
29. Immunohistochemical expression of activated caspase-3 as a marker of apoptosis in glomeruli of human lupus nephritis.
Jeruc J, Vizjak A, Rozman B, Ferluga D.
Am J Kidney Dis. 2006 48 (3): 410-8.
30. Association of alpha-actinin-binding anti-double-stranded DNA antibodies with lupus nephritis.
Renaudineau Y, Croquefer S, Jousse S, Renaudineau E, Devauchelle V, Gueguen P, Hanrotel C, Gilburd B, Saraux A, Shoenfeld Y, Putterman C, Youinou P.
Arthritis Rheum. 2006 54 (8): 2523-32.
31. Characterization of the expanded T-cell populations in patients with Wegener’s granulomatosis.
Giscombe R, Wang XB, Kakoulidou M, Lefvert AK.
J Intern Med. 2006 260 (3): 224-30.
32. Persistent expansion of CD4 (+) effector memory T cells in Wegener’s granulomatosis.
Abdulahad WH, van der Geld YM, Stegeman CA, Kallenberg CG.
Kidney Int. 2006 Jul 12; [Epub ahead of print]
33. B lymphocyte maturation in Wegener’s granulomatosis: A comparative analysis of VH genes from endonasal lesions.
Voswinkel J, Mueller A, Kraemer JA, Lamprecht P, Herlyn K, Holl-Ulrich K, Feller AC, Pitann S, Gause A, Gross WL.
Ann Rheum Dis. 2006 65 (7): 859—64.
34. Henoch-Schonlein purpura: Polymorphisms in thrombophilia genes.
Dagan E, Brik R, Broza Y, Gershoni-Baruch R.
Pediatr Nephrol. 2006 21 (8): 1117-21.
35. Role of podocyte slit diaphragm as a filtration barrier.
Kawachi H, Miyauchi N, Suzuki K, Han GD, Orikasa M, Shimizu F.
Nephrology (Carlton). 2006 11 (4): 274-81.
36. Tissue factor pathway inhibitor in childhood nephrotic syndrome.
Al-Maugeiren MM, Abdel Gader AG, Al-Rasheed SA, Al-Salloum AA.
Pediatr Nephrol. 2006 21 (6): 771-7.
37. Low protein Z levels in children with nephrotic syndrome.
Ozkaya O, Bek K, Fisgin T, Aliyazicioglu Y, Sultansuyu S, Acikgoz Y, Albayrak D, Baysal K.
Pediatr Nephrol. 2006 21 (8): 1122-6.
38. Nephrotic syndrome associated with chronic graft-versus-host disease after allogenic hematopoietic stem cell transplantation.
Reddy P, Johnson K, Uberti JP, Reynolds C, Silver S, Ayash L, Braun TM, Ratanatharathorn V.
Bone Marrow Transplant. 2006 38 (5): 351-7.
39. Renal corpuscle morphometry with increased reliability and high level of automation.
Caruntu ID, Covic A.
Pathol Res Pract. 2006 Sep 6; [Epub ahead of print]
40. Mechanisms of neutrophil transmigration across renal proximal tubular HK-2 cells.
Bijuklic K, Sturn DH, Jennigns P, Kountchev J, Pfaller W, Wiedermann CJ, Patsch JR, Joannidis M.
Cell Physiol Biochem. 2006 17 (5-6): 233-44.
41. Loss of podocyte dysferlin expression is associated with minimal change nephropathy.
Izzedine H, Brocheriou I, Eymard B, Le Charpentier M, Romero NB, Lenaour G, Bourry E, Deray G.
Am J Kidney Dis. 2006 48 (1): 143-50.
42. Proliferating cells in HIV and pamidronate-associated collapsing focal segmental glomerulosclerosis are parietal epithelial cells.
Dijkman HB, Weening JJ, Smeets B, Verrijp KC, van Kuppevelt TH, Assmann KK, Steenbergen EJ, Wetzels JF.
Kidney Int. 2006 70 (2): 338-44.
43. Cell-cycle regulator proteins in the podocyte in collapsing glomerulopathy in children.
Srivastava T, Garola RE, Singh HK.
Kidney Int. 2006 Jun 14; [Epub ahead of print]
44. Glomerular clusterin is associated with PKC-alpha/beta regulation and good outcome of membranous glomerulonephritis in humans.
Rastaldi MP, Candiano G, Musante L, Bruschi M, Armelloni S, Rimoldi L, Tardanico R, Cherci SS, Ferrario F, Montinaro V, Haupt R, Parodi S, Carnevali ML, Allegri L, Camussi G, Gesualdo L, Scolari F, Ghiggeri GM.
Kidney Int. 2006 Jun 14. [Epub ahead of print]
45. Study of hepatitis B virus pre-S/S gene mutations of renal tissues in children with hepatitis B virus-associated membranous nephropathy.
Kim SE, Park YH, Chung WY.
Pediatr Nephrol. 2006 21 (8): 1097-103.
46. Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with membranoproliferative glomerulonephritis type II (dense deposit disease).
Abrera-Abeleda MA, Nishimura C, Smith JL, Sethi S, McRae JL, Murphy BF, Silvestri G, Skerka C, Jozsi M, Zipfel PF, Hageman GS, Smith RJ.
J Med Genet. 2006 43 (7): 582-9.
47. Mycoplasma pneumoniae detection with PCR in renal tissue of a patients with acute glomerulonephritis.
Del Carmen Laso M, Cadario ME, Haymes L, Grimoldi I, Balbarrey Z, Casanueva E.
Pediatr Nephrol. 2006 Jul 4; [Epub ahead of print]
48. Relationship between PAI-1 gene 4G/5G polymorphism and clinical profile of IgA nephropathy.
Ding R, Chen X, Liu S, Lv Y, Wu J.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2006 (4): 449-51.
49. Impact of selectin gene polymorphisms on rapid progression to end-stage renal disease in patients with IgA nephropathy.
Watanabe Y, Inoue T, Okada H, Kotaki S, Kanno Y, Kikuta T, Suzuki H.
Intern Med. 2006 45 (16): 947-51.
50. Association of uteroglobin G38A polymorphism with IgA nephropathy: A meta-analysis.
Yong D, QingQing W, Hua L, Yang LX, QingLing Z, Ying H, QiaoJing Q, HanChao S.
Am J Kidney Dis. 2006 48 (1): 1-7.
51. Roles of TGF-beta1 and apoptosis in the progression of glomerulosclerosis in human IgA nephropathy.
Chihara Y, Ono H, Ishimitsu T, Ono Y, Ishikawa K, Rakugi H, Ogihara T, Matsuoka H.
Clin Nephrol. 2006 65 (6): 385-92.
52. Histological differences in newly onset IgA nephropathy between children and adults.
Ikezumi Y, Suzuki T, Imai N, Ueno M, Narita I, Kawachi H, Shimizu F, Nikolic-Paterson DJ, Uchiyama M.
Nephrol Dial Transplant. 2006 Aug 25; [Epub ahead of print]
53. 24h ambulatory blood pressure is linked to chromosome 18q21-22 and genetic variation of NEDD4L associates with cross-sectional and longitudinal blood pressure in Swedes.
Fava C, von Wowern F, Berglund G, Carlson J, Hedblad B, Rosberg L, Burri P, Almgren P, Melander O.
Kideny Int. 2006 Jun 21; [Epub ahead of print]
54. Research into the glomerular podocyte – is it relevant to diabetic nephropathy?
White KE.
Diabet Med. 2006 23 (7): 715-9.
55. A disease haplotype for advanced nephropathy in type 2 diabetes at the ACE locus.
Ng DP, Placha G, Choo S, Chia KS, Warram JH, Krolewski AS.
Diabetes. 2006 55 (9): 2660-3.
56. Impact of renin-angiotensin system modulation on the hyperfiltration state in type 1 diabetes.
Sochett EB, Cherney DZ, Curtis JR, Dekker MG, Scholey JW, Miller JA.
J Am Soc Nephrol. 2006 17 (6): 1703-9.
57. The relationship between genetic and haemodynamic factors in diabetic nephropathy (DN): Case-control study in type 1 diabetes mellitus (T1DM).
Shestakova MV, Vikulova OK, Gorashko NM, Voronko OE, Babunova NB, Nosikov VV, Dedov II.
Diabetes Res Clin Pract. 2006 Jul 24; [Epub ahead of print]
58. Connective tissue growth factor plays an important role in advanced glycation end product-induced tubular epithelial-to-mesenchymal transition: Implications for diabetic renal disease.
Burns WC, Twigg SM, Forbes JM, Pete J, Tikellis C, Thallas-Bonke V, Thomas MC, Cooper ME, Kantharidis P.
J Am Soc Nephrol. 2006 17 (9): 2484-94.
59. Aberrant heparan sulfate profile in the human diabetic kidney offers new clues for therapeutic glycomimetics.
Wijnhoven TJ, Lensen JF, Rops AL, van der Vlag J, Kolset SO, Bangstad HJ, Pfeffer P, van den Hoven MJ, Berden JH, van den Heuvel LP, van Kuppevelt TH.
Am J Kidney Dis. 2006 48 (2): 250-61.
60. Association of lipoprotein lipase S447X, apolipoprotein E exon 4, apoC3 -455T>C polymorphisms on the susceptibility to diabetic nephropathy.
Ng M, Baum L, So WY, Lam V, Wang Y, Poon E, Tomlinson B, Cheng S, Lindpaintner K, Chan J.
Clin Genet. 2006 70 (1): 20-8.
61. MTHFR C677T and A1298C gene polymorphisms and hyperhomocysteinemia as risk factors of diabetic nephropathy in type 2 diabetes patients.
Mtiraoui N, Ezzidi I, Chaieb M, Marmouche H, Aouni Z, Chaieb A, Mahjoub T,Vaxillaire M, Almawi WY.
Diabetes Res Clin Pract. 2006 Jul 4; [Epub ahead of print]
62. Redistribution of connexin43 expression in glomerular podocytes predicts poor renal prognosis in patients with type 2 diabetes and overt nephropathy.
Sawai K, Mukoyama M, Mori K, Yokoi H, Koshikawa M, Yoshioka T, Takeda R, Sugawara A, Kuwahara T, Saleem MA, Ogawa O, Nakao K.
Nephrol Dial Transplant. 2006 Jul 4; [Epub ahead of print]
63. ADMA, proteinuria, and insulin resistance in non-diabetic stage I chronic kidney disease.
Caglar K, Yilmaz MI, Sonmez A, Cakir E, Kaya A, Acikel C, Eyileten T, Yenicesu M, Oguz Y, Bilgi C, Oktenli C, Vural A, Zoccali C.
Kidney Int. 2006 Jul 5; [Epub ahead of print]
64. Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes.
Sampson MJ, Hughes DA.
Diabetologia. 2006 49 (8): 1726-31.
65. Lipotoxicity.
Weinberg JM.
Kidney Int. 2006 Sep 6; [Epub ahead of print]
66. Alterations of uromodulin biology: a common denominator of the genetically heterogenous FJHN/MCKD syndrome.
Vylet’al P, Kublova M, Kalbacova M, Hodanova K, Baresova V, Stiburkova B, Sikora J, Hulkova H, Zivny J, Majewski J, Simmonds A, Fryns JP, Venkat-Raman G, Elleder M, Kmoch S.
Kidney Int. 2006 70 (6): 1155-69.
67. Update on HIV-associated nephropathy.
Shah SN, He CJ, Klotman P.
Curr Opin Nephrol Hypertens. 2006 15 (4): 450-5
68. Quantitative imaging of basic functions in renal (patho) physiology.
Kang JJ, Toma I, Sipos A, McCulloch F, Peti-Peterdi J.
Am J Physiol Renal Physiol. 2006 291 (2): F495-502.
III. CLINICAL PRESENTATION
1. Cardiovascular biomarkers in CKD: Pathophysiology and implications for clinical management of cardiac disease.
Roberts MA, Hare DL, Ratnaike S, Ierino FL.
Am J Kidney Dis. 2006 48 (3): 341-60.
2. Impaired basal NO activity in patients with glomerular disease and the influence of oxidative stress.
Schaufele TG, Schlaich MP, Delles C, Klingbeil AU, Fleischmann EH, Schmieder RE.
Kidney Int. 2006 Aug 2; [Epub ahead of print]
3. Microalbuminuria as an early marker for cardiovascular disease.
De Zeeuw D, Parving HH, Henning RH.
J Am Soc Nephrol. 2006 17 (8): 2100-5.
4. Macroalbuminuria is a better risk marker than low estimated GFR to identify individuals at risk for accelerated GFR loss in population based screening.
Halbesma N, Kuiken DS, Brantsma AH, Bakker SJ, Wetzels JF, De Zeeuw D, De Jong PE, Gansevoort RT.
J Am Soc Nephrol. 2006 Aug 9; [Epub ahead of print]
5. Adiponectin and mortality in patients with chronic kidney disease.
Menon V, Li L, Wang X, Greene T, Balakrishnan V, Madero M, Pereira AA, Beck GJ, Kusek JW, Collins AJ, Levey AS, Sarnak MJ.
J Am Soc Nephrol. 2006 Aug 2; [Epub ahead of print]
6. The urinary activity of angiotensin-converting enzyme in preterm, full-term newborns, and children.
Lopes Del Ben G, Redublo Quinto BM, Casarini DE, Bueno Ferreira LC, Sousa Ayres S, de Abreu Carvalhaes JT.
Pediatr Nephrol. 2006 21 (8): 1138-43.
7. Clinical characteristics of chronic kidney disease patients with and without diabetes: A subanalysis of the PAERI study.
Lorber D, Reddan D.
Clin Nephrol. 2006 66 (1): 11-6.
8. Chronic kidney disease in long-term survivors of hematopoietic cell transplantation: Epidemiology, pathogenesis, and treatment.
Hingorani S.
J Am Soc Nephrol. 2006 17 (7): 1995-2005.
9. Coeliac disease and risk of renal disease - - a general population cohort study.
Ludvigsson JF, Montogomery SM, Olen O, Ekbom A, Ludvigsson J, Fored M.
Nephrol Dial Transplant. 2006 21 (7): 1809-15.
10. WT1 mutations in nephrotic syndrome revisited. High prevalence in young girls, associations and renal phenotypes.
Aucella F, Bisceglia L, De Bonis P, Gigante M, Caridi G, Barbano G, Mattioli G, Perfumo F, Gesualdo L, Ghiggeri GM.
Pediatr Nephrol. 2006 Aug 15; [Epub ahead of print]
11. Low protein Z levels in children with nephrotic syndrome.
Ozkaya O, Bek K, Fisgin T, Aliyazicioglu Y, Sultansuyu S, Acikgoz Y, Albayrak D, Baysal K.
Pediatr Nephrol. 2005 21 (8): 1122-6.
12. Urine proteomic profiling of pediatric nephrotic syndrome.
Khurana M, Traum AZ, Aivado M, Wells MP, Guerrero M, Grall F, Libermann TA, Schachter AD.
Pediatr Nephrol. 2006 Jun 30; [Epub ahead of print]
13. Urinary proteome of steroid-sensitive and steroid resistant idiopathic nephrotic syndrome of childhood.
Woroniecki RP, Orlova TN, Mendelev N, Shatat IF, Hailpern SM, Kaskel FJ, Goligorsky MS, O’riordan E.
Am J Nephrol. 2006 26 (3): 258-67.
14. Expression of P-glycoprotein in lymphocytes from children with nephrotic syndrome, depending on their steroid response.
Wasilewska A, Zoch-Zwierz W, Pietruczuk M, Zalewski G.
Pediatr Nephrol. 2006 Jun 8; [Epub ahead of print]
15. Nephrotic syndrome in a child after umbilical-cord-blood transplantation.
Lee JH, Kwon BS, Ha IS, Cheong HI, Moon KC, Ahn HS, Choi Y.
Pediatr Nephrol. 2006 Jun 22; [Epub ahead of print]
16. Steroid-responsive nephrotic syndrome in a patient with nail-patella syndrome.
Hari P, Mantan M, Dinda A, Hari S, Bagga A.
Pediatr Nephrol. 2006 21 (8): 1197-9.
17. The role of 99mTc DMSA renal scintigraphy in Joubert syndrome.
Kara Gedik G, Lay Ergun E, Fani Bozkurt M.
Rev Esp Med Nucl. 2006 25 (4): 258-62.
18. IgA nephropathy in two adolescent sisters heterozygous for Fabry disease.
Whybra C, Schwarting A, Kriegsmann J, Gal A, Mengel E, Kampmann C, Baehner F, Schaefer E, Beck M.
Pediatr Nephrol. 2006 Jul 13; [Epub ahead of print]
19. Prognosis of lupus membranous nephropathy in children.
Nathanson S, Salomon R, Ranchin B, Macher MA, Lavocat MP, Krier MJ, Baudouin V, Azema C, Bader-Meunier B, Deschenes G.
Pediatr Nephrol. 2006 21 (8): 1113-6.
20. Prognostic factors in lupus nephritis: Diagnostic and therapeutic delay increases the risk of terminal renal failure.
Faurschou M, Starklint H, Halberg P, Jacobsen S.
J Rheumatol. 2006 33 (8): 1563-9.
21. Lupus nephritis im Chinese children - A terrritory-wide chort study in Hong Kong.
Wong SN, Tse KC, Lee TL, Lee KW, Chim S, Lee KP, Wai-Po Chu R, Chan W, Fong KW, Hui J, Po-Siu Li S, Yeung PS, Yuen SF, Chi-Hang Ho A, Chuk-Kwan Leung L, Luk D, Chan SY, Cheung HM, Chow CM, Lau D.
Pediatr Nephrol. 2006 21 (8): 1104-12.
22. Full-house nephropathy in a patient with negative serology for lupus.
Baskin E, Agras PI, Menekse N, Ozdemir H, Cengiz N.
Rheumatol Int. 2006 Sep 14; [Epub ahead of print]
23. Lupus nephropathy and cardiopulmonary and hepatic dysfunctions in a child.
Olowu WA.
Pediatr Nephrol. 2006 Jul 4; [Epub ahead of print]
24. Strongyloides stercoralis hyperinfection in systemic lupus erythematosus and the antiphospholipid syndrome.
Mora CS, Segami MI, Hidalgo JA.
Semin Arthritis Rheum. 2006 Aug 30; [Epub ahead of print]
25. Fanconi’s syndrome and distal (type 1) renal tubular acidosis in a patient with primary Sjogren’s syndrome with monoclonal gammopathy of undetermined significance.
Kobayashi T, Muto S, Nemoto J, Miyata Y, Ishiharajima S, Hironaka M, Asano Y, Kusano E.
Clin Nephrol. 2006 65 (6): 427-32.
26. Myeloma renal disease: Presentation and outcome.
Chan DT, Craig K, Donovan K, Phillips A.
Nephron Clin Pract. 2006 104 (3): c126-31.
27. Hyper-IgE syndrome and autoimmunity in Mexican children.
Yamazaki-Nakashimada M, Zaltzman-Girshevich S, Garcia de la Puente S, De Leon-Bojorge B, Espinosa-Padilla S, Saez-de-Ocariz M, Carrasco-Daza D, Hernandez-Bautista V, Perez-Fernandez L, Espinosa-Rosales F.
Pediatr Nephrol. 2006 21 (8): 1200-5.
28. Proliferative glomerulonephritis and primary antiphospholipid syndrome.
Abdalla AH, Kfoury HK, Al-Suleiman M, Al-Khader AA.
Saudi Med J. 2006 27 (7): 1063-5.
29. Clinical and histologic determinants of renal outcome in ANCA-associated vasculitis: A prospective analysis of 100 patients with severe renal involvement.
de Lind van Wijngaarden RA, Hauer HA, Wolterbeek R, Jayne DR, Gaskin G, Rasmussen N, Noel LH, Ferrario F, Waldherr R, Hagen EC, Bruijn JA, Bajema IM.
J Am Soc Nephrol. 2006 17 (8): 2264-74.
30. A new international classification of childhood vasculitis.
Dillon MJ, Ozen S.
Pediatr Nephrol. 2006 Jul 4; [Epub ahead of print]
31. EULAR/PReS endorsed consensus criteria for the classification of childhood vasculitides.
Ozen S, Ruperto N, Dillon MJ, Bagga A, Barron K, Davin JC, Kawasaki T, Lindsley C, Petty RE, Prieur AM, Ravelli A, Woo P.
Ann Rheum Dis. 2006 65 (7): 936-41.
32. Antineutrophil cytoplasmic antibody-positive crescentic glomerulonephritis in scleroderma - A different kind of renal crisis.
Kamen DL, Wigley FM, Brown AN.
J Rheumatol. 2006 33 (9): 1886-8.
33. Nephropathy, polyneuropathy, and gastroenteritis in a child with Churg-Strauss syndrome.
Olowu WA.
Clin Rheumatol. 2006 Aug 2; [Epub ahead of print]
34. Micrsocopic polyangiitis associated with primary biliary cirrhosis: A causal or casual association?
Amezcua-Guerra LM, Prieto P, Bojalil R, Pineda C, Amigo MC.
J Rheumatol. 2006 Sep 15; [Epub ahead of print]
35. A case of Takayasu arteritis complicated with glomerulonephropathy mimicking membranoproliferative glomerulonephritis: A case report and review of the literature.
Kuroda T, Ueno M, Sato H, Murakami S, Sakatsume M, Nishi S, Nakano M, Gejyo F.
Rheumatol Int. 2006 Jul 8; [Epubahead of print]
36. PR3-ANCA-positive crescentic necrotizing glomerulonephritis accompained by isolated pulmonic valve infective endocarditis, with reference to previous reports of renal pathology.
Fukuda M, Motokawa M, Usami T, Oikawa T, Morozumi K, Yoshida A, Kimura G.
Clin Nephrol. 2006 66 (3): 202-9.
37. Minimal change nephrotic syndrome and classical Hodgkin’s lymphoma: Report of 21 cases and review of the literature.
Audard V, Larousserie F, Grimbert P, Abtahi M, Sotto JJ, Delmer A, Boue F, Nochy D, Brousse N, Delarue R, Remy P, Ronco P, Sahali D, Lang P, Hermine O.
Kidney Int. 2006 69 (12): 2251-60.
38. Minimal change disease following exposure to mercury-containing skin lightening cream.
Tang HL, Chu KH, Mak YF, Lee W, Cheuk A, Yim KF, Fung KS, Chan HW, Tong KL.
Hong Kong Med J. 2006 12 (4): 316-8.
39. Predictive factors of chronic kidney disease in primary focal segmental glomerulosclerosis.
Abrantes MM, Cardoso LS, Lima EM, Penido Silva JM, Diniz JS, Bambirra EA, Oliveira EA.
Pediatr Nephrol. 2006 21 (7): 1003-12.
40. C1q nephropathy in association with Gitelman syndrome: A case report.
Hanevold C, Mian A, Dalton R.
Pediatr Nephrol. 2006 Sep 6; [Epub ahead of print]
41. Idiopathic membranous nephropathy in children.
Lee BH, Cho HY, Kang HG, Ha IS, Cheong HI, Moon KC, Lim IS, Choi Y.
Pediatr Nephrol. 2006 21 (11): 1707-15.
42. Acute renal failure due to IgM-lambda glomerular thrombi and MPGN-like lesions in a patient with angioimmunoblastic T-cell lymphoma.
Miura N, Suzuki K, Yoshino M, Kitagawa W, Yamada H, Ohtani H, Joh K, Imai H.
Am J Kidney Dis. 2006 48 (1): e3-9.
43. Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II).
Licht C, Heinen S, Jozsi M, Loschmann I, Saunders RE, Perkins SJ, Waldherr L, Skerka C, Kirschfink M, Hoppe B, Zipfel PF.
Kidney Int. 2006 70 (1): 42-50.
44. Long-term outcome 19 years after childhood IgA nephritis: A retrospective cohort study.
Ronkainen J, Ala-Houhala M, Autio-Harmainen H, Jahnukainen T, Koskimies O, Merenmies J, Mustonen J, Ormala T, Turtinen J, Nuutinen M.
Pediatr Nephrol. 2006 21 (9): 1266-73.
45. A scoring system to predict renal outcome in IgA nephropathy: From a nationwide prospective study.
Wakai K, Kawamura T, Endoh M, Kojima M, Tomino Y, Tamakoshi A, Ohno Y, Inaba Y, Sakai H.
Nephrol Dial Transplant. 2006 Jul 5; [Epub ahead of print]
46. IgA-containing immune complexes in the urine of IgA nephropathy patients.
Matousovic K, Novak J, Yanagihara T, Tomana M, Moldoveanu Z, Kulhavy R, Julian BA, Konecny K, Mestecky J.
Nephrol Dial Transplant. 2006 21 (9): 2478-84.
47. Cholestatic jaundice and IgA nephropathy induced by OTC muscle building agent Superdrol.
Jasiurkowski B, Raj J, Wisinger D, Carlson R, Zou L, Nadir A.
Am J Gastroenterol. 2006 Sep 4; [Epub ahead of print]
48. The –374 T/A polymorphism in the gene encoding RAGE is associated with diabetic nephropathy and retinopathy in type 1 diabetic patients.
Lindholm E, Bakhtadte E, Sjogren M, Cilio CM, Agardh E, Groop L, Agardh CD.
Diabetologia. 2006 Sep 13; [Epub ahead of print]
49. Association between serum levels of soluble receptor for advanced glycation end products and circulating advanced glycation end products in type 2 diabetes.
Tan KC, Shiu SW, Chow WS, Leng L, Bucala R, Betteridge DJ.
Diabetologia. 2006 Sep 13; [Epub ahead of print]
50. Urinary tumour necrosis factor-{alpha} excretion independently correlates with clinical markers of glomerular and tubulointerstitial injury in type 2 diabetic patients.
Navarro JF, Mora C, Muros M, Garcia J.
Nephrol Dial Transplant. 2006 Aug 25; [Epub ahead of print]
51. Redistribution of connexin43 expression in glomerular podocytes predicts poor renal prognosis in patients with type 2 diabetes and overt nephropathy.
Sawai K, Mukoyama M, Mori K, Yokoi H, Koshikawa M, Yoshioka T, Takeda R, Sugawara A, Kuwahara T, Saleem MA, Ogawa O, Nakao K.
Nephrol Dial Transplant. 2006 21 (9): 2472-7.
52. Vascular defect beyond the endothelium in type II diabetic patients with overt nephropathy and moderate renal insufficiency.
Chan WB, Chan NN, Lai CW, So WY, Lo MK, Lee KF, Chow CC, Metreweli C Chan JC.
Kidney Int. 2006 70 (4): 711-6.
53. Clinical characteristics of chronic kidney disease patients with and without diabetes: A subanalysis of the PAERI study.
Lorber D, Reddan D.
Clin Nephrol. 2006 66 (1): 11-6.
54. Management of cardiovascular risk factors in advanced type 2 diabetic nephropathy: A comparative analysis in nephrology, diabetology and primary care settings.
Minutolo R, Sasso FC, Chiodini P, Cianciaruso B, Carbonara O, Zamboli P, Tirino G, Pota A, Torella R, Conte G, Nicola LD.
J Hypertens. 2006 24 (8): 1655-61.
55. Homocysteine and vitamin B (12) concentrations and mortality rates in type 2 diabetes.
Looker HC, Fagot-Campagna A, Gunter EW, Pfeiffer CM, Sievers ML, Benneth PH, Nelson RG, Hanson RL, Knowler WC.
Diabetes Metab Res Rev. 2006 Jul 17; [Epub ahead of print]
56. Possible relationship between adiponectin and renal tubular injury in diabetic nephropathy.
Fujita H, Morii T, Koshimura J, Ishikawa M, Kato M, Miura T, Sasaki H, Narita T, Ito S, Kakei M.
Endocr J. 2006 Sep 12; [Epub ahead of print]
57. A classification of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura and related disorders.
Besbas N, Karpman D, Landau D, Loirat C, Proesmans W, Remuzzi G, Rizzoni G, Taylor CM, Van de Kar N, Zimmerhackl LB.
Kidney Int. 2006 Jun 14; [Epub ahead of print]
58. Urinary neutrophil gelatinase-associated lipocalcin in D+HUS: A novel marker of renal injury.
Trachtman H, Christen E, Cnaan A, Patrick J, Mai V, Mishra J, Jain A, Bullington N, Devarajan P; Investigators of the HUS-SYNSORB Pk Multicenter Clinical Trial.
Pediatr Nephrol. 2006 21 (7): 989-94.
59. Glomerular involvement in adults with sickle cell hemoglobinopathies: Prevalence and clinical correlates of progressive renal failure.
Guasch A, Navarrete J, Nass K, Zayas CF.
J Am Soc Nephrol. 2006 17 (8): 2228-35.
60. Autosomal dominant Alport’s syndrome: Study of a large Tunisian family.
Kharrat M, Makni S, Makni K, Kammoun K, Charfeddine K, Azaeiz H, Jarraya F, Ben Hmida M, Gubler MC, Ayadi H, Hachicha J.
Saudi J Kidney Dis Transpl. 2006 17 (3): 320-5.
61. Hereditary periodic fever with systemic amyloidosis: Is hyper-IgD syndrome really a benign disease?
Siewert R, Ferber J, Horstmann RD, Specker C, Heering PJ, Timann C.
Am J Kidney Dis. 2006 48 (3): e41-5.
62. A case of Weber-Christian disease with collapsing glomerulopathy.
Nahar N, Pardo V, Sadhu S, Young L, Gonzalez N, Jaimes EA.
Am J Kidney Dis. 2006 48 (3): 484-8.
63. Mesangial proliferative glomerulonephritis after autologous stem cell transplantation.
Forslund T, Anttinen J, Hallman H, Heinonen K, Pitkanen R.
Am J Kidney Dis. 2006 48 (2): 314-20.
64. Polyclonal IgG4 hypergammaglobulinemia associated with plasmatic lymphadenopathy, anemia and nephropathy.
Boulanger E, Fuentes V, Meignin V, Mougenot B, Labaume S, Gouilleux-Gruart V, Cogne M, Aucouturier P, Clauvel JP, Ronco P, Lassoued K.
Ann Hematol. 2006 Jul 27; [Epub ahead of print]
65. Ten-year prognosis of Puumala hantavirus-induced acute interstitial nephritis.
Miettinen MH, Makela SM, Ala-Houhala IO, Huhtala HS, Koobi T, Vaheri AI, Pasternack AI, Porsti IH, Mustonen JT.
Kidney Int. 2006 69 (11): 2043-8.
66. Symmetric dimethylarginine (SDMA) as endogenous marker of renal function- -A meta-analysis.
Kielstein JT, Salpeter SL, Bode-Boeger SM, Cooke JP, Fliser D.
Nephrol Dial Transplant. 2006 Jul 4; [Epub ahead of print]
67. Cystatin C, kidney function and cardiovascular disease.
Bokenkamp A, Herget-Rosenthal S, Bokenkamp R.
Pediatr Nephrol. 2006 Jul 13; [Epub ahead of print]
68. GFR is better estimated by considering both serum cystatin C and creatinine levels.
Bouvet Y, Bouissou F, Coulais Y, Seronie-Vivien S, Tafani M, Decramer S, Chatelut E.
Pediatr Nephrol. 2006 Jul 22; [Epub ahead of print]
69. Outpatient versus inpatient renal biopsy: A retrospective study.
Lin WC, Yang Y, Wen YK, Chang CC.
Clin Nephrol. 2006 66 (1): 17-24.
70. Mortality after acute renal failure: Models for prognostic stratification and risk adjusment.
Chertow GM, Soroko SH, Paganini EP, Cho KC, Himmelfarb J, Ikizler TA, Mehta RL.
Kidney Int. 2006 Jul 19; [Epub ahead of print]
71. Comparison of 2 acute renal failure severity scores to general scoring systems in the critically ill.
Ahlstrom A, Kuitunen A, Peltonen S, Hynnien M, Tallgren M, Aaltonen J, Pettila V.
Am J Kidney Dis. 2006 48 (2): 262-8.
72. Validity of International Classification of Diseases, Ninth Revision, Clinical Modification codes for Acute Renal Failure.
Waikar SS, Wald R, Chertow GM, Curhan GC, Winkelmayer WC, Liangos O, Sosa MA, Jaber BL.
J Am Soc Nephrol. 2006 17 (6): 1688-94.
73. Childhood acute renal failure: 22-year experience in a university hospital in southern Thailand.
Vachvanichsanong P, Dissaneewate P, Lim A, McNeil E.
Pediatrics. 2006 Aug 7; [Epub ahead of print]
74. Neutrophil-gelatinase-associated lipocalin and renal function after percutaneous coronary interventions.
Bachorzewska-Gajewska H, Malyszko J, Sitniewska E, Malyszko JS, Dobrzycki S.
Am J Nephrol. 2006 26 (3): 287-92.
75. Acute renal failure with acyclovir in a 42-year-old patient without previous renal dysfunction.
De Deyne S, De la Gastine B, Gras G, Dargere S, Verdon R, Coquerel A.
Rev Med Interne. 2006 Jun 27; [Epub ahead of print]
IV. TREATMENT
1. Effect of fosinopril in children with steroid-resistant idiopathic nephrotic syndrome.
Yi Z, Li Z, Wu XC, He QN, Dang XQ, He XJ.
Pediatr Nephrol. 2006 21 (7): 967-72.
2. Mesangial hypercellularity predicts antiproteinuric response to dual blockade of RAS in primary glomerulonephritis.
Minutulo R, Balletta MM, Catapano F, Chiodini P, Tirino G, Zamboli P, Fuiano G, Russo D, Marotta P, Iodice C, Conte G, De Nicola L.
Kidney Int. 2006 70 (6): 1170-6.
3. Combination therapy with an angiotensin receptor blocker and an ACE inhibitor in proteinuric renal disease: A systemic review of the efficacy and safety data.
MacKinnon M, Shurraw S, Akbari A, Knoll GA, Jaffey J, Clark HD.
Am J Kidney Dis. 2006 48 (1): 8-20.
4. Rationale and design of a study to evaluate management of proteinuria in patients at high risk for vascular events: The IMPROVE trial.
Bakris GL, Ruilope L, Locatelli F, Ptaszynska A, Pieske B, Raz I, Voors AA, Dechamplain J, Weber MA.
J Hum Hypertens. 2006 20 (9): 693-700.
5. Add-on therapy with angiotensin II receptor 1 blocker in children with chronic kidney disease already treated with angiotensin-converting enzyme inhibitors.
Litwin M, Grenda R, Sladowska J, Antoniewicz J.
Pediatr Nephrol. 2006 Aug 15; [Epub ahead of print]
6. Antiproteinuric effect of losartan in non-diabetic renal disease is not dependent on ACE insertion/deletion polymorphism.
Park HC, Choi HY, Kim BS, Kang SW, Choi KH, Ha SK, Lee HY, Han DS.
Kidney Blood Press Res. 2006 29 (4): 216-24.
7. Gender differences in the renal response to renin-angiotensin system blockade.
Miller JA, Cherney DZ, Duncan JA, Lai V, Burns KD, Kennedy CR, Zimpelmann J, Gao W, Cattran DC, Scholey JW.
J Am Soc Nephrol. 2006 Aug 16; [Epub ahead of print]
8. Candesartan cilexetil in children with hypertension or proteinuria: Preliminary data.
Child Project; Simonetti GD, von Vigier RO, Konrad M, Rizzi M, Fossali E, Bianchetti MG.
Pediatr Nephrol. 2006 Jun 27; [Epub ahead of print]
9. Comparison between valsartan and valsartan plus cilnidipine in type II diabetics with normo- and microalbuminuria.
Katayama K, Nomura S, Ishikawa H, Murata T, Koyabu S, Nakano T.
Kidney Int. 2006 70 (1): 151-6.
10. Role of endothelin and endothelin receptor antagonists in renal disease.
Neuhofer W, Pittrow D.
Eur J Clin Invest. 2006 36 (Suppl 3): 78-88.
11. Statins for diabetic cardiovascular complications.
Ludwig S, Shen GX.
Curr Vasc Pharmacol. 2006 4 (3): 245-51.
12. Simvastatin maintains steady patterns of GFR and improves AER and expression of slit diaphragm proteins in type II diabetes.
Tonolo G, Velussi M, Brocco E, Abaterusso C, Carraro A, Morgia G, Satta A, Faedda R, Abhyankar A, Luthman H, Nosadini R.
Kidney Int. 2006 70 (1): 177-86.
13. Protection of the kidney by thiazolidinediones: An assessment from bench to bedside.
Sarafidis PA, Bakris GL.
Kidney Int. 2006 Aug 2; [Epub ahead of print]
14. Effect of pioglitazone on urinary liver-type fatty acid-binding protein concentrations in diabetes patients with microalbuminuria.
Nakamura T, Sugaya T, Kawagoe Y, Ueda Y, Koide H.
Diabetes Metab Res Rev. 2006 22 (5): 385-9
15. Effect of 15d-PGJ (2) on the expression of CD40 and RANTES induced by IFN-gamma and TNF-alpha on renal tubular epithelial cells (HK-2).
Zhang YJ, Yang X, Kong QY, Zhang YF, Chen WY, Dong XQ, Li XY, Yu XQ.
Am J Nephrol. 2006 26 (4): 356-62.
16. Long-term treatment with EPO increases serum levels of high-density lipoprotein in patients with CKD.
Siamopoulos KC, Gouva C, Katopodis KP, Tzallas C, Nikolopoulos P, Papavasiliou EC, Tselepis AD.
Am J Kidney Dis. 2006 48 (2): 242-9.
17. Modulating the progression in IgA nephropathy.
Chan JC, Trachtman H.
Nephron Clin Pract. 2006 104 (1): c61-8.
18. Pharmacodynamics and pharmacokinetics of the urotensin II receptor antagonist palosuran in macroalbuminuric, diabetic patients.
Sidharta PN, Wagner FD, Bohnemeier H, Jungnik A, Halabi A, Krahenbuhl S, Chadha-Boreham H, Dingemanse J.
Clin Pharmacol Ther. 2006 80 (3): 246-56.
19. Effects of pentoxyfylline on the urinary protein excretion profile of type 2 diabetic patients with microproteinuria. A double-blind, placebo-controlled randomized trial.
Rodríguez-Morán M, González-Gomnzález G, Bermúdez-Barba MV, Medina de la Garza CE, Tamez-Pérez HE, Martínez-Martínez FJ, Guerrero-Romero F.
Clin Nephrol. 2006 66 (1): 3-10.
20. Enzyme replacement therapy and renal function in 201 patients with Fabry disease.
Schwarting A, Dehout F, Feriozzi S, Beck M, Mehta A, Sunder-Plassmann G. on behalf of the European FOS Investigators.
Clin Nephrol. 2006 66 (2): 77-84.
21. Iloprost for prevention of contrast-mediated nephropathy in high-risk patients undergoing a coronary precedure. Results of a randomized pilot study.
Spargias K, Adreanides E, Giamouzis G, Karagiannis S, Gouziouta A, Manginas A, Voudris V, Pavlides G, Cokkinos DV.
Eur J Clin Pharmacol. 2006 62 (8): 589-95.
22. Role of carbon monoxide and biliverdin in renal ischemia/reperfusion injury.
Li Volti G, Rodella LF, Di Giacomo C, Rezzani R, Bianchi R, Borsani E, Gazzolo D, Motterlini R.
Nephron Exp Nephrol. 2006 104 (4): e135-9.
23. Update on the treatment of lupus nephritis.
Waldman M, Appel GB.
Kidney Int. 2006 Aug 23; [Epub ahead of print]
24. Azathioprine/methylprednisolone versus cyclophosphamide in proliferative lupus nephritis. A randomized controlled trial.
Grootscholten C, Ligtenberg G, Hagen EC, van den Wall Bake AW, de Glas-Vos JW, Bijl M, Assmann KJ, Bruijn JA, Weening JJ, van Houwelingen HC, Derksen RH, Berden JH.
Kidney Int. 2006 70 (4): 732-42.
25. Long-term mizoribine intermittent pulse therapy for young patients with flare of lupus nephritis.
Tanaka H, Tsugawa K, Suzuki K, Nakahata T, Ito E.
Pediatr Nephrol. 2006 21 (7): 962-6.
26. Pathogenesis and treatment of systemic lupus erythematosus nephritis.
Davidson A, Aranow C.
Curr Opin Rheumatol. 2006 18 (5): 468-75.
27. Direct effects of dexamethasone on human podocytes.
Xing CY, Saleem MA, Coward RJ, Ni L, Witherden IR, Mathieson PW.
Kidney Int. 2006 Jul 12; [Epub ahead of print]
28. Complete remission of minimal-change nephrotic syndrome by apheresis monotherapy.
Kobayashi T, Ando Y, Umino T, Miyata Y, Muto S, Hironaka M, Asano Y, Kusano E.
Clin Nephrol. 2006 65 (6): 423-6.
29. Immunosuppressive treatment of idiopathic focal segmental glomerulosclerosis: A five-year follow-up study.
Goumenos DS, Tsagalis G, El Nahas AM, Shortland JR, Davlouros P, Vlachojannis JG, Brown CB.
Nephron Clin Pract. 2006 104 (2): c75-82.
30. Cyclosporin-A in the treatment of nephrotic syndrome: The importance of monitoring C0 (trough) and C2 (two hours after its administration) blood levels.
Goumenos DS, Kalliakmani P, Tsakas S, Savidaki I, Vlachojannis JG.
Med Chem. 2006 2 (4): 391-3.
31. Induction and long-term treatment with cyclosporine in membranous nephropathy with the nephrotic syndrome.
Alexopoulos E, Papagianni A, Tsamelashvili M, Leontsini M, Memmos D.
Nephrol Dial Transplant. 2006 Sep 12; [Epub ahead of print]
32. Independent risk factors for chronic cyclosporine induced nephropathy in children with nephrotic syndrome.
Fujinaga S, Kaneko K, Muto T, Ohtomo Y, Murakami H, Yamashiro Y.
Arch Dis Child. 2006 91 (8): 666-70.
33. Steroid pulse therapy impaired endothelial function while increasing plasma high molecule adiponectin concentration in patients with IgA nephropathy.
Uchida HA, Nakamura Y, Kaihara M, Norii H, Hanayama Y, Sugiyama H, Maeshima Y, Yamasaki Y, Makino H.
Nephrol Dial Transplant. 2006 Sep 2, [Epub ahead of print]
34. Succesful therapeutic use of rituximab in refractory membranous glomerulonephritis.
Cobo M, Hernández D, Rodrigez C, Pérez-Tamajón L.
Clin Nephrol. 2006 66 (1): 54-7.
35. Tacrolimus in steroid-resistant and steroid-dependent nephrotic syndrome.
Westhoff TH, Schmidt S, Zidek W, Beige J, van der Giet M.
Clin Nephrol. 2006 65 (6): 393-400.
36. Meta-analysis: Anti-viral therapy of hepatitis B virus-associated glomerulonephritis.
Fabrizi F, Dixit V, Martin P.
Aliment Pharmacol Ther. 2006 24 (5): 781-8.
37. Nephrotoxicity as a complication of antiretroviral therapy.
Valle R, Haragsim L.
Adv Chronic Kidney Dis. 2006 13 (3): 314-9.
38. HIV-associated nephropathy.
Khan S, Haragsim L, Laszik ZG.
Adv Chronic Kidney Dis. 2006 13 (3): 307-13.
39. Antiretroviral therapy in the treatment of HIV-associated nephropathy.
Atta MG, Gallant JE, Hafizur Rahman M, Nagajothi N, Racusen LC, Scheel PJ, Fine DM.
Nephrol Dial Transplant. 2006 Jul 24; [Epub ahead of print]
40. FK506 in the treatment of children with nephrotic syndrome of different pathological types.
Xia Z, Liu Y, Gao Y, Fan Z, Fu Y, Zhang LF, Ren X, Gao C.
Clin Nephrol. 2006 66 (2): 85-8.
41. Modulator of bone morphogenetic protein activity in the progression of kidney diseases.
Yanagita M.
Kidney Int. 2006 70 (6): 989-93.
42. Effect of tranilast in early-stage diabetic nephropathy.
Soma J, Sato K, Saito H, Tsuchiya Y.
Nephrol Dial Transplant. 2006 Jul 4. [Epub ahead of print]
43. The management of tumor lysis syndrome.
Rampello R, Fricia T, Malaguarnera M.
Nat Clin Pract Oncol. 2006 3 (8): 438-47.
44. Isolation and characterization of multipotent progenitor cells from the Bowman’s capsule of adult human kidneys.
Sagrinati C, Netti GS, Mazzinghi B, Lazzeri E, Liotta F, Frosali F, Ronconi E, Meini C, Gacci M, Squecco R, Carini M, Gesualdo L, Francini F, Maggi E, Annunziato F, Lasagni L, Serio M, Romagnani S, Romagnani P.
J Am Soc Nephrol. 2006 Aug 2; [Epub ahead of print]
45. Regrow or repair: Potential regenerative therapies for the kidney.
Little MH.
J Am Soc Nephrol. 2006 Jul 26; [Epub ahead of print]
46. Secondary failure of plasma therapy in factor H deficiency.
Nathanson S, Ulinski T, Fremeaux-Bacchi V, Deschenes G.
Pediatr Nephrol. 2006 Aug 15; [Epub ahead of print]
47. Neutrophil gelatinase-associated lipocalin-mediated iron traffic in kidney epithelia.
Schmidt-Ott KM, Mori K, Kalandadze A, Li JY, Paragas N, Nicholas T, Devarajan P, Barasch J.
Curr Opin Nephrol Hypertens. 2006 15 (4): 442-9.
V. TRANSPLANTATION
1. Subclinical rejection impairs glomerular adaptation after renal transplantation.
Ibernon M, Goma M, Moreso F, Fulladosa X, Hueso M, Cruzado JM, Torras J, Bestard O, Grinyo JM, Seron D.
Kidney Int. 2006 70 (3): 557-61.
2. Experience with an organ procurement organization-based non-directed living kidney donation programme.
Mark PJ, Baker K, Aguayo C, Sorensen JB.
Clin Transplant. 2006 20 (4): 427-37.
3. Kidney transplantation without prior dialysis in children: The eurotransplant experience.
Cransberg K, Smits JM, Offner G, Nauta J, Persijn GG.
Am J Transplant. 2006 6 (8): 1858-64.
4. Reflux nephropathy in kidney transplants, demonstrated by dimercaptosuccinic acid scanning.
Coulthard MG, Keir MJ.
Transplantation. 2006 82 (2): 205-10.
5. Pediatric live-donor kidney transplantation in Mansoura Urology & Nephrology Center: A 28-year perspective.
El-Husseinin AA, Foda MA, Shokeir AA, Sobh MA, Ghonein MA.
Pediatr Nephrol. 2006 Jun 22; [Epub ahead of print]
6. The advantage of allocating kidneys from old cadaveric donors to old recipients: A single-center experience.
Bodingbauer M, Pakrah B, Steininger R, Berlakovich G, Rockenschaub S, Wekerle T, Muehlbacher F.
Clin Transplant. 2006 20 (4): 471-5.
7. Early posttransplant serum osteoprotegerin levels predict long-term (8-year) patient survival and cardiovascular death in renal transplant patients.
Hjelmesaeth J, Ueland T, Flyvbjerg A, Bollerslev J, Leivestad T, Jenssen T, Hansen TK, Thiel S, Sagedal S, Roislien J, Hartmann A.
J Am Soc Nephrol. 2006 17 (6): 1746-54.
8. Color Doppler ultrasonography in the diagnostic evaluation of renal allografts.
Schwenger V, Hinkel UP, Nahm AM, Morath C, Zeier M.
Nephron Clin Pract. 2006 104 (3): c107-12.
9. Agreement of immunosuppression regimens described in Medicare pharmacy claims with the Organ Procurement and Transplantation Network Survey.
Stirnemann PM, Takemoto SK, Schnitzler MA, Brennan DC, Abbott KC, Salvalaggio P, Burroughs TE, Gavard JA, Willoughby LM, Lentine KL.
J Am Soc Nephrol. 2006 Jul 6; [Epub ahead of print]
10. Effect of induction therapy protocols on transplant outcomes in crossmatch positive renal allograft recipients desensitized with IVIG.
Vo AA, Toyoda M, Peng A, Bunnapradist S, Lukovsky M, Jordan SC.
Am J Transplant. 2006 Jul 25; [Epub ahead of print]
11. Living donor transplantation using alemtuzumab induction and tacrolimus monotherapy.
Tan HP, Kaczorowski DJ, Basu A, Unruh M, McCauley J, Wu C, Donaldson J, Dvorchik I, Kayler L, Marcos A, Randhawa P, Smetanka C, Starzl TE, Shapiro R.
Am J Transplant. 2006 Aug 4; [Epub ahead of print]
12. Pharmacodynamics of rituximab in kidney allotransplantation.
Genberg H, Hansson A, Wernerson A, Wennberg L, Tyden G.
Am J Transplant. 2006 Aug 21; [Epub ahead of print]
13. Late corticosteroid withdrawal can be safely performed for kidney recipients with stable graft function under pathological confirmation.
Harada H, Miura M, Ogawa Y, Seki T, Taniguchi A, Takenouchi T, Togashi M, Hirano T.
Clin Transplant. 2006 Jul 20; [Epub ahead of print]
14. Steroid-free immunosuppression after renal transplantation - - long-term experience from a single centre.
El-Faramawi M, Rohr N, Jespersen B.
Nephrol Dial Transplant. 2006 21 (7): 1966-73.
15. Safety and efficacy of a calcineurin inhibitor avoidance regimen in pediatric renal transplantation.
Harmon W, Meyers K, Ingelfinger J, McDonald R, McIntosh M, Ho M, Spaneas L, Palmer JA, Hawk M, Geehan C, Tinckam K Hancock WW, Sayegh MH.
J Am Soc Nephrol. 2006 17 (6): 1735-45.
16. Long-term safety and efficacy after conversion of maintenance renal transplant recipients from mycophenolate mofetil (MMF) to enteric-coated mycophenolate sodium (EC-MPS), myfortic®).
Budde K, Knoll G, Curtis J, Chan L, Pohanka E, Gentil M, Seifu Y, Marrast A.-C, Neumayer H.-H on behalf of the ERL B302 Study Group.
Clin Nephrol. 2006 66 (2): 103-11.
17. Tacrolimus and quality of life after kidney transplantation - - A multicenter study.
Bohlke M, Rocha M, Gomes RH, Marini SS, Terhorst L, Barcellos FC, Hallal PC, Casarini D, Irigoyen MC.
Clin Transplant. 2006 20 (4): 504-8.
18. A prospective, randomized, multicenter trial of tacrolimus-based therapy with or without basiliximab in pediatric renal transplantation.
Grenda R, Watson A, Vondrak K, Beattie J, Fitzpatrick M, Saleem MA, Trompeter R, Milford DV, Moghal NE, Hughes D, Perner F, Friman S, Van Damme-Lombaerts R, Janssen F.
Am J Transplant. 2006. 6 (7): 1666-72.
19. Ketoconazole-tacrolimus coadministration in kidney transplant recipients: Two-year results of a prospective randomized study.
El-Dahshan KF, Bakr MA, Donia AF. Badr AE, Sobh MA.
Am J Nephrol. 2006 26 (3): 293-8.
20. Everolimus in clinical practice - - renal transplantation.
Pascual J.
Nephrol Dial Transplant. 2006 21 Suppl 3: iii18-23.
21. Potential role of proliferation signal inhibitors on atherosclerosis in renal transplant patients.
Andres V, Castro C, Campistol JM.
Nephrol Dial Transplant. 2006 21 (Suppl 3): iii14-7.
22. Treatment of erectile dysfunction with sildenafil citrate in renal allograft recipients: A randomized, double-blind, placebo-controlled, crossover trial.
Sharma RK, Prasad N, Gupta A, Kapoor R.
Am J Kidney Dis. 2006 48 (1): 128-33.
23. Soluble CD30 concentrations in ESRD patients with and without panel reactive HLA antibodies.
Vaidya S, Partlow D, Barnes T, Thomas P, Gugliuzza K.
Clin Transplant. 2006 20 (4): 461-4.
24. Late and early C4d-positive acute rejection: Different clinico-histopathological subentities in renal transplantation.
Sun Q, Liu ZH, Ji S, Chen J, Tang Z, Zeng C, Zheng C, Li LS.
Kidney Int. 2006 70 (2): 377-83.
25. Association of high pretransplant sIL-6R plasma levels with acute tubular necrosis in kidney graft recipients.
Sadeghi M, Daniel V, Naujokat C, Mehrabi A, Opelz G.
Transplantation. 2006 81 (12): 1716-24.
26. Noninvasive immune monitoring assessed by flow cytometry and real time RT-PCR in urine of renal transplantation recipients.
Galante NZ, Camara NO, Kallas EG, Salomao R, Pacheco-Silva A, Medina-Pestana JO.
Transpl Immunol. 2006 16 (2): 73-80.
27. Upregulation of ADAM19 in chronic allograft nephropathy.
Melenhorst WB, van den Heuvel MC, Stegeman CA, van der Leij J, Huitema S, van den Berg A, van Goor H.
Am J Transplant. 2006 6 (7): 1673-81.
28. Post-transplant sCD30 and neopterin as predictors of chronic allograft nephropathy: Impact of different immunosuppressive regimens.
Weimer R, Susal C, Yildiz S, Staak A, Pelzl S, Renner F, Dietrich H, Daniel V, Kamali-Ernst S, Ernst W, Padberg W, Opelz G.
Am J Transplant. 2006 6 (8): 1865-74.
29. Post-transplant anti-HLA class II antibodies as risk factor for late kidney allograft failure.
Campos EF, Tedesco-Silva H, Machado PG, Franco M, Medina-Pestana JO, Gerbase-Delima M.
Am J Transplant. 2006 Aug 21; [Epub ahead of print]
30. Adeno-associated virus-mediated CTLA4Ig gene transfer protects MHC-mismatched renal allografts from chronic rejection.
Benigni A, Tomasoni S, Turka LA, Longaretti L, Zentilin L, Mister M, Pezzotta A, Azzollini N, Noris M, Conti S, Abbate M, Giacca M, Remuzzi G.
J Am Soc Nephrol. 2006 17 (6): 1665-72.
31. Hepatocyte growth factor: New arsenal in the fights against renal fibrosis?
Liu Y, Yang J.
Kidney Int. 2006 70 (2): 238-40.
32. HGF gene therapy attenuates renal allograft scarring by preventing the profibrotic inflammatory-induced mechanisms.
Herrero-Fresneda I, Torras J, Franquesa M, Vidal A, Cruzado JM, Lloberas N, Fillat C, Grinyo JM.
Kidney Int. 2006 70 (2): 265-74.
33. Recurrent glomerulonephritis after kidney transplantation.
Choy BY, Chan TM, Lai KN.
Am J Transplant. 2006 Aug 29; [Epub ahead of print]
34. Secondary focal segmental glomerulosclerosis following kidney transplantation in a patient with type I diabetes mellitus.
Yamamoto I, Yamamoto H, Mitome J, Tanno Y, Utsunomiya Y, Miyazaki Y, Yamaguchi Y, Hosoya T.
Clin Transplant. 2006 20 Suppl (15): 7-10.
35. IL-6 promoter polymorphism -174 is associated with new-onset diabetes after transplantation.
Bamoulid J, Courivaud C, Deschamps M, Mercier P, Ferrand C, Penfornis A, Tiberghien P, Chalopin JM, Saas P, Ducloux D.
J Am Soc Nephrol. 2006 Jul 12; [Epub ahead of print]
36. Mineralocorticoid receptor blockade confers renoprotection in preexisting chronic cyclosporine nephrotoxicity.
Perez-Rojas J, Blanco JA, Cruz C, Trujillo J, Vaidya VS, Uribe N, Bonventre JV, Gamba G, Bobadilla NA.
Am J Physiol Renal Physiol. 2006 Jul 11; [Epub ahead of print]
37. Infectious complications after kidney transplantation: Current epidemiology and associated risk factors.
Alangaden GJ, Thyagarajan R, Gruber SA, Morawski K, Garnick J, El-Amm JM, West MS, Sillix DH, Chandrasekar PH, Haririan A.
Clin Transplant. 2006 20 (4): 401-9.
38. The prevalence of BK viremia and urinary viral shedding in a pediatric renal transplant population: A single-center retrospective analysis.
Alexander RT, Langlois V, Tellier R, Robinson L, Hebert D.
Pediatr Transplant. 2006 10 (5): 586-92.
39. Clinical utility of histological features of polyomavirus allograft nephropathy.
Gaber LW, Egidi MF, Stratta RJ, Lo A, Moore LW, Gaber AO.
Transplantation. 2006 82 (2): 196-204.
40. De novo gastrointestinal tumours after renal transplantation: Role of CMV and EBV viruses.
Adani GL, Baccarani U, Lorenzin D, Gropuzzo M, Tulissi P, Montanaro D, Curro G, Sainz M, Risaliti A, Bresadola V, Bresadola F.
Clin Transplant. 2006 20 (4): 457-60.
41. Reduction in chronic allograft nephropathy by inhibition of p38 mitogen-activated protein kinase.
Wada T, Azuma H, Furuichi K, Sakai N, Kitagawa K, Iwata Y, Matsushima K, Takahara S, Yokoyama H, Kaneko S.
Am J Nephrol. 2006 26 (4): 319-25.
..
C O N T E N T S
Part Two
SECTIONS
I. EPIDEMILOGY
II. ETIOPATHOGENESIS
III. CLINICAL PRESENTATION
IV. TREATMENT
V. TRANSPLANTATION
TITLE OF PUBLICATIONS – AUTHORS – SUMMARY OF PUBLICATIONS
..
Part Two
I. EPIDEMIOLOGY
1. DNA polymorphisms and renal disease: A critical appraisal of studies presented at the annual ERA/EDTA and ASN conferences in 2004 and 2005.
Mondry A, Loh M, Laurence KB et al.
Nephrol Dial Transplant. 2006 Jul 4; [Epub ahead of print]
Countless studies try to associate single DNA polymorphisms with disease, while there is growing evidence that many of these studies are of flawed design. Based on the Journal of the American Society of Nephrology (JASN) requirements for gene-disease association study quality, the abstracts presented at the two major international nephrology conferences in 2004 and 2005 organized by European Renal Association/European Dialysis and Transplantation Association (ERA/EDTA) and American Society of Nephrology (ASN) are analysed to show how this problem affects nephrology. Over time, average sample numbers have increased, as have the numbers of abstracts compliant with JASN requirements. This indicates a potential beneficial effect of the published stricter guidelines on study quality. Alternative options include pre-registration of studies in dedicated databases, secondary assessment of association studies through meta-analysis and participation in network approaches, such as Human Genome Epidemiology Network (HuGE Net) and the Renal Genome Network.
2. Lessons in ethnonephrology.
Hoy WE.
Kidney Int. 2006 70 (2): 251-7.
Only recently has the nephrology community moved beyond singular focus on terminal kidney failure to embrace population-based studies of early stages of disease, its markers and risk factors, and of interventions. Observations in developing countries, and in minority, migrant, and disadvantaged groups in westernized countries, have promoted these developments. We are only beginning to interpret renal disease in the context of public health history, social and health transitions, changing population demography, and competing mortality. Its intimate reletionships to other health issues are being progressively exposed. Perspectives on the multideterminant etiology of most disease and the pedestrian nature of most risk factors are maturing. We are challenged to reconcile epidemilogic patterns with morphology in diseased renal tissue, and to consider structural markers, such as nephron number and glomerular size, as determinants of disease susceptibility. New work force models are mandated for population-based studies and intervention programs. Intervention programs need to be integrated with other chronic disease initiatives and nested in a matrix of systematic pimary care, and although flexible to changing needs, must be sustained over the long term. Cross-disciplinary collaboration is essential in designing those programs, and in promoting them to health-care funders. Substatntial expansion and restructuring of the discipline is need for the nephrology community to participate effectively in those processes.
3. Racial disparities in the association between birth weight in the term infant and blood pressure at age 7 years: Results from the Collaborative Perinatal Project.
Hemachandra AH, Klebanoff MA, Furth SL.
J Am Soc Nephrol. 2006 Jul 26; [Epub ahead of print]
BP has been inversely associated with birth weight in studies worldwide, but few studies have included black individuals. The US National Collaborative Project followed 58,960 pregnant women and their resultant offspring for 7 yr. In this post hoc analysis, all term white or black children without kidney or heart disease were included (n = 29,710). The effect of birth weight and other risk factors on systolic (SBP) and diastolic BP (DBP) was evaluated at 7 yr. Mean birth weight and body mass index at 7 yr were slightly lower for black compared with white children (birth weight 3.14 +/- 0.48 versus 3.32 +/- 0.46 kg [P < 0.001]; body mass index 15.8 +/- 2.0 versus 16.3 +/- 2.0 [P < 0.001]). Compared with white mothers, black mothers were less likely to smoke (41 versus 52%), were more anemic (23 versus 7%), and were more likely to live in poverty (72 versus 39%). In linear regression, there was significant interaction between race and birth weight in predicting SBP (P = 0.002). In bivariate analysis, birth weight was positively associated SBP (beta = 0.87) and DBP (beta = 1.14) in black children (P < 0.001) but not associated with either in white children. With maternal poverty, educational level, and anemia during pregnancy added to the model, birth weight remained a significant positive predictor of SBP (beta = 0.89, P < 0.001) in black but not in white children (beta = 0.02, P = 0.17). The association between birth weight and SBP differs between black and white children. The cause of intrauterine growth restriction-associated hypertension seems to be race sensitive; therefore, future studies of racial disparities in the „Barker hypothesis” may help in the understanding of the mechanism of fetal programming of hypertension.
4. The enigma of hypertensive ESRD: Observation on incidence and trends in 18 European, Canadian, and Asian-Pacific populations, 1998 to 2002.
Stewart JH, McCredie MR, Williams SM et al.
Am J Kidney Dis. 2006 48 (2): 183-91.
Background Despite improved of hypertension and decreasing rates of stroke and coronary heart disease, the reported incidence of hypertensive end-stage renal disease (ESRD) increased during the 1990s. However, bias, particularly from variations in acceptance into ESRD treatment (ascertainment) and diagnosis (classification), has been a major source of error when comparing ESRD incidences or estimating trends. Methods Age-standardized rates were calculated in persons aged to 44, 45 to 64, and 65 to 74 years for 15 countries or region (separately for the Europid and non-Europid populations of Canada, Australia, and New Zealand), and temporal trends were estimated by means of Poisson regression. For 10 countries or regions, population-based estimates of mean systolic blood pressure and prevalences of hypertension were extracted from published sources. Results Hypertensive ESRD, comprising ESRD attributed to essential hypertension or renal artery occlusion, was least common in Finland, non-Aboriginal Australians, and non-Polynesian New Zealanders; intermediate in most European and Canadian populations; and most common in Aboriginal Australians and New Zealand Maori and Pacific Island people. Rates correlated with the incidence of all other nondiabetic ESRD, but not with diabetic ESRD or community rates of hypertension. Between 1998 and 2002, hypertensive ESRD did not increase in Northwestern Europe or non-Aboriginal Canadians, although it did so in Australia. Conclusion Despite the likelihood of classification bias, the probability remains of significant variation in incidence of hypertensive ESRD within the group of Europid populations. These between-population differences are not explained by community rates of hypertension or ascertainment bias.
5. Glomerular hyperfiltration predicts the development of microalbuminuria in stage 1 hypertension: The HARVEST.
Palatini P, Mormino P, Dorigatti F et al.
Kidney Int. 2006 Jun 21; [Epub ahead of print]
Factors related to the development of microalbuminuria in hypertension are not well known. We did a prospective study to investigate wether glomerular hyperfiltration precedes the development of microalbuminuria in hypertension. We assessed 502 never-treated subjects screened for stage 1 hypertension without microalbuminuria at baseline and followed up for 7.8 years. Creatinine clearence was measured at entry. Urinary albumin and ambulatory blood pressure were measured at entry and during follow-up until subjects developed sustained hypertension needing antihypertensive treatment. Subjects with hyperfiltration (creatinine clearence > 150 ml/min/1.73 m(2), top quintile of the distribution) were younger and heavier than the rest of the group and had a greater follow-up increase in urinary albumin than subjects with normal filtration (P/=1+) were 317 (13.7%), 39 (1.7%), and 103 (4.4%), respectively. Age, hypertension, and diabetes were independently associated with microalbuminuria in men. In addition to the classical risk factors detected in men, estimated 24-h urinary sodium excretion and uric acid were also independently associated with microalbuminuria in women. Among the 668 subjects with renal insufficiency (CCr 90 ml/min per 1.73 m (2), the prevalence of myocardial infarction, stroke, and total CVD of individuals with eGFR 60 to 89 ml/min per 1.73 m (2) was increased by 91.4, 71.7 and 67.6%, respectively. For individuals with eGFR 30 to 59 ml/min per 1.73 m (2), the percentage was 105.2, 289.1, and 200%, respectively. For each eGFR category, stroke was more prevalent than myocardial infarction. Compared with individuals with eGFR > 90 ml/min per 1.73 m (2), participants with eGFR 60 to 89 and 30 to 59 ml/min per 1.73 m (2) tended to have more cardiovascular risk factors, and there were strong unadjusted and adjusted associations between CVD with different stages of eGFR (eGFR > 90 ml/min per 1.73 m (2) as reference). This first report on the prevalence and spectrum of CVD in early stages of CKD in a community-based Chinese population. The spectrum of CVD in this Chinese population is different from reports of Western countries. Individuals with subtle decreased renal function seem much more likely to have multiple cardiovascular risk factors and have higher prevalence of CVD than those without CKD.
9. Identifying genetic susceptibilities to diabetes-related complications among individuals at low risk of complications: An application of tree-structured survival analysis.
Costacou T, Chang Y, Ferrell RE et al.
Am J Epidemiol. 2006 Aug 23; [Epub ahead of print]
The authors hypothesized that genetic predisposition to diabetes complications would be more evident among low-risk individuals and aimed to identify genes related developing complications (confirmed distal symmetric polyneuropathy, overt nephropathy, or coronary artery disease) in low-risk groups. Participants in the Pittsburgh, Pennsylvania, Epidemiology of Diabetes Complications Study of childhood-onset type 1 diabetes, first seen in 1986-1988 (mean age, 28 years; diabetes duration, 19 years), were reexamined biennially for 10 years. For each complication, subgroups with lowest disease risk were identified by using tree-structured survival analysis, and 15 candidate genes were compared between subjects with and without complications. In the group with the lowest incidence of confirmed distal symmetric polyneuropathy (n = 123), confirmed distal symmetric polyneuropathy risk increased fivefold for those with the eNOS GG genotype (p < 0.05). In the group with lowest risk of overt nephropathy (n = 340), the ACE D polymorphism increased overt nephropathy risk twofold (p = 0.05), whereas a protective effect was observed for the LIPC CC genotype (p < 0.05). In the group with the lowest incidence of coronary arterty disease (n = 331), the MTHFR CC genotype increased coronary artery disease risk threefold (p < 0.05). Tree-structured analysis may help identify genetic predispositions among individuals who, despite low risk, develop diabetes-related complications.
10. A cohort analysis of type 1 diabetes mortality in Havana and Allegheny County, Pittsburgh, PA.
Barcelo A, Bosnyak Z, Orchard T.
Diabetes Res Clin Pract. 2006 Jul 27; [Epub ahead of print]
Objective To examine the mortality of type 1 diabetes (T1D) in two countries with very different health care systems using two population-based registries of childhood-onset T1D one in Havana (HA), Cuba, and the other in Allegheny County (AC), USA. Research Design Methods Cases diagnosed with T1D between 1965 and 1980 in HA and between 1965 and 1979 in AC were included. Follow-up started with diagnosis in each individual and ended as of 1 January 1991, or with death. Life-table analyses were used to examine the mortality rates in both populations by duration of diabetes. Results Cumulative mortality by January 1991 in HA (14% in males and females, respectively) was higher than in AC (7% in males and 9% in females) for both genders (males, p = 0.0005; females, p = 0.0491). Mortality rates were considerably higher in HA for both men and women than in AC however, among females confidence intervals overlapped. Overall mortality rate for Caucasians (AC) was significantly lower than that for African-Americans (AC) or Hispanics (HR). An analysis of causes of death showed a greater proportion of deaths attributed to nephropathy (48.6%) in HA while acute complications (36%) and infections (27%) were frequent in AC. Conclusions This study shows a two-fold greater mortality among people with childhood-onset T1D in Havana, Cuba, than Allegheny, USA. Different strategies may be needed to increase survival among those with type 1 diabetes in the USA and Cuba.
11. Diabetic microvascular complications - - can the presence of one predict the development of another?
Girach A, Vignati L.
J Diabetes Complications. 2006 20 (4): 228-37.
The number of people with diabetes is increasing dramatically worldwide. The rising prevalence of obesity in childhood and adolescence has also been linked to a startling increase in the number of diagnosed cases of type 2 diabetes in these younger age groups. Despite the introduction of treatment strategies, diabetes remains a major cause of new-onset blindness, end-stage renal disease, and lower lag amputation, all of which contribute to the excess morbidity and mortality in people with diabetes. Furthermore, the management of diabetes-related complications generates substantial costs. In order that timely treatment can be given, it is essential that patients at risk for the development of diabetic microvascular complications are identified earlier. Diabetes duration and glycemic, blood pressure, and lipid control have consisitently been shown to correlate with diabetic retinopathy, neuropathy, nephropathy, but to date, the relationship of one diabetic microvascular complication to another has not been clearly described. A review of the literature has raised the question that apart from known risk factors, there is a possible relationship among the diabetic microvascular complications themselves, and this appears to be much stronger than the sparse published data on it would suggest. A scoring system that can predict the development of diabetic microvascular complications may facilitate the early identification of those patients at risk and, consequently, have a positive impact on patients’ quality of life and reduce the economic burden of diabetes and its complications.
12. Relationship between common functional polymorphisms of the p22phox gene (-930A > G and +242C > T) and nephropathy as a result of type 2 diabetes in a Chinese population.
Lim SC, Goh SK, Lai YR et al.
Diabet Med. 2006 23 (9): 1037-41.
Objective Genetic determinants are important in diabetic nephropathy (DN). Oxidative stress has also emerged as an important pathogenic factor in DN and vascular NADH oxidase is a major source of reactive oxygen species (ROS). Previous small studies reported a strong but contradictory association between functional genetic variation of p22(phox), an important subcomponent of NADH oxidase, and DN. We investigated the association between two common functional single nucleotide polymorphisms (SPNs) (-930 A > G and +242 C > T) and DN in a much larger group of Chinese patients with type 2 diabetes mellitus (T2DM). Research and Methods Case-control study of Chinese subjects with long-standing T2DM (> 10 years). Cases (n = 306) were subjects with a spot urinary albumin : creatinine ratio (ACR) of > 113 mg/mmol or elevated serum creatinine. Control subjects (n = 306) had ACR < 3.3 mg/mmol and normal serum creatinine. Genotyping was carried out by standard PCR and restriction fragment length polymorphism analysis. Results Gender distribution, age, duration of diabetes and HbA(1c) were similar in case and control subjects. Distribution of genotypes in the control subjects for both SNPs was consistent with the Hardy-Weinberg equilibrium. Disturbation of genotypes did not differ significantly between cases and control subjects for both polymorphisms-+2424 C > T: cases CC 84.6%, CT 15.0%, TT 0.4% and control subjects CC 87.6%, CT 11.8%, TT 0.6% (P = 0.45); -930A > G: cases AA 40.5%, AG 41.8%, GG 17.7% and control subjects AA 38.2%, AG 49.0%, GG 12.8% (P = 0.12). Distribution of alleles was also similar-2424 C > T: cases C 92.2%, T 7.8% and control subjects C 93.5%, T 6.5% (P = 0.66); -930 A > G cases A 61.4%, G 38.6% and control subjects A 62.7%, G 37.3% (P = 0.38). We estimated that our study has approximately 80% power to detect a relative risk of 1.65 (for +242 C > T) and 1.35 (for –930 A > G) conferred by the minor allele, respectively. Conclusions In contrast with prevoius small studies, our data suggest that these SNPs do not confer significantly increased susceptibility to DN secondary to T2DM in Chinese subjects.
13. Metabolic syndrome and CKD in a general Japanese population: The Hisayama Study.
Ninomiya T, Kiyohara Y, Kubo M et al.
Am J Kidney Dis. 2006 48 (3): 383-91.
Background Metabolic syndrome has been linked with various atherosclerotic disease, but has not been evaluated sufficiently as a risk for the development of chronic kidney disease (CKD) in the general population. Methods We followed up 1,440 community-dwelling individuals without CKD aged 40 years or older for 5 years and examined the effects of metabolic syndrome, defined by the modified National Cholesterol Education Program Adult Treatment Panel III criteria, on the development of CKD. Results During follow-up, 88 subjects experienced CKD. The age- and sex-adjusted 5-year cumulative incidence of CKD was significantly greater in subjects with than without metabolic syndrome (10.6% versus 4.8%; P < 0.01). In multivariate analysis, even after adjusment for other confounding factors, including insulinemia, metabolic sydrome remained an independent risk factor for occurence of CKD (odds ratio, 2.08; 95% confidence interval [CI], 1.23 to 3.52). Compared with subjects with 1 or fewer metabolic syndrome component, multivariate-adjusted odd ratios for CKD in subjects with 2, 3, and 4 or more metabolic syndrome components were 1.13 (95% CI, 0.60 to 2.12), 1.90 (95% CI, 0.98 to 3.69), and 2.79 (95% CI, 1.31 to 9.90), respectively. The rate of change in kidney function during 5 years decreased significantly in subjects with 4 or more metabolic sndrome components compared with those with 1 or fewer component in the age group of 40 to 59 years, whereas it also was significantly low in subjects with 3 metabolic syndrome components in the group aged 60 years or older. Conclusion Our findings suggest that metabolic syndrome is a significant risk factor for the development of CKD in the general population.
14. The relationship of microalbuminuria with metabolic syndrome.
Choi HS, Ryu SH, Lee KB.
Nephron Clin Pract. 2006 104 (2): c85-93.
Background/Aims Microalbuminuria and the metabolic syndrome are risk factors for cardiovascular disease. The aim of this study is to examine the prevalence of microalbuminuria and to document the relationship of microalbuminuria with the metabolic syndrome in a large population of Korean subjects. Methods We examined the cross-sectional association of microalbuminuria with the components of the matabolic syndrome and with other cardiovascular risk factors in 6,588 Korean adults who took part a health examination program. Results The prevalence of microalbuminuria was 4.2% in the non-metabolic syndrome group (n = 5,902), and 14.8% in the metabolic group ( n = 686). The odds ratio of microalbuminuria in the adults with the metabolic syndrome compared with those adults without the metabolic syndrome was 1.53 (1.13-2.07 95% CI). In the multiple logistic regression analysis, as compared with the subjects without an elevated blood pressure, a low high-density lipoprotein cholesterol level, a high triglyceride level, a high plasma glucose level and a large waist circumference, the odds ratios for microalbuminuria with these components, after adjusment was made for the body mass index, the high-sensitivity C-reactive protein level and the homeostasis model assessment, were 2.17 (95% CI 1.71-2.76), 2.84 (95% CI 1.55-5.21), 1.30 (95% CI 1.03-1.65) and 2.68 (95% CI 2.04-3.51), respectively. The corresponding multivariate-adjusted odds ratios of microalbuminuria for the participants with 1, 2, 3, and 4 and 5 components of metabolic syndrome were 1.79 (95% CI 1.24-2.59), 2.35 (95% CI 1.58-3.51), 3.23 (95% CI 2.07-5.25), and 4.22 (95% CI 2.13-8.35), respectively. Conclusion There was a significantly graded relationship between the number of metabolic syndrome components and the corresponding prevalence of microalbuminuria. These findings suggest microalbumnuria is strongly related with the components of the metabolic syndrome.
15. Racial differences in the prevalence of chronic kidney disease among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Cohort Study.
McClellan W, Warnock DG, McClure L et al.
J Am Soc Nephrol. 2006 17 (6): 1710-5.
The racial disparity in the incidence of ESRD exemplified by the three- to four fold excess risk among black compared with white individuals in the United States is not reflected in the prevalence of less severe degrees of impaired kidney function among black compared with white individuals. The four-variable Modification of Diet in Renal Disease study equation was used to evaluate the black-to-white prevalence of impaired kidney function with increasing severity of impairment among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a nationally, representative, population-based cohort of individuals who are 45 yr and older. An estimated GFR (eGFR) 90 ml/min per 1.73 m(2) and albuminuria, 2.7% (SE 0.3); stage 2 (GFR 60 to 89 ml/min per 1.73 m(2) and albuminuria), 3.2% (SE 0.4); stage 3 (GFR 30 to 59 ml/min per 1.73 m(2), 4.2% (SE 0.1); and stage 4 (GFR 15 to 29 ml/min per 1.73 m(2), 0.2% (SE 0,01). This closely approximates reported US CKD prevalence (11.0% in 1988 through 1994 and 11.7% in 1999 through 2000). The relative risk for progression from CKD stages 3 or 4 to ESRD in US white patients compared with Norwegian patients was 2.5. This was only modestly modified by adjusment for age, gender, and diabetes. AGE and GFR at start of dialysis were similar, hypertension and cardiovascular mortality in the populations were comparable, but US white patients were referred later to a nephrologist and had higher prevalence of obesity and diabetes. In conclusion, CKD prevalence in Norway was similar to that in the United States, suggesting that lower progression to ESRD rather than a smaller pool of individuals at risk accounts for the lower incidence of ESRD in Norway.
17. Ethnic disparities in cardiovascular risk factors and coronary disease prevalence among individuals with chronic kidney disease: Findings from the Third National Health and Nutrition Examination Survey.
Nguyen HT, Stack AG.
J Am Soc Nephrol. 2006 17 (6): 1716-23.
Differences in coronary disease have been reported among ethnic minorities in the US population. Whether these persist in patients with chronic kidney disease is unknown. The prevalence of myocardial infarction (MI) and angina was compared by race and GFR in the Third National Health and Nutrition Examination Survey using the Modification of Diet in Renal Disease Study equation. Age-gender standardized estimates were computed for each GFR category (>/=90, 60 to 89, and /=90, 60to 89, and /=90 ml/min; odds ratio 1.00), Mexican-American individuals with GFR of 60 to 89 and 6 years of diabetes. None of the individual markers showed significant disease association when considered on their own. However, haplotype analyses revealed a near doubling in the prevalence of the A.T.D risk haplotype in case subjects (0.136). compared with control subjects (0.075) (P = 0.009), thus providing first evidence for a disease haplotype for advanced diabetic nephropathy at the ACE locus.
56. Impact of renin angiotensin system modulation on the hyperfiltration state in type 1 diabetes.
Sochett EB, Cherney DZ, Curtis JR et al.
J Am Soc Nephrol. 2006 17 (6): 1703-9.
The initial stage of diabetic nephropathy are characterized by glomerular hyperfiltration and hypertension, processes that have been linked to initiation and progression of renal disease. Renin angiotensin system (RAS) blockade is commonly used to modify the hyperfiltration state and delay progression of renal disease. Despite this therapy, many patients progress to ESRD, suggesting heterogeneity in the response to RAS modulation. The role of the RAS in the hyperfiltration state in adolescents with uncomplicated type 1 diabetes was examined, segregated on the basis of the presence of hyperfiltration. Baseline renal hemodynamic function was charaterized in 22 patients. Eleven patients exhibited glomerular hyperfiltration (GFR >/= 135 ml/min), and in the remaining 11 patients, the GFR was /= 20 years (DN’’-”) 63 with overt DN and T1DM C polymorphisms on the susceptibility to diabetic nephropathy.
Ng M, Baum L, So WY et al.
Clin Genet. 2006 70 (1): 20-8.
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. In DN patients, triglyceride (TG) level is elevated and lipoprotein lipase (LPL) activity, which hydrolyzes TG, is decreased. The LPL S447X and apolipoprotein E (APOE) exon 4 polymorphisms affect TG levels, and the APOC3-455T>C polymorphism affects LPL activity. Our aim was to examine the association of these polymorphisms with nephropathy in type 2 diabetes. We examined these polymorphisms in a case-control study of type 2 diabetic patients including 374 with DN and 392 without DN. LPL 447X-containing genotypes (447X+) were significantly decreased in DN patients [18.6 vs 25.6%, odds ratio (OR) = 0.66, p = 0.021], as were APOE3/3 genotypes (64.8 vs 73.1%, OR = 0.68, p = 0.01). In addition, combination of genotypes [APOE3/3 and lPL 447+ (OR = 0.56), APOC3 CC and LPL 447+ (OR = 0.31), APOE3/3 and APOC3 CC (OR = 0.61] were protective for DN compared with the most common combination of the respective polymorphisms. Our findings suggest the importance of interactions among lipid genes in modulating the risk of DN.
61. MTHFR C677T and A1298C gene polymorphisms and hyperhomocysteinemia as risk factors of diabetic nephropathy in type 2 diabetes patients.
Mtiraoui N, Ezzidi I, Chaieb M et al.
Diabetes Res Clin Pract. 2006 Jul 4; [Epub ahead of print]
Point mutations in methylenetetrahydrofolate reductase (MTHFR) and hyperhomocysteinemia were implicated in the pathogensis of diabetic nephropathy (DN) in many ethnic groups. This study addressed the association of C677T and A1298C single nucleotide polymorphisms (SNPs) of MTHFR gene with DN in Tunisian type 2 diabetes (T2DM) patients. Study subjects comprised 93 DN patients, 267 patients with normoalbuminuria, and 400 control subjects. C677T and A1298C genotypes were determined by PCR-RFLP analysis, and homocysteine levels were measured by ELISA. A1298C and C677T were highly prevalent among T2DM patients, with allele frequencies of 0.26 and 0.36, respectively. Higher mutant 677T allele and 677C/T and 677T/T SNP, not A1298C SNP, together with 677C/1298A, 677T/1298A haplotypes were seen in DN patients compared to normoalbuminuric patients, (p/= 300 mg albumin/24 h urine), erythrocyturia (>/= 250/L, without leukocyturia), and impaired renal function (both 24-h creatinine clearence and Modification of Diet in Renal Disease clearence below the fifth percentile of age- and gender-matched control subjects). The 8592 patients who were included in this study were followed for a 4-yr period. We identified 134 patients with macroalbuminuria, 128 with erythrocyturia, and 103 with impaired renal function. There was only a little overlap among the three groups. The prevalence of macroalbuminuria, erythrocyturia, and impaired renal function was calculated to be in the general population 0.6, 1.3, and 0.9%, respectively. In all three groups, fewer than 30% of patients were known to have this laboratory abnormality before screening. The incidence of cardiovascular disease was high in the macrolabuminuria grouop (e.g., the age- and gender-adjusted hazard ratio for mortality as a result of cardiovascular disease is 2.6 [1.1 to 6.0]) and for the impaired renal function group (3.4 [1.5 to 8.0]). After a mean follow-up of 4.2 yr, the macroalbuminuria group showed a -7.2 ml/min per 1.73 m(2) estimated GFR (eGFR) loss, compared with -2.3 ml/min per 1.73 m(2) in the control group (difference P < 0.001), whereas the rate of eGFR loss in the impaired renal function group (-0.2 ml/min per 1.73 m(2); P = 0.18), and the erythrocyturia group (-2.6 ml/min per 1.73 m(2)) was not different from control group. Macroalbuminuria and impaired renal function both predict a worse prognosis with respect to cardiovascular morbidity and mortality. However, macroalbuminuria is a better risk marker than low eGFR or erythrocyturia to identify in population screening of individuals who are at risk for accelerated GFR loss.
5. Adiponectin and mortality in patients with chronic kidney disease.
Menon V, Li L, Wang X et al.
J Am Soc Nephrol. 2006 Aug 2; [Epub ahead of print]
Adiponectin is presumed to possess antiatherogenic and cardioprotective properties. Limited data exist on the relationship between adiponectin and mortality in the earlier stages of chronic kidney disease. The modification of Diet in Renal Disease study was randomized, controlled trial that was conducted between 1989 and 1993. Adiponectin in frozen samples that were obtained at baseline (N = 820). Survival status and cause of death, up to Dcemeber 31, 2000, were obtained from the National Death Index. Multivariable Cox models were used to examine the relationship of adiponectin with all-cause and cardiovascular mortality. Mean +/- SD age was 52 +/- 12 yr, and mean +/- SD glomerular filtration rate (GFR) was 33 +/- 12 ml/min per 1.73 m(2). Eighty-five percent of participants were white, and 60% were male. Mean +/- SD adiponectin was 12.8 +/- microg/ml. Triglycerides, insulin resistance, glucose, body mass index, GFR, C-reactive protein, and albumin were inversely related and proteinuria and HDL cholesterol were directly related to adiponectin. During the 10-year follow-up period, 201 (25%) participants died of any cause, and 122 (15%) from cardiovascular disease. In multivariable adjusted Cox models, a 1-microg/ml increase in adiponectin was associated with a 3% (hazard ratio 1.03; 95% confidence interval 1.01 to 1.05, P = 0.02) increased risk for all-cause and 6% (hazard ratio 1.06; 95% confidence interval 1.03 to 1.09; P < 0.001) increased risk for cardiovascular mortality. High, rather than low, adiponectin is associated with increased mortality in this cohort of patients with chronic kidney disease stages 3 to 4. Further studies are necessary to confirm this association and to elucidate the underlying mechanisms.
6. The urinary activity of angiotensin-converting enzyme in preterm, full-term newborns, and children.
Lopes Del Ben G, Redublo Quinto BM, Casarinin DE et al.
Pediatr Nephrol. 206 21 (8): 1138-43.
The urinary activity of the angiotensin-converting enzyme (U (ACE)) is not yet completely documented in human neonates. We measured the U (ACE) in 36 premature neonates on the 1st, 2nd, 3rd, and 4th weeks of life, in 22 full-term neonates between the 1st and 2nd days, and in 30 nursing and preschool children between 1 months and 6 years of age. The urinary excretion of sodium (U (Na) / (Cr) ) and the potassium / sodium index (U (K) / (Na) ) were analyzed in the neonates. U (ACE) was greater in premature than in full-term neonates and greater in both than in older children (p < 0.001). In the premature neonates, U (ACE) peaked at 2nd week, U (Na) / U (Cr) index decreased, and the U (K) / U (Na) index increased between the 1st day and 2nd week (p < 0.001). The U (Na) / U (Cr) index on the 1st day and in the 1st and 2nd weeks was greater in premature than in full-term neonates (p < 0.001). There was no significant correletaion between the U (ACE) and U (Na) / U (Cr) index. In conclusion, the U (ACE) profile was shown to be age dependent and related to postnatal renal development. The increase in U (ACE) activity may reflect the high activity of the neonatal intrarenal renin-angiotensin system (RAS).
7. Clinical characteristics of chronic kidney disease patients with and without diabetes: A subanalysis of the PAERI study.
Lorber D, Reddan D.
Clin Nephrol. 2006 66 (1): 11-6.
Abstract. Aims Diabetes is the leading cause of chronic kidney disease (CKD) in the United States, and cardiac disease is the primary cause of death in patients with CKD and diabetes. The Prevalence in Early Renal Insufficiency (PAERI) study evaluated the prevalence of anemia associated comorbidities in a community based sample of patients with CKD. The purpose of this post hoc analysis was to identify differences, if any, in the prevalence and severity of anemia (hemoglobin < 12 g/dl (120 g/l)) and other clinical characteristics between CKD patients with diabetes and patients with CKD who did not have diabetes. Materials and Methods The PAERI study was a prospective, cross-sectional, multicenter survey. Eligible patients were > 18 years old with CKD, defined as serum creatinine 1.5 – 6.0 mg/dl (132.6 – 530.4 umol/l) in females and 2.0 – 6.0 mg/dl (176.8 – 530.4 umol/l) in males within 12 months before enrollment. Study duration for each patient was a single site visit. Results Of the original 5,222 patients enrolled, 3,361 had diabetes and 1,861 did not. A family history of diabetes was present in 72.7% of diabetic patients vs. 27.2% of nondiabetic patients (p < 0.0001). Patients with diabetes had a significantly higher prevalence of anemia (52.7 vs 39.4%, p < 0.0001) and cardiac disease (55.7 vs. 42.9%, p < 0.0001) The prevalence of hypertension was higher in both groups (91.5 and 89.3%). Significantly more diabetic patients than nondiabetic patients received angiotensin-converting enzyme inhibitors (60.4 vs 43.8%, p < 0.0001). Hyperlipidemia was more common in patients with diabetes (73.9 vs. 55.4%, p < 0.0001). Patients with diabetes were significantly younger and had a significantly higher mean body mass index and lower transferrin saturation compared with nondiabetic patients. In diabetic and nondiabetic patients, more than 97% had glomerular filtration rate < 60 ml/min/1.73 m^2 and more than 70% had serum creatinine < 2.5 mg/dl (221.0 umol/l). Conclusions These findings underscore the extent and severity of concurrent illness in patients with both diabetes and CKD. In those patients, diabetes was associated with greater prevalence of serious cardiac-related comorbidities than observed in nondiabetic patients.
8. Chronic kidney disease in long-term survivors of hematopoietic cell transplantation: Epidemiology, pathogenesis, and treatment.
Hingorani S.
J Am Soc Nephrol. 2006 17 (7): 1995-2005.
High-dose myeloablative hematopoietic cell transplantation is becoming an increasingly common treatement modality for variety of disease. Patient survival may be limited by substantial treatment-related toxicities, including chronic kidney disease (CKD). Although the majority of CKD after transplantation is idiopathic, thrombotic microangiopathic syndromes and nephrotic syndrome have been described. Epidemiology, pathogenesis, and potential treatment options for the various clinical syndromes that are associated with CKD in hematopoietic cell transplantation patients is reviewed. As the indications for and the number of transplants that are performed worldwide increases so will the burden of CKD. The nephrologists and oncologists will have to work together to identify patients who are at risk for CKD early to prevent its development and progression to end-stage kidney disease.
9. Coeliac disease and risk of renal disease - - A general population cohort study.
Ludvigsson JF, Montgomery SM, Olen O et al.
Nephrol Dial Transpant. 2006 21 (7): 1809-15.
Background Coeliac disease (CD) may be a risk factor for renal disease. Methods We investigated the risk of any form of glomerulonephritis (GN) (acute, chronic and non-specified), chronic glomerulonephritis (CGN) and renal replacement therapy including dialysis and kidney transplantation (KT) in patients with CD in ageneral population-based cohort study. We used Cox regression to assess the rik of renal disease in 14 336 patients who had received a diagnosis CD (1964-2003) and 69 875 reference individuals matched for age, calendar year, sex and county. Patients were identified using the Swedish Hospital Discharge Registry. Follow-up began 1 year after study entry. Results CD was associated with an increased risk of any form of GN (hazard ratio (HR) = 1.64; 95% confidence intervals (CI) = 1.02-2.66; P = 0.046; 89 events), CGN (HR = 2.65; 95% CI = 1.34-5.24; P = 0.005; 39 events), dialysis (HR = 3.48; 95% CI = 2.26-5.37; P < 0.001; 102 positive events) and KT (HR = 3.15; 95% CI = 1.29-7.71; P = 0.012; 22 events). Conclusion We suggest that immune characteristics associated with CD increase the risk of chronic renal disease. Individuals with CD may also be et a moderately increased risk of any form of GN.
10. WT1 mutations in nephrotic syndrome revisited. High prevalence in young girls, associations and renal phenotypes.
Aucella F, Bisceglia L, De Bonis P et al.
Pediatr Nephrol. 2006 Aug 15; [Epub ahead of print]
WT1 mutations have been considered a rare cause of nephrotic syndrome but recent reports challenge this assumption. Exclusion of inherited forms is a basic point in any therapeutic strategy to nephrotic syndrome since they not respond to drugs. We screened for WT1 mutations in 200 patients with nephrotic syndrome: 114 with steroid resistance (SRNS) and 86 with steroid dependence (SDNS) for whom other inherited forms of nephrotic syndrome (NPHS2, CD2AP) had been previously excluded. Three girls out of 32 of the group with steroid resistance under 18 years presented classical WT1 splice mutations (IVS9+5G>A, IVS9+4C>T) of Frasier syndrome. Another on presented a mutation coding an amino acid change (D396N) at exon 9 that is typical of Denys-Drash syndrome. All presented resistance to drugs and developed end stage renal failure within 15 years. Two girls the Frasier group presneted a 46 XY karyoptype with streak gonads while one was XX and had normal gonad morphology. In the two cases with IVS9+5G>A renal pathology was characterized by capillary wall thickening with deposition of IgG and C3 in one that was interpreted as a membrane pathology. Foam cells were diffuse in tubule-interstitial areas. In conclusion, WT1 splice mutations are not rare in females under 18 years with SRNS. This occurs in absence of a clear renal pathology picture and frequently in absence of phenotype change typical Frasier syndrome. In adults and children with SDNS, screening analysis is of no clinical value. WT1 hot spot mutation analysis should be routinely done in children with SRSN; if the molecular screening anticipate any further therapeutic approach it may modify the long term therapeutic strategy.
11. Low protein Z levels in children with nephrotic syndrome.
Ozkaya O, Bek K, Fisgin T et al.
Pediatr Nephrol. 2006 21 (8): 1122-6.
Acquired deficiency of anticoagulant proteins, due to loss in the urine, has been proposed as one of the major thrombogenic alterations in nephrotic syndrome (NS). Protein Z (PZ) is a single-chain vitamin K-dependent glycoprotein. Low PZ levels are reported to be a risk factor for thrombosis. The aim of this study was to investigate protein Z and other natural anticoagulant levels in children with NS. Thirty children aged between 1.5 and 12 years with NS (Groups I and II) and 19 age-and-sex-matched healthy controls (Group III) were enrolled into the study. Patients were divided into two groups: group I (proteinuria >40 mg/m(2)/hr) and Group II (patients in remission). Plasma PZ levels in roup I were significantly lower than Group II (p = 0.009) and group III (p = 0.018). Plasma levels of AT III for groups II and III (p = 0.009, p = .005, respectively). Protein C levels in Group I were higher than in Group II and Group III (p = 0.002, p = 0.000, respectively). Protein Z levels positively correlated with serum total protein and albumin levels (p = 0.003, p = 0.003, respectively) and negatively with the degree of proteinuria (p = 0.000). Protein Z levels were positively correlated with AT III (R = 0.037, p = 0.04). Along with the other coagulation abnormalities, decreased protein Z may contribute to increased risk of thromboembolic complications in children with NS. The negative correlation between proteinuria and PZ level suggest the possibility of renal PZ loss. Further studies are needed to incvestigate the mechanism and role of decreased PZ in NS.
12. Urine proteomic profiling of pediatric nephrotic syndrome.
Khurana M, Traum AZ, Aivado M et al.
Pediatr Nephrol. 2006 Jun 30; [Epub ahead of print]
The prognosis of pediatric nephrotic syndrome (NS) correlates with the responsiveness to glucocorticoid therapy. Steroid-resistant NS (SRNS) patients progress to end-stage renal disease, while steroid-sensitive NS (SSNS) and steroid-dependent (SDNS) patients not. We have performed proteomic profiling of urine samples from a cross section of pediatric and adolescent subjects with SSNS, SRNS, and orthostatic proteinuria (OP) to identify urinary biomarkers of steroid resistance. We performed surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF MS) on urine from 19 subjects with SSNS/SDNS in remission, 14 with SSNS/SDNS in relapse, 5 with SRNS in relapse, and 6 with OP. genetic algorithm search of principal component space revealed a group of five peaks distinguishing SRNS subjects, with mass/charge (m/z) values of 3,917.07, 4,155.53, 6,329.68, 7,036.96, and 11,117.4. Our analyses identified the peak at m/z 11,117.4 with an accuracy of 95% for classifying SRNS. Multidimensional protein fractionation and mass spectrometric analysis of SRNS urine samples combined with immunodepletion identified the 11,117.4 protein as beta(2)-microglobulin (B2M). using an unbiased protein profiling approach, we have validated previously reported findings of B2M as a biomarker associated with SRNS. Prospective studies are warranted to estabilish additonal biomarkers that would be predictive of SRNS.
13. Urinary proteome of steroid-sensitive and steroid-resistant idiopathic nephrotic syndrome in childhood.
Woroniecki RP, Orlova TN, Mendelev N et al.
Am J Nephrol. 2006 26 (3): 258-67.
The response to steroid therapy is used to characterize the idiopathic nephrotic syndrome (INS) of childhood as either steroid-sensitive (SSNS) or steroid-resistant (SRNS), a classification with a better prognostic capability than renal biopsy. The majority (approximately 80%) of INS is due to minimal change disease but the percentage of focal and segmental glomerulosclerosis is increasing. We applied a new technological platform to examine the urine proteome to determine if different urinary protein excretion profiles could differentiate patients with SSNS from those with SRNS. Twenty-five patients with INS and 17 control patients were studied. Mid-stream urines were analyzed using surface enhanced laser desorption and ionization mass spectrometry (SELDI-MS). Data were analyzed using multiple bioinformatic techniques. Patient classification was performed using Biomarker Pattern Software (TM) and a generalized form of Adaboost and predictive models were generated using a supervised algorithm with cross-validation. Urinary proteomic data distinguished INS patients from control patients, irrespective of steroid response, with a sensitivity of 92.3%, specificity of 93.7%, positive predictive value of 96% and a negative predictive value of 88.2%. Classification of patients as SSNS or SRNS was 100%. A protein of mass 4,144 daltons was identified as the single most important classifier in distinguishing SSNS from SRNS. SELDI-MS combined with bioinformatics can identify different proteomic patterns in INS. Characterization of the proteins of interest identified by this proteomic approach with prospective clinical validation may yield a valuable clinical tool for the non-invasive prediction of treatment response and prognosis.
14. Expression of P-glycoprotein in lymphocytes from children with nephrotic syndrome, depending on their steroid response.
Wasilewska A, Zoch-Zwierz W, Pietruczuk M et al.
Pediatr Nephrol. 2006 Jun 8; [Epub ahead of print]
The aim of this study was to examine the expression of P-glycoprotein (P-gp) in CD3 lymphocytes of children with nephrotic syndrome (NS) in relation to their clinical response to glucocorticoid (GC) treatment. The examinations were performed on two groups. The study group (I) consisted of 88 children aged 2.0-20.0 years with NS, divided according to their clinical response to GC: NFR-non-frequent relapse NS; FR-frequent relapse NS; SD-steroid-dependent NS. The control group (II) consisted of 18 healthy children never treated with GC. We measured P-gp expression on CD3 lymphocytes of patients with NS using a flow cytometric assay. The CD3/P-gp was significantly higher than in controls. The difference was higher in SD (P=0.0001) and FR – (P=0.0002) group. The difference in NFR was smaller. Mean CD3/P-gp (in percent was twice as high in SD children than in NFR, and the difference, as between FR and NFR, was statistically significant ( 6 months prior to biopsy, s-creatinine > 140 micromol/l, diffuse proliferative glomerulonephritis, and tubular atrophy emerged as the strongest combination of independent risk factors (relative hazard ratios: 9.3, 5.6, 8.9, and 3.1, respectively). Conclusion Our results confirm the negative prognostic impact of hypercreatininemia, class IV histopathology, and tubular atrophy in lupus nephritis. Our data show that delay between onset of nephritis and renal biopsy constitutes an important risk factor of ESRD. Patients with SLE should have kidney biopsy as soon as clinical signs of nephritis are evident in order to accelerate treatment decisions and minimize risk of inflammation-induced irreversible kidney damage.
21. Lupus nephritis in Chinese children - A territory-wide cohort study in Hong Kong.
Wong SN, Tse KC, Lee TL et al.
Pediatr Nephrol. 2006 21 (8): 1104-12.
We report a multicenter study of Chinese children in Hong Kong with systemic lupus erythematosus (SLE) nephritis. Children were included if: they fulfilled the ACR criteria, had significant proteinuria or casturia, were Chinese and younger than 19 years and had been diagnosis with SLE between January 1990 and December 2003. Investigators in each center retrieved data on clinical features, biopsy reports, treatment and outcome of these patients. There were 128 patients (eight boys, 120girls; mean age: 11.9 +/- 2.8 years). About 50% presented with multisystem illness and 40% with nephritic/nephrotic symptoms. Negative anti-dsDNA antibodies were found in 6% of the patients. Renal biopsy revealed WHO Class II, III, IV, and V nephritis in 13 (10%), 22 (17%). 69 (54%) and 13 (10%) patients, respectively. The clinical severity of the nephritis did not accurately predict renal biopsy findings. The follow-up period ranged from 1 to 16.5 years (mean +/- SD: 5.76 +/- 3.61 years). During the study five patients died (two from lupus flare, one from cardiomyopathy, two from infections). Four patients had end-stage renal failure (ESRF) (one died during a lupus flare). All deaths and end-stage renal failure occured in the Class IV nephritis group. Chronic organ damage was infrequent in the survivors. The actuarial patient survival rates at 5, 10, and 15 years of age 95.3, 91.8, and 91.8%, respectively. For Class IV nephritis patients, the survival rates without ESRF at 5, 10, and 15 years were 91.5, 82.3 and 76%, respectively. The survival and chronic morbidity rates of Chinese SLE children in the present study are comparable to those of other published studies.
22. Full-house nephropathy in a patient with negative serology for lupus.
Baskin E, Agras PI, Menekse N et al.
Rheumatol Int. 2006 Sep 14; [Epub ahead of print]
A 10-year-old girl presented with a complaint of recurrent abdominal pain. Physical examination findings were unremarkable. Laboratory investigations revealed BUN of 17 mg/dl and creatinine of 1 mg/dl, and complement levels were normal. She had neither hematuria nor proteinuria, and glomerular filtration rate was 60.9 ml/min/1.73 m(2). ANA, anti-DNA, p-ANCA and c-ANCA were all negative. Renal biopsy revealed findings of class III lupus nephritis in light, ’’full-house’’ nephropathy in immune fluorescent and tubuloreticular inclusions in electron microscopic examinations. After 17 months of treatment, her last creatinine is 2.5 mg/dl and GFR 17.9 ml/m,in/1.73 m(2) and ANA and anti-DNA remain still negative. This case presents an example that decreased GFR can be the first presenting symptom of full-house nephropathy. Those patients who have negative lupus serology and renal biopsy findings of full-house nephropathy and tubuloreticular inclusions may behave and should be treated as lupus nephritis.
23. Lupus nephropathy and cardiopulmonary and hepatic dysfunctions in a child.
Olowu WA.
Pediatr Nephrol. 2006 Jul 4; [Epub ahead of print]
Systemic lupus erythematosus (SLE) is a potentially fatal autoimmune multi-systemic rheumatologic disorder. An unusual case is reported of an 11.9-year-old Nigerian girl who was diagnosed after 2.8 years of non-specific symptoms and six episodes of recurrent haemolysis and pancytopenia warranting blood transfusions. At diagnosis, she had hepatitis, polyarthritis, nephropathy, and cardiopulmonary and bone-marrow dysfunctions. Lymphopaenia, thrombocytopaenia, and direct antiglobulin-test positive haemolytic anaemia were present. Rapid resolution of disease activity followed exchange blood transfusion after an initial poor response to corticosteroid and cyclophosphamide therapy. Any child with recurrent haemolysis and pancytopaenia of unknown aetiology should be invesgated for SLE.
24. Strongyloides stercoralis hyperinfection in systemic lupus erythematosus and the antiphospholipid syndrome.
Mora CS, Segami MI, Hidalgo JA.
Semin Arthritis Rheum. 2006 Aug 30; [Epub ahead of print]
Objective The Strongyloides stercoralis hyperinfection syndrome (SHS) may develop in individuals with asymptomatic infection receiving immunosuppressive treatment. This report summarizes current knowledge regarding SHS in patients with systemic lupus erythematosus (SLE) and associated antiphospholipid syndrome (APS). Methods Two patients with active SLE and associated APS presenting with SHS are reported. Additional cases of strongyloides in SLE were identified and reviewed. Results Patient 1: A 34-year-old woman with SLE and APS characterized by active glomerulonephritis, stroke, and several hospital-acquired infections presented with womiting and diffuse abdominal pain. Intestinal vasculitis was suspected, and treatment with methylprednisolone and cyclophosphamide was given. Response was partial. A gastric biopsy revealed S. stercoralis larvae. She received ivermectin and eventually recovered. Patient 2: A 37-year-old man with active glomerulonephritis and APS with recurrent thrombosis presented with digital necrosis. Necrotizing vasculitis was suspected and treated with immunosuppressants. He suddenly developed respiratory failure secondary to alveolar hemorrhage and bronchoalveolar lavage was performed. The patient deveploped Gram-negative septic shock and died. The postmortem result of bronchoalveolar lavage yielded Strongyloides larvae. Nine cases of strongyloidiasis and SHS in SLE patients reported in the literature were identified and reviewed. Five of these patients died; none had associated APS. Conclusions These cases suggest that the SHS can exacerbate SLE and APS, predisposing to Gram-negative sepsis and death. Immunocompromised patients need an early diagnosis and specific treatment of parasitic diseasea and their comlications. The SHS should be considered in the differential diagnosis of lupus complications in patients from endemic areas.
25. Fanconi’s syndrome and distal (type 1) renal tubular acidosis in a patient with primary Sjogren’s syndrome with monoclonal gammopathy of undetermined significance.
Kobayashi T, Muto S, Nemoto J et al.
Clin Nephrol. 2006 65 (6): 427-32.
Tubulointerstitial nephritis is a well-recognized complication in primary Sjogren’s syndrome. Fanconi’s syndrome is a far less frequent complication compared with distal tubular dysfunction. We here describe a 49-year-old woman with primary Sjogren’s syndrome. In 1997, she was diagnosed with primary Sjogren’s syndrome with tubuointerstitial nephritis, and was then treated with oral prednisolone for the tubulointerstitial nephritis. In 2002, she was referred to our hospital because of progressive fatigue. At that time, biclonal spike on serum protein (IgG-kappa and IgA-kappa) and Bence-Jones protein in urine found. Bone marrow aspiration showed 1.0% plasma cell infiltration. Thus, a diagnosis of monoclonal gammopathy of undetermined significance (MGUS) was made. In 2004, she was again admitted to our hospital because of mild renal dysfunction and hypokalemia. Laboratory evaluation showed inappropriate, alkaline urine in hyperchloremic metabolic acidosis and positive urine anion gap, indicating the presence of distal (Type 1) renal tubular acidosis (RTA). The urine concentration defect was also found. Further studies revealed proximal tubular dysfunction, including renal glycosuria, generalized aminoaciduria, phosphaturia, uricosuria and proximal RTA. The kidney biopsy represented diffuse and severe tubulointerstitial nephritis with dense infiltrates of lymphocytes and IgA and K light chain-positive plasma cells. No findings of multiple myeloma or malignat lymphoma were observed. In conclusion, our patients had Sjogren’s syndrome with MGUS and exhibited dysfunction of both proximal tubule (Fanconi’s syndrome) and distal tubule, which may be attributed to diffuse tubulointerstitial nephritis.
26. Myeloma renal disease: Presentation and outcome.
Chan DT, Craig K, Donovan K et al.
Nephron Clin Pract. 2006 104 (3): c126-31.
Background Renal disease can be the first presentation of multiple myeloma (MM) or develop during the disease process. Aim To define the mode of presentation of MM to nephrologists and determine the association with patient characteristics and outcome. Methods MM patients referred to a tertiary renal unit were studied retrospectively. Group I presented to nephrologists prior to MM diagnosis (n = 36); group II was referred to nephrology after diagnosis (n = 27), and group III was known only to haematlogy and never referred (n = 91). Age presentation, gender, paraprotein type, need for dialysis, haematlogical and biochemical parameters, and survival were examined. Results Of the 154 MM patients, 23.4% presented with renal impairment (group I), 17.5% were referred to nephrology after MM diagnosis (group II) and 59.1% did not receive renal input (group III). On presentation, group I had a median serum creatinine (sCr) of 700 (range 341-.1,023) mumol/l and 80% required dialysis. Although the median sCr on presentation for group II was 131 (range 103-373) mumol/l, median sCr on renal referral was 554 (range 181-807) mumol/l and 57% needed dialysis. In contrast, the median sCr on presentation for group III was only 99 (range 85-117) mumol/l. Group I was more anaemic (p < 0.001) and had higher beta(2)-microglobulin levels (p 500 micromol/L). One hundred patients who were enrolled in an international, randomized, clinical trial to compare plasma exchange with intravenous methylprednisolone as an additional initial treatment were analyzed prospetively. Diagnostic renal biopsies were performed upon entry into the study. Thirty-nine histologic and nine clinical parameters were determined as candidate predictors of renal outcome. The end points were renal function at the time of diagnosis (GFR0) and 12 mo after diagnosis (GFR12), dialysis at entry and 12 mo after diagnosis, and death. Multivariate analyses were performed. Predictive of GFR0 were age (r = -0.4, P = 0.04), arteriosclerosis (r = -0.53, P = 0.01), segmental crescents (r = 0.35, P = 0.07), and eosinophilic infiltrate (r = -0.41, P = 0.04). Prognostic indicators for GRF12 were age (r = -0.32, P = 0.01), normal glomeruli (r = 0.24, P = 0.04), tubular atrophy (r = -0.28, P = 0.02), intraepithelial infiltrate (r = -0.26, P = 0.03), and GFR0 (r = 0.29. P = 0.01). Fibrous crescents (r = 0.22, P = 0.03) were predictive of dialysis of entry. Normal glomeruli (r = -0.30, P = 0.01) and treatment arm (r = -0.28, P = 0.02) were predictive of dialysis after 12 mo. No parameter predicted death. Both chronic and acute tubulointerstitial lesions predicted GFR12 in severe ANCA-associated glomerulonephritis, whereas plasma exchange was a positive predictor of dialysis independence after 12 mo for the entire patient group. Plasma exchange remained a positive predictor when patients who were dialysis dependent at presentatin were analyzed separately (r = -0.36, P = 0.01). Normal glomeruli were a positive predictor of dialysis independence and improved renal function after 12 mo, indicating that the unaffected part of the kidney is vital in determining renal outcome.
30. A new international classification of childhood vasculitis.
Dillon MJ, Ozen S.
Pediatr Nephrol. 2006 Jul 4; [Epub ahead of print]
There has been, for many years, a need for an accepteble classification of childhood vasculitis as well as criteria for classifying specific sub-categories of vasculitic disease affecting the young. Hitherto, there has been, with certain exceptions, much reliance on adult classification systems and criteria that have not proved entirely satisfactory. A recent International Consensus Conference held in Vienna in June 2005 attempted to rectify this state of affairs. It resulted in a new proposal for childhood vasculitis classification and proposal of classification criteria for several important categories of chidlhhod vasculits including Henoch-Schonlein purpura, Kawasaki disease, polyarteritis nodosa (with additional definitions for cutaneous and microscopic polyarteritis), Wegener granulomatosis and Takayasu arteritis. The process involved the Delphi technique to a gather a wide spectrum of opinion from pediatric rheumatologists and nephrologists followed by the Consensus Conference attended by a group of pediatricians with extensive vasculitis experience where nominal group techniques were utilized to agree on a general classification and classification criteria for individual childhood vasculitides. The consensus that was reached will hopefully provide pediatricians with a valuable tool in the study of childhood vasculitides but will require appropriate validation using patients and control groups.
31. EULAR/PReS endorsed consensus criteria for the classification of childhood vasculitides.
Ozen S, Ruperto N, Dillon MJ et al.
Ann Rheum Dis. 2006 65 (7): 936-41.
Background There has been a lack of appropriate classification criteria for vasculitis in children. Objective To develop a widely accepted general classification for the vasculitides observed in children and specific and realistic classification criteria for common childhood vasculitides (Henoch-Schonlein purpura (HSP), Kawasaki disease (KD), childhood polyarteritis nodosa (PAN), Wegener’s granulomatosis (WG), and Takayasu arteritis (TA)). Methods The project was divided into two phases: (1) the Delphi technique was used to gather opinions from a wide spectrum of paediatric rheumatologists and nephrologists; (2) a consensus conference using nominal group technique was held. Ten international experts, all paediatricians, met for the consensus conference. Agreement of at least 80% of the participants was defined as consensus. Results Consensus was reached to base the general working classification for childhood vasculitides on vessel size. The small vessel disease was further subcategorised into „granulomatous” and „non-granulomatous”. Final criteria were developed to classify a child as HSP, KD, childhood PAN , WG, or TA, with changes introduced based on paediatric experience. Mandatory criteria were suggested for all disease except WG. Conclusions It is hoped that the suggested criteria will be widely accepted around the world because of the reliable techniques used and the international and multispecialist composition of the expert group involved.
32. Antineutrophil cytoplasmic antibody-positive crescentic glomerulonephritis in scleroderma - A different kind of renal crisis.
Kamen DL, Wigley FM, Brown AN.
J Rheumatol. 2006 33 (9): 1886-8.
Objective Renal disease remains a major source of morbidity and mortality in patients with scleroderma (systemic sclerosis, SSc). We describe the clinical course of 3 patients with diffuse cutaneous SSc presenting with renal disease subsequently found to have antibodies to myeloperoxidase (anti-MPO) and crescentic glomerulonephritis. The presence of antineutrophil cytoplasmic antibodies (ANCA) and anti-MPO defines a subset of patients with SSc who are susceptible to crescentic glomerulonephritis. These patients may present in a manner identical to scleroderma renal crisis, yet treatment requirements differ significantly. We suggest that the presence of ANCA be routinely evaluated when faced with renal failure in the setting of SSc.
33. Nephropathy, polyneuropathy, and gastroenteritis in child with Churg-Strauss syndrome.
Olowu WA.
Clin Rheumatol. 2006 Aug 2; [Epub ahead of print]
Churg-Strauss syndrome (CSS) is a serious but rare pauci-immune vasculitis of small- and medium-sized blood vessels. It is commonly seen in association with bronchial asthma and/or allergic disorders. The syndrome is characterized by the presence of asthma, hypereosinophilia, and vasculitis in any part of the body. Vasculitis is often associated with significant distortion of normal functions. A rather severe case of CSS in an 8-year-old Nigerian girl with asthma and allergic rhinoconjunctivitis is reported. She present with multiple morbidities, namely, vasculitic polyneuropathy and also nephritic-nephrotic syndrome that eventuated in acute renal failure after onset of vasculitic gastroenteritis. Routine screening of all asthmatic patients for CSS is advocated.
34. Microscopic polyangiitis associated with primary biliary cirrhosis: A causal or casual association?
Amezcua-Guerra LM, Prieto P, Bojalil R et al.
J Rheumatol. 2006 Sep 15; [Epub ahead of print]
Objective The association between microscopic polyangiitis (MPA) and primary biliary cirrhosis (PBC) has seldom reported. We describe a patients with PBC and MPA who presented with polyarthritis and pulmonary nodules followed by pauci-immune crescentic glomerulonephritis and liver dysfunction. Detection of p-ANCA, antimyeloperoxidase, and antimitochondrial antibodies along with liver and renal histopathology allowed a diagnosis of MPA and PBC. We also discuss 2 other cases that could be unreciognized associations of both diseases. Further reports are necessary to clarify if the coexistence between PBC and MPA is causal or casual.
35. A case of Takayasu arteritis complicated with glomerulonephropathy mimicking membranoproliferative glomerulonephritis: A case report and review of the literature.
Kuroda T, Ueno M, Sato H et al.
Rheumatol Int. 2006 Jul 8; [Epub ahead of print]
In this report, we describe the case of a 50-year-old Japanese women with Takayasu arteritis who developed severe proteinuria and renal dysfunction. Abdominal computed tomography did not narrowing of both renal arteries. Although her levels of C-reactive protein were negative, plasma vascular endothelial growth factor (VEGF) and serum interleukin (IL)-6 levels were elevated. Renal biopsy showed glomerulonephropathy mimicking membranoproliferative glomerulonephritis (MPGN) with glomerular capillary wall thickening (double contour). This was accompanied by mesangial cell proliferation and moderate increase of mesangial matrix without deposits of C3. These findings are quite different from MPGN as electron microscopy did not show subendothelial deposit and circumferential mesangial interposition. Here, we present the case of Takayasu arteritis associated with MPGN-like renal manifestation and elevated VEGF and IL-6. The presence of elevated VEGF and IL-6 could be factors that might contribute to MPGN-like appearence.
36. PR3-ANCA-positive crescentic necrotizing glomerulonephritis accompained by isolated pulmonic valve infective endocarditis, with reference to previous reports of renal pathology.
Fukuda M, Motokawa M, Usami T et al.
Clin Nephrol. 2006 66 (3): 202-9.
Abstract Patients with infective endocarditis (IE) often have renal complications which may include infarcts, abscesses and glomerulonephritis (GN). Furthermore, it is generally accepted that there is an association between IE and anti-neutrophil cytoplasmic antibody (ANCA). Here, we report the case of a 24-year-old man who developed rapidly progressive GN in the course of IE due to infection with alpha-streptococcus. The initial clinical manifestation of the condition was severe sacroiliitis without fever. Sandwich ELISA showed that the patients was positive for PR3-ANCA at low titer, and the classical complement pathway was also activated. Renal biopsy demonstrated several lesions: focal embolic GN, GN with immune deposits and focal and segmental crescentic necrotizing GN. Treatment with antibiotics and steroids led to eradication of the infection, and resolution of the renal disease was accompained by immediate disappearance of PRS-ANCA and hypocomplementemia. During a 4-year follow-up period, no recurrence was observed. Here have only been 7 case reports of GN associated with IE and PR-ANCA in which the renal pathology has been described, and the current report is the first to document renal pathology in a patient with isolated pulmonic valve IE and PR3-ANCA. Moreover, this report is the first to show a change in renal biopsy findings in response to treatment. A review of the 7 literature cases and that of our patient showed that none involved pauci-immune GN. Hence, further studies are needed to clarify the prevalence of pauci-immune GN in ANCA-positive IE patients.
37. Minimal change nephrotic syndrome and classical Hodgkin’s lymphoma: Report of 21 cases and review of the literature.
Audard V, Larousserie F, Grimbert P et al.
Kidney Int. 2006 69 (12): 2251-60.
Minimal change nephrotic syndrome (MCNS) is described as a paraneoplastic manifestation of classical Hodgkin’s lymphoma (cHL). We reassessed the pathophysiological and clinical significance of this association. A retrospective study was performed to evaluate a cohort of adult patients who developed MCNS and cHL. Twenty-one patients recruited in 15 French centers were analyzed. cHL was associated with inflammatory and general symptoms in most cases. The morphological subtype was predominantly nodular sclerosis (71.4%). MCNS appeared before the diagnosis of lymphoma in eight patients (38.1%) and in this case, it was characterized by a nephrotic syndrome (NS) frequently resistant (50%) or dependent (12.5%) to steroid treatment. Interestingly, diagnosis (3-120months after MCNS) and effective treatment of the hemopathy were associated with the disappearence of the MCNS. cHL was diagnosed before MCNS in nine patients in nine patients (42.9%), and in this case, glomerulopathy was associated with cHL relapse in 55.5% of cases. In four patients (19%), the two diseases occured simultaneously. Extensive immunohistochemical study of lymph nodes was performed in eight patients and did not reveal particular features. In conclusion, MCNS associated with cHL is frequently dependent or resistant to steroid regimen, but remission of NS is obtained the cure of lymphoma.
38. Minimal change disease following exposure to mercury-containing ligthening cream.
Tang HL, Chu KH, Mak YF et al.
Hong Kong Med J. 2006 12 (4): 316-8.
A 34-year-old woman developed nephrotic syndrome after using a skin lightening cream that contained an extremely high level of mercury. Blood and urine mercury levels were elevated and a renal biopsy revealed minimal change disease. Membranous nephropathy was excluded using immunoflorescence and electron microscopy. Her proteinuria remitted 9 months after she stopped using the cosmetic cream. This is the first reported case in the English literature of proven minimal change disease secondary to mercury exposure. It is important that mercury poisoning due to to cosmetic cream is considered in the differential diagnoses for any woman who presents with nephrotic syndrome.
39. Predictive factors of chronic kidney disease in primary focal segmental glomerulosclerosis.
Abrantes MM, Cardoso LS, Lima EM et al.
Pediatr. Nephrol. 2006 21 (7): 1003-12.
Renal histological features of focal segmental glomerulosclerosis (FSGS) are found in 75% of pediatric patients with steroid-resistant nephrotic syndrome. In order to evaluate the predictive factors of chronic kidney disease (CKD), we retrospectively reviewed the records of 110 children with biopsy-proven FSGS admitted between 1972 and 2004. Renal survival was analyzed by the Kaplan-Meier method and Cox’s regression model. Two multivariate models were developed: (1) from the onset of symptoms to the occurence of CKD and (2) the time of renal biopsy to CKD. Mean follow-up time was 10 years [standard deviation (SD) 5.5], and 24 patients (21.8%) progressed to CKD. At baseline, after adjusment three variables remained as independent predictors of CKD: age >6.5 years (RR=3.3, 95% CI=1.3-7.8), creatinine >1 mg/dl (RR=2.5, 95% CI=0.97-6.5), and non-response to steroids (RR=7.3, 95% CI=2.7-19.7). In a model with continuous variables only age and non-response to steroids were associated with CKD. At the time of renal biopsy, after adjusment two variables remained as independent predictors of CKD: hematuria (RR=3.0, 95% CI=1.2-7.3) and creatinine >0.8 mg/dl (RR=4.3, 95% CI=1.7-10.6). In a model with continuous variables four factors predicted CKD: age, creatinine, hematuria, and percentage of global sclerosis.
40. C1q nephropathy in association with Gitelman syndrome: A case report.
Hanevold C, Mian A, Dalton R.
Pediatr Nephrol. 2006 Sep 6; [Epub ahead of print]
There have been rare reports of glomerulopathies developing in patients with Bartter syndrome (BS) and its milder variant, Gitelman syndrome (GS). We present the first case of C1q nephropathy (C1qN) in an African American child with GS. This child was diagnosed with GS at 9 years of age and subsequently developed nephrotic range proteinuria 3 years later. Renal biopsy revealed mesangial hypercellularity and focal segmental glomerulosclerosis (FSGS). The segmental lesions were generally located at the vascular pole. Dominant C1q (2+) staining along with IgG (1-2+) was demonstrated in the mesangium, which correlated with scattered electron dense mesangial deposits demonstrated by electron microscopy. Treatment with an angiotensin-converting enzyme inhibitor led to an improvement in proteinuria to near-normal values (urine protein/creatinine ratio down to 0.5), but the creatinine clearence declined to approximately 58 ml/min/1.73 m(2). This case highlights the possible association between the milder hypokalemic tubulopathy, GS, and glomerular disease, including C1qN. Prompt evaluation of proteinuria with renal biopsy in these patients is recommended to detect significant glomerular pathology. Further research is needed to define risk factors for this complication.
41. Idiopathic membranous nephropathy in children.
Lee BH, Cho HY, Kang HG et al.
Pediatr Nephrol. 2006 21 (11): 1707-15.
Idiopathic membranous nephropathy (MN) is a rare cause of asymptomatic proteinuria (AP) or nephrotic syndrome (NS) in childhood. To improve our understanding of its clinical course, we retrospectively reviewed 19 cases of idiopathic MN seen in our hospital a period of 28.5 years, i.e., from January 1977 to July 2005. Eight patients (39%) had AP and 11 (61%) presented with NS. All eight AP patients achieved remission, regardless of treatment modality. Oral corticosteroid was given to all 11 NS patients, but only three of them responded to corticosteroid. Of the eight steroid non-responders, three achieved remissions with the addition of cyclosporine, and the five who were not administered additional immunosuppressive drugs had persistent NS. At the latest evaluation, all six NS patients achieved remission remained free of proteinuria and had a normal renal function. Moreover, two of the 5 steroid non-responders showed persistent nephrotic-range proteinuria but a stable renal function. The remaining three steroid non-responders progressed into chronic renal insufficiency, and this progression was preceded by renal vein thrombosis (RVT) in two of the three patients. Presentation with NS (P=0.045) and the development of RVT (P=0.010) were identified as poor prognostic factors.
42. Acute renal failure due to IgM-lambda glomerular thrombi and MPGN-like lesions in a patient with angioimmunoblastic T-cell lymphoma.
Miura N, Suzuki K, Yoshino M et al.
Am J Kidney Dis. 2006 48 (1): e3-9.
A 70-year-old man with angioimmunoblastic T-cell lymphoma developed acute renal failure. Laboratory data showed decreased levels of serum C3, C4, and CH50, elevated immunoglobulin M (IgM) levels, and the presence of cryoglobulinemia (IgM-lambda). Renal biopsy showed membranoproliferative glomerulonephritis-like lesions with azan-red-stained thrombi in the glomerular capillary lumen. Immunofluorescence showed that IgM-lambda stained strongly in the glomerular capillary lumen. Equal to the azan-red-stained thrombi, whereas C3 and C4 staining was negative. Electron microscopy showed electron-dense deposits in the subendothelial space and glomerular thrombi lacking fine fibrillar structure. These findings suggest that cryoglobulin which consists of monoclonal IgM-lambda, induced glomerular and acute renal failure in a patients with angioimmunoblastic T-cell lymphoma.
43. Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II).
Licht C, Heinen S, Jozsi M et al.
Kidney Int. 2006 70 (1): 42-50.
We report a novel pathomechanism for membranoproliferative glomerulonephritis type II (MPGN II) caused by a mutant factor H protein expressed in the plasma. Genetic analyses of two patients revealed deletion of a single Lys residue (K224) located within the complement regulatory region in domain 4 of Factor H. This deletion resulted in defective complement control: mutant protein purified from the plasma of patients showed severely reduced cofactor and decay-accelerating activity, as well as reduced binding to the central complement component C3b. However, cell-binding activity of the mutant protein was normal and comparable to wild-type Factor H. The patients are daughters of consanguineous parents. As both patients but also their healthy mother were positive for C3 nephritic factor, the mutant Factor H protein is considered relevant for unrestricted activation of the disease-causing activation of the alternative complement pathway. Replacement of functional Factor H by fresh frozen plasma (10-15 ml/kg days) was well tolerated, prevented so far disease progression in both patients, and is in the long run expected to preserve kidney function.
44. Long-term outcome 19 years after childhood IgA nephritis: A retrospective cohort study.
Ronkainen J, Ala-Houhala M, Autio-Harmainen H et al.
Pediatr Nephrol. 2006 21 (9): 1266-73.
We evaluated the natural long-term outcome after childhood IgA nephritis. Altogether 55 patients with biopsy-proven IgA nephritis were identified, 37 (67%) responded to the health questionnaire and 31 (56%) participated in the medical examination after a mean follow-up of 18.7 years (SD 6.2; range 8.5-29.8). The results of medical examination, onset data and the re-analysis of original biopsies of 31 participants were used when analyzing the predictive factors for persistent nephropathy, i.e. constant proteinuria/hematuria or end-stage renal disease (ESRD) All patients’ medical history data were obtained from regional hospitals and renal survival data from the national kideny register. Six (11%) of the 55 identified patients had developed ESRD. Sixteen (52%) of the 31 participants were not attending for regular follow-up visits after acute phase. Twenty-two (71%) had renal symptoms and 12 (39%) were receiving drugs for hypertension/proteinuria at their latest follow-up visit. The chronicity index and total biopsy score in the first renal biopsy were higher in patients with persistent nephropathy or ESRD than in those without (P=0.022 and p=0.014, respectively). Nine (69%) of the 13 subjects who had been over 16 years of age at diagnosis had persistent nephropathy or ESRD, compared with 4 (22%) of the 18 subjects who had been under 16 years of age (relative risk 3.1, 95% CI 1.2-8.0). Pregnancy complications were common: 12 (55%) of the 22 pregnancies had been complicated by proteinuria and/or hypertension, and the prematurity rate was 30%. Long-term follow-up during adulthood is needed even after mild childhood IgA nephritis, espacially in women during and after pregnancy.
45. A scoring system to predict renal outcome in IgA nephropathy: From a nationwide prospective study.
Wakai K, Kawamura T Endoh M et al.
Nephrol Dial Transplant. 2006 Jul 5; [Epub ahead of print]
Background Immunoglobulin A (IgA) nephropathy is the most commom form of feature glomerulonephritis in the world, and a substantial number of patients develop end-stage renal disease (ESRD). Although there are several prognostic indicators, it remains difficult to predict the renal outcome in individual patients. Methods A prospective cohort study was conducted in 97 clinical units in Japan from 1995 to 2002. We analysed the data from 2269 patients using proportional hazards models in order to determine the predictors of ESRD in IgA nephropathy and develop a scoring system to estimate ESRD risk. Results During follow-up (median, 77 months), 207 patients developed ESRD. Systolic hypertension, proteinuria, hypoproteinemia, azotemia and a high histological grade at initial renal biopsy were independently associated with the risk of ESRD. Mild haematuria predisposed patients to ESRD more than severe haematuria. A scoring system was developed to estimate the 7-year ESRD risk from eight clinical and pathological variables. Actually, this prognostic score accurately classified patients by risk: patients with estimates of 0.0-0.9, 1.0-4.9, 5.0-19.9, 20.0-49.9, and 50.0-100.0% had a 0.2, 2.4, 12.2, 40.2 and 80.8% of ESRD incidence over 7 years, respectively. The corresponding area under the reciver operating characteristic curve was 0.939 [95% confidence interval (CI), 0.921-0.958]. This score was verified in repetions of the deriavtion-validation technique. Conclusions Although the quality of some data collected by the mail survey is limited and the influence of therapy could not be considered, this scoring system will serve as a useful prognostic tool for IgA nephropathy in clinical practice.
46. IgA-containing immune complexes in the urine of IgA nephropathy patients.
Matousovic K, Novak J, Yanagihara T et al.
Nephrol Dial Transplant. 2006 21 (9): 2478-84.
Background Sera of IgA nephropathy (IgAN) patients contain high levels of circulating immune complexes composed of IgA1 molecules with aberrantly glycosylated hinge-region O-linked oligosaccharides and IgG or IgA1 antibodies with anti-glycan or anti-hinge-region peptide specificities. Due to damaged sieving properties of the glomerular capillary wall in IgAN, these immune complexes may appear in the urine. Methods We collected urine samples from 29 patients with biopsy-proven IgAN (Group I), 27 proteinuric patients with non-IgA nephropathies (Group II) and 28 healthy volunteers (Group III). The levels of urinary IgA and IgG and IgA-IgG-conataining immune complexes were measured by ELISA and standardized for urinary creatinine concentrations. Results The urinary IgA and IgG levels were significantly higher in Groups I and II than in Group III. Although the excretion of IgA as a fraction of total urinary protein was not significantly greater in IgAN patients than in patients with other renal diseases, the excretion of aberrantly glycosylated IgA1 was observed by western blot in 68% of the IgAN patients but in none of healthy controls. The urinary levels of IgA-IgG immune complexes were significantly higher in Group I than Groups II (P < 0.01) and III (P < 0.05). There was no significant difference in the levels between Groups II and III. These immune complexes had a molecular mass between 650-850 kDa, as shown by size-exclusion chromatography. Conclusion The amounts of urinary IgA-IgG-conatining immune complexes were significantly higher in patients with IgAN than in patients with non-IgA nephropathies or healthy controls.
47. Cholestatic jaundice and IgA nephropathy induced by OTC muscle building agent Superdrol.
Jasiurkowski B, Raj J, Wisinger D et al.
Am J Gastroenterol. 2006 Sep 4; [Epub ahead of print]
Over the counter (OTC) medicines are commonly used in the United States despite a lack of scientific evidence for clinical utility and toxicity associated with their use. A case of jaundice and IgA nephropathy as a consequence of use of a muscle enhancing OTC supplement that was advertised as innocuous with no hormonal activity is described. IgA nephropathy has not been described previously in association with the use of testosterone. The case highlights that, besides adulteration, the misrepresentation of chemicals present in OTC medications and supplements can create confusion and a false sense of security with their use.
48. The -374 T/A polymorphism in the gene encoding RAGE is associated with diabetic nephropathy and retinopathy in type 1 diabetic patients.
Lindholm E, Bakhtadze E, Sjogren M et al.
Diabetologia. 2006 Sep 13; [Epub ahead of print]
Aims/Hypothesis The receptor for AGE (RAGE) is considered to be mainly an intracellular signal-transducer or pro-inflammatory peptide of possible importance for inflammation and autoimmune diseases. Our aim was to study whether the -374 T/A polymorphism in the gene encoding RAGE (AGER) is associated with diabetes and presence of diabetic complications. Methods The AGER -374 T/A polymorphism was genotyped in 867 type 1 diabetic patients, 2,467 type 2 diabetic patiens and 205 non-diabetic control subjects of Scandinavian origin. Results AGER polymorphism was related to different HLA-DQB1 genotypes and the presence of diabetic complications. Type 1 diabetic patients had a higher frequency of the AGER -374 A/A or T/A genotypes than type 2 diabetic patients (51.1 vs 44.9%, p = 0.002) and control subjects (51.1 vs 47.6%, p = 0.0006). The RAGE -374 T/A polymorphism was associated with HLA-DQB1 genotypes; patients with HLA risk genotypes had a higher frequency of the A/A or T/A genotypes than patients with other HLA-DQB1 genotypes (60.3 vs 40.3%, p < 0.000001). In type 1 diabetic patients, the frequency of the A/A or T/A genotypes was higher in patients with diabetic nephropathy than without (61.1 vs 46.8%, p = 0.006) and with sight-threatening retinopathy than without (56.1 vs 47.6%, p = 0.03). In type 2 diabetic patients with HbA(1c) values below the median, the T/T genotype was more frequent in patients with diabetic nephropathy than without (54.3 vs 38.2%, p = 0.02). Conclusion/Interpretation Our results show an association between the AGER -374 T/A polymorphism and type 1 diabetes. This association was HLA-DQB1-dependent. The polymorphism was associated with diabetic nephropathy in both type 1 and type 2 diabetes, in an HbA(1c)-dependent manner in latter group, and also with sight-threatening retinopathy in type 1 diabetic patients.
49. Association between serum levels of soluble receptor for advanced glycation end products and circulating advanced glycation end products in type 2 diabetes.
Tan KC, Shiu SW, Chow WS et al.
Diabetologia. 2006 Sep 13; [Epub ahead of print]
Aims/Hypothesis Activation of the the receptor for advanced glycation end products (RAGE, also known as AGE-specific receptor [AGER]) has been implicated in the development of diabetic vascular complications. Blockade of RAGE using a soluble form of the receptor (sRAGE) suppressed vascular hyperpermeability and atherosclerosis in animal models. Since little is known about the regulation of endogenous sRAGE levels, we determined whether serum sRAGE is influenced by circulating AGEs and the severity of nephropathy in type 2 diabetic patients. Materials/Methods We recruited 150 healthy control and 318 diabetic subjects. Diabetic subjects were subdivided into those with proteinuria, microalbuminuria or normoalbuminuria. Serum sRAGE was assayed by ELISA and serum AGEs by competitive ELISA using a polyclonal rabbit antiserum raised against AGE-Rnase. Results Diabetic subjects had higher sRAGE (1,029.5 pg/ml [766.1-1,423.0] interquartile range vs 1,002.6 [726.5-1,345.3], p < 0.05) and AGEs (4.07 +/- 1.13, SD, unit/ml vs 3.49 +/- 1.05, p < 0.01) than controls. Proteinuric subjects had the highest sRAGE levels and there was a significant trend between the severity of nephropathy and sRAGE (p = 0.01). In diabetic subjects, serum log(sRAGE) correlated with AGES (r = 0.27, p < 0.001), log(plasma creatinine) (r = 0.31, p < 0.001), log(urine AER) (r = 0.24, p < 0.01) and log(triglycerides) (r = 0.15, p < 0.01). On stepwise linear regression analysis, AGEs and creatinine levels were the main independent determinants of sRAGE concentration. Conclusions/Interpretation Serum sRAGE levels and circulating AGEs associated with the severity of nephropathy in type 2 diabetic patients. Prospective studies are required to determine whether endogenous sRAGE potentially influences the development of diabetic vascular complications.
50. Urinary tumour necrosis factor-{alpha} excretion independently correlates with clinical markers of glomerular and tubulointerstitial injury in type 2 diabetic patients.
Navarro JF, Mora C, Muros M et al.
Nephrol Dial Transplant. 2006 Aug 25; [Epub ahead of print]
Background Inflammation is a potential factor in the development and progression of diabetic nephropathy. The aim of this study to analyse the relationship between the pro-inflammatory cytokine tumour necrosis factor-alpha (TNFalpha) and clinical markers of glomerular and tubulointerstitial damage [urinary albumin excretion (UEA) and urinary N-acetyl-beta-glucosaminidase (UNAG), respectively] in a large group of type 2 diabetic patients. Methods A total of 160 diabetic patients and 32 healthy controls were included in the study. High-sensitive C-reactive protein (hs-CRP) as well as serum and urinary levels of TNFalpha were measured. UAE and UNAG were determined by 24-h urine collection. Results Serum hs-CRP and TNFalpha were significantly higher in diabetic than in control subjects, as well as UAE and UNAG. Diabetic patients had increased urinary TNFalpha compared to non-diabetics [14.5 (2-29) vs 4 (0.8-12), P < 0.001]. Serum hs-CRP and TNFalpha in diabetics with increased UEA were elevated compared to diabetics having normoalbuminuria. Urinary TNFalpha was also higher in diabetic subjects with micro- or macroalbuminuria than in patients with normal UAE [10.5 (4-20) and 18 (2-18) pg/mg, P < 0.0001, respectively]. Multiple regression analysis showed that urinary TNFalpha (P < 0.0001), hs-CRP (P < 0.0001) serum TNFalpha (P < 0.01) and HbA1c (P < 0.05) were independent of and significantly associated with UAE, whereas duration of diabetes (P < 0.001), urinary TNFalpha (P < 0.01), HbA1c (P = 0.01), hs-CRP (P < 0.05) and serum creatinine (P < 0.05) were associated with UNAG. Conclusions In patients with type 2 diabetes, urinary TNFalpha excretion is elevated and correlates with severity of renal disease in terms of both glomerular and tubulointerstitial damage, suggesting a significant role for TNFalpha in the pathogenesis and progression of renal injury in diabetes mellitus.
51. Redistribution of connexin43 expression in glomerular podocytes predicts poor renal prognosis in patients with type 2 diabetes and overt nephropathy.
Sawai K, Mukoyama M, Mori K et al.
Nephrol Dial Transplant. 2006 21 (9): 2472-7.
Background Significance of podocyte injury in the progression of diabetic nephropathy is not well-understood. In this study, we examined whether alteration of gap junction protein connexin43 (Cx43) expression in podocytes is associated with the progression of overt diabetic nephropathy. Methods We recruited 29 type 2 diabetic patients with overt nephropathy who underwent renal biopsy. Nephrectomized kidney samples obtained from seven subjects with localized neoplasm and biopsy specimens from five patients diagnosed as minor glomerular abnormalities were used as controls. Cx43 staining on paraffin-embedded kidney sections were studied by immunohistochemistry. Results In controls, Cx43 was expressed at podocytes in a linear pattern along the glomerular basement membrane. In contrast, downregulation and loss of uniformly linear staining of Cx43 (Cx43 heterogeneity) in podocytes were observed in diabetic nephropathy. Cx43 intensity correlated with current renal function (R = 0.647, P < 0.005), whereas the magnitude of Cx43 heterogeneity correlated well with degree of future decline in renal function (R = -0.705, P < 0.001). Conclusions Alteration of Cx43 expression in podocytes was closely associated with the progression of overt diabetic nephropathy. These results indicate that change in Cx43 expression at podocytes represents a progressive stage in overt diabetic nephropathy and that it may be a convenient way to predict future decline in renal function.
52. Vascular defect beyond the endothelium in type II diabetic patients with overt nephropathy and moderate renal insufficiency.
Chan WB, Chan NN, Lai CW et al.
Kidney Int. 2006 70 (4): 711-6.
There is a paucity of data on the effects of overt nephropathy and moderate renal impirment on endothelial function in diabetic patients. A total of 26 type II diabetic (DM) patients with nephropathy (DMN+) (mean +/- s.d. age: 63.7 +/- 6.3 years), 32 diabetic patients without nephropathy (MN-) (59.4 +/- 10.1 years), and 52 non-diabetic subjects (54.9 +/- 8.2 years) were recruited. High-resolution ultrasound scan was used to measure carotid intima media thickness (IMT) and flow-mediated dilation (FMD) of brachial artery. Endothelium dependent dilation was determined by maximal vascular dilation after sublingual nitroglycerine (glycerol trinitrate (GTN-induced dilation). The mean carotid IMT increased progressively from non-DM to MNN- to DMN+ groups (0.74 +/- 0.23 vs 0.80 +/- 0.25 vs 1.03 +/- 0.38 mm; P = 0.001 for trend) whereas FMD (4.3 +/- 2.5 vs 3.9 +/- 1.7 vs 1.9 +/- 2.0%, P < 0.001 for trend) and GTN-induced dilation (14.7 +/- 4.0 vs 14.5 +/- 3.9 vs 10.3 +/- 3.2%; P < 0.001 for trend) declined in an opposite manner. On multivariate analysis, age (beta = 0.257, P = 0.009), glomerular filtration rate (beta = -0.364, P < 0.001), and smokong (beta = 0.25, P = 0.013) were independently associated with carotid IMT (F = 15.76, R(2) = 0.340, P < 0.001). After adjusment for baseline brachial arterial diameter, history in smoking (beta = -0.039, P < 0.001), fasting plasma glucose (beta = -0.033, P = 0.002) and total cholesterol (beta = -0.023, P = 0.024) were independently associated with vessel diameter after FMD (F = 2446.5, R(2) = 0.992, P < 0.001); whereas age (beta = -0.069, P = 0.001) and urinary albumin excretion (beta = -0.048, P = 0.018) were independently associated with vessel diameter after GTN (F = 851.6, R(2) = 0.967, P < 0.001). Type II diabetic patients with overt nephropathy and moderate renal impairment had both structural and functional vascular abnormalities beyond endothelium.
53. Clinical characteristics of chronic kidney disease patients with and without diabetes: A subanalysis of the PAERI study.
Lorber D, Reddan D.
Clin Nephrol. 2006 66 (1): 11-6.
Aims Diabetes is the leading cause of chronic kidney disease (CKD) in the United States, and cardiac disease is the primary cause of death in patients with CKD and diabetes. The Prevalence of Anemia in Early Renal Insufficiency (PAERI) study evaluated the prevalence of anemia and association comorbidities in community-based sample of patients with CKD. The purpose of this post hoc analysis was to identify differences, if any, in the prevalence and severity of anemia (hemoglobin < or = 12 g/dl (120 g/l) and other clinical characteristics between CKD patients with diabetes and patients with CKD who did not have diabetes. Material and Methods The PAERI study was a prospective, cross-sectional, multicenter survey. Eligible patients were > or = 18 years old with CKD, defined as serum creatinine 1.5 - 6.0 mg/dl (132.6 - 530.4 micromol/l) in females and 2.0 - 6.0 mg/dl (176.8 - 530.4 micromol/l) in males within 12 months before enrollment. Study duration for each patient was a single site visit. Results Of the original 5,222 patients enrolled, 3,361 had diabetes and 1,861 did not. A family history of diabetes was present in 72.7% of diabetic patients vs 27.2% of nondiabetic patients (p < 0.0001). Patients with diabetes had a significantly higher prevalence of anemia (52.7 vs. 39.4%, p < 0.0001) and cardiac disease (55.7 vs. 42.9%, p < 0.0001). The prevalence of hypertension was high in both groups (91.5 vs. 89.3%). Significantly more diabetic patients than nondiabetic patients received angiotensin-converting enzyme inhibitors (60.4 vs. 43.8%, p < 0.0001). Hyperlipidemia was more common in patients with diabetes (73.9 vs. 55.4%, p < 0.0001). Patients with diabetes were slightly younger and had a significantly higher mean body mass index and lower transferrin saturation compared with nondiabetic patients. In diabetic and nondiabetic patients, more than 97% had glomerular filtration rate < 60 ml/min/1.73 m^2 and more than 70% had serum creatinine < 2.5 mg/dl (221.0 micromol/l). Conclusions These findings underscore the extent and severity of concurrent illness in patients with both diabetes and CKD. In those patients, diabetes was associated with a greater prevalence of serious cardiac-related comorbidities than observed in nondiabetic patients.
54. Management of cardiovascular risk factors in advanced type 2 diabetic nephropathy: A comparative analysis in nephrology, diabetology and primary care settings.
Minutolo R, Sasso FC, Chiodini P et al.
J Hypertens. 2006 24 (8): 1655-61.
Objectives Advanced diabetic nephropathy (DN) is characterized by a marked development of cardiovascular and renal disease. These patients are frequently managed by different health professionals with the consequence that the quality of care may differ substantially. To compare the management of cardiovascular risk factors in patients with type 2 DN and an estimated glomerular filtration rate (GFR) of 15-60 ml/min per 1.73 m (2) followed in nephrology, diabetology and primary care. Methods This multicentre cross-sectional study verified the control of blood pressure (BP), total cholesterol, triglycerides, glycosylated haemoglobin A1c (HbA1c) and haemoglobin in patients exclusively followed in either nephrology (n = 266), diabetology (n = 246) or primary care (n = 195) of the same metropolitan area for at least 1 year. Results Primary care patients were older and had a greater prevalence of previous cardiovascular events. The GFR was lower in nephrology than in diabetology and primary care (33 +/- 13 versus 47 +/- 9 and 40 +/- 12 ml/min/1.73 m(2), P < 0.0001). the prevalence of BP target ( ................
................
In order to avoid copyright disputes, this page is only a partial summary.
To fulfill the demand for quickly locating and searching documents.
It is intelligent file search solution for home and business.