KENdensed Renal Pathophysiology Notes I
KENdensed Renal Pathophysiology Notes I
Glomerular disease thru Acute Renal Failure pgs 62-130 in Renal PPD notes
Glomerular diseases:
Histologic Alterations
1. Glomerular hypercellularity – cellular proliferation, leukocytic infiltration
2. Basement Membrane thickening- thickening of BM, deposition of electron dense material (most common thickening is by extensive subepithelial deposition, as in membranous glomerulonephritis)
3. Hyalinization- accumulation of material that is homogenous, and eosinophilic by LM
4. Sclerosis- Loss of structural detail of Glomerular tuft by increased BM or mesangial matrix, other alterations include fibrin deposition, amyloid, lipid
I. The Clinical Syndromes:
|Syndrome |Clinical Findings |Causes |
|Acute |Hematuria, azotemia, variable proteinuria, |Post streptococcal |
|Nephritic Syndrome |oliguria, edema, HTN |SLE |
| | |Polyarteritis nodosa |
|Rapidly progressive GN |Acute nephritis, proteinuria, ARF |Postinfectious |
| | |Systemics: |
| | |SLE |
| | |Goodpastures |
| | |Vasculitis |
| | |Henoch-Schonlein purpura |
|Nephrotic Syndrome |Proteinuria, hypoalbuminemia, |Membranous GN |
| |hypercholesterolemia, edema |Minimal Change Disease (Lipoid nephrosis) |
| | |FS glomerulosclerosis |
| | |Membranoproliferative GN |
| | |IgA Nephropathy |
| | |Sytemics: |
| | |DM |
| | |Amyloidosis |
| | |SLE |
| | |Drugs ( Gold, penicillamine) |
| | |Infectious (malaria, syphilis, Hep B, HIV) |
| | |Carcinoma |
|Chronic Renal Failure |Azotemia progressing to uremia |Almost any glomerulopathy! |
|Asymptomatic heamturia or |Glomerular hematuria, subnephrotic proteinuria|(incidental finding in routine exam) |
|proteinuria | | |
|Disease |Clinical Presentation |Pathogenesis |Clinical Course |LM |IF |EM |
|Poststrep | | | | | | |
|glomerulonephritis |Acute nephritis |Ab mediated, circulating |Case: young child w/ malaise, fever, |Enlarged, hypercellular bloodless |Granular IgG, C3 in |Subepithelial humps |
| | |or planted Ag |nausea, oliguria, hematuria after sore |glomeruli, |GBM and mesangium | |
| | | |throat. RBC casts in urine, mild |Diffuse proliferation, leukocytic | | |
| | | |proteinuria, periorbital edema, some HTN. |infiltration | | |
| | | |Labs: ASO titer, serum C3 | | | |
| | | |Tx: 95% recover w/ conservative Na/H20 | | | |
| | | |balance therapy | | | |
|Goodpasture’s |RPGN |Anti GBM Ag |RBC casts in urine, moderate proteinuria, |Crescents, formed by proliferation |Granular immune |Distinct ruptures in GBM, |
| | | |variable HTN, edema |of parietal cells and by |deposits |some subepithelial |
| | | | |monocyte/macrophage migration into | |deposits |
| | | |Tx: intensive plasmapheresis, steroids, |Bowman’s space | | |
| | | |cytotoxic agents (these also relieves | | | |
| | | |pulmonary failure) | | | |
|Idiopathic RPGN |RPGN |Anti GBM immune complex |Therapy as with Goodpastures, but results |Proliferation, crescents |Linear IgG, C3 or |Deposits or none |
| | | |not as dramatic | |granular, or none | |
|Membranous |Nephrotic Syndrome |Ab mediated, in situ |Major cause of Nephrotic syndrome in |Uniform, Diffuse capillary wall |Granular IgG, C3 |subepithelial deposits |
|Glomerulonephritis | | |adults: Tumor, ALE, gold, mercury, Drugs, |thickening, BM spikes between | | |
| | | |Hep B, syphilis, schisto, malaria, |deposits | | |
| | | |idiopathic. | | | |
| | | | | | | |
| | | |Case: insidious nephrotic syndrome, | | | |
| | | |hematuria, HTN, w/ increasing sclerosis of | | | |
| | | |glomeruli, rising BUN… notoriously variable| | | |
| | | |course | | | |
|Minimal Change (Lipoid |Nephrotic Syndrome |Unknown |Children w/ massive proteinuria, renal |Normal |Negative |Loss of foot processes |
|nephrosis) | | |function remains good, | | | |
| | | |Tx: corticosteroids | | | |
|Focal Segmental |Nephrotic syndrome, |Unknown |Compared to Minimal change disease: inc |Hallmark is degeneration and focal |Focal IgM and C3 |Loss of foot processes, |
|glomerulo sclerosis |non-nephrotic | |hematuria, red GFR, inc HTN, poor steroid |disruption of visceral epithelial | |epithelial denudation |
| |proteinuria | |response, many progress to chronic GN, IF |cells. Focal and segmental | | |
| | | |shows deposits. |sclerosis, collapse of BM, inc | | |
| | | |Rare spontaneous remission. |mesangial matrix and hyalinosis | | |
|Disease |Clinical Presentation |Pathogenesis |Clinical Course |LM |IF |EM |
|Membranoproliferative GN| | | | | | |
|Type I |Nephrotic Syndrome |Immune complex |Older children, young adults. Some patients|Large hypercellular glomeruli, |IgG, C3, C1, C4 |Subendothelial deposits |
| | | |develop crescents, and RPGN, 50% develop |Mesangial proliferation, GBM | | |
| | | |CRF. |thickening, splitting, some | | |
| | | |Tx of steroids, immunosuppressive agents |crescents | | |
| | | |not very effective. | | | |
|Membranoproliferative GN| | | | | | |
|Type II |Hematuria, CRF |AutoAb, alternative |Older children, young adults. Some patients|Large hypercellular glomeruli, |C3, some IgG |Dense deposits |
| | |complement pathway |develop crescents, and RPGN, 50% develop |Mesangial proliferation, GBM | | |
| | | |CRF. |thickening, splitting, some | | |
| | | |Tx of steroids, immunosuppressive agents |crescents | | |
| | | |not very effective. | | | |
| | | |Recurrence is common in Type II | | | |
|IgA Nephropathy |Recurrent hematuria and |Unknown |Affects children/young adults in 1-2 days |Focal proliferative GN; mesangial |IgA, IgG, IgM, C3 in|Mesangial and |
|(Berger’s disease) |/or proteinuria | |of mucosal infections of Resp, GI or |widening |mesangium |paramesangial dense |
| | | |urinary tracts, slowly progressive disease | | |deposits |
|Chronic |CRF |Variable |Insidious development slowly progresses to |Hyalinized glomeruli |Granular or negative|none |
|glomerulonephritis | | |death in uremia. Most patients have HTN, | | | |
| | | |manifested by cerebral or cardio symptoms. | | | |
Chronic renal failure:
Major Causes of CRF
1. Glomerulopathies
2. Hypertension
3. Obstructive uropathy
4. Interstitial nephritis
5. Hereditary (PCKD)
I. Intact Nephron hypothesis – nephrons in damaged kidneys operate at a higher functional level so that gross kidney function is preserved
II. Discrimination between ARF and CRF
1. H & P- Previous serum Creatinine, nocturia, history of foray urine, edema, orthostatic HTN, muscle tenderness, etc
2. Kidney size – small, CRF
3. Renal Osteodystrophy – yes- CRF
4. Carbamylated HgB – yes- CRF
5. Anemia – no- ARF
Stages of renal failure
1. Decreased renal reserve – excretory regulatory capacity intact, GFR dec. but labs normal
2. Renal insufficiency – mild azotemia, impaired concentrating ability, nocturia, anemia
3. Renal failure – anemia inc, hypocalcemia, hyperphosphatemia, hyponatremia, impaired concentrating ability, nocturia, isothenuria, metabolic acidosis
4. Uremia – constellation of signs/symptoms
a. Signs and symptoms of uremia:
i. Nervous- stupor, coma, fatigue, malaise, insomnia, memory, speech slurred, tics, dementia, headache, cramps
ii. GI – hiccup, parotitis, gastritis, anorexia, pancreatitis, ulcer, nausea/vomiting
iii. Hematology – anemia, bleeding
iv. Immunology – inc infection/ cancers
v. Cardio – pericarditis, atheromatosis, edema HTN, cardiomyopathy
vi. Pulmonary – pleuritis, edema
vii. Skin –pruritus, nail atrophy, melanosis
viii. Endocrine – glucose intolerance, hyperlipidemia, hyperPTH, hypogonadism, growth retardation
ix. Bone – renal osteodystropy, amyloidosis
x. Misc – thirst, weight loss, uremic fetor, hyperthermia
Functions of the Kidney
1. Fluid-electrolyte balance, acid/base homeostasis
a. Types of filtrate products
i. Non regulated – plasma concentration falls w/GFR (creatinine, BUN)
ii. Partial regulation – balanced until GFR < 30-40 ml/min
(Hydrogen ion, uric acid, phosphate, calcium)
iii. Complete regulation – balance maintained until GFR < 10-15 ml/min (Na+, K+, H20)
b. CRF loss of renal concentrating ability
i. At max urine output, CRF patients make less urine than normal and at higher osmolarity—more Na+ loss
ii. At min urine output, CRF patients make more urine than normal—and at less osmolarity—unable to excrete enough Na+
c. Signs of abnormal fluid balance
i. Abnormal concentration
• Nocturia
• Volume depletion/hypernatremia w/o access to H20 or impaired thirst
ii. Abnormal dilution
• Hyponatremia
• Greater susceptibility to H20 intoxication
d. Na+ excretion with CRF
i. CRF patients excrete same amount of Na+ as normal patients, but they have dec GFR, so they lose higher % of Na+
ii. Regulation of Na+ by CRF patients
• Adaptation occurs in distal tubule
• Aldosterone levels normal to high
•ANP inc
iii. Uremic symptoms from abnormal Na+
•Hypernatremia-- edema, CHF, hypertension
• Hyponatremia—volume contraction, ARF
e. e. K+ excretion with CRF
i. K+ regulation with CRF
f. • Maintained until GFR ................
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