University of Edinburgh



Gray scale Ultrasound, color Doppler Ultrasound and Contrast-enhanced Ultrasound in Renal Parenchymal DiseasesAbstractUltrasound (US), which may be combination of gray scale and spectral Doppler US, color and power Doppler US, with or without microbubble contrast agents, is usually the first imaging modality to be employed in renal parenchymal diseases. The most typical appearance of diffuse renal parenchymal diseases on grayscale US is an increased renal cortical echogenicity and increased or reduced corticomedullary differentiation. Spectral Doppler analysis of intrarenal flows may reveal an increase in intrarenal resistive index value >0.70 in native kidneys, and >0.8 in renal transplants. Gray scale US and spectral Doppler US do not exhibit high specificity and sensitivity since different renal parenchymal diseases often display the same US appearance, whereas the same renal parenchymal disease may present different appearances on US according to disease stage. Consequently, correlation of the US pattern with patient’s history and clinical background is essential for a correct characterization. Key words: Kidney – disease – Ultrasound – Doppler – contrast - microbubblesLearning objectives:Discuss the fundamental US appearance of renal parenchymal diseasesExplain current concepts of gray scale US, Doppler US, and contrast-enhanced US in the evaluation of renal parenchymal diseasesIdentify the current most important indications for gray-scale US of the kidney and the added value of this technique Optimize and interpretate color and spectral Doppler information to identify diffuse renal parenchymal diseasesDefine the specific features of each renal parenchymal disease in terms of gray-scale US, spectral Doppler and color DopplerDefine the role of contrast-enhanced US in renal parenchymal diseasesUS techniques and normal renal anatomy Gray scale ultrasound (US), with addition of harmonic and compound speckle-reduction modes and colour Doppler (CD) USmodes, is the first imaging modality for the study of kidney diseases and for the guidance of interventional procedures including renal parenchymal biopsy [1, 2]. Convex-array US transducers (broadband frequency probes of 1–8 MHz in adults, and 3–10 MHz in pediatric patients) are usually employed in the US scanning of the kidneys.At gray scale US, the renal cortex – containing renal glomeruli and proximal and distal tubules - presents a lower echogenicity than the liver, spleen and renal sinus [2], while renal inner medulla (renal pyramids) - containing vasa rectae, medullary capillary plexus, loops of Henle, and collecting ducts - may be differentiated from renal cortex in most of adult patients being hypoechoic in comparison to the renal cortex [2] although the relative hypoechoic appearance of inner medulla depends on the echogenicity of renal cortext which can be altered by the fluid status of the patient . Spleen echogenicity is used as a standard reference to evaluate the echogenicity of the renal cortex in the presence of fatty liver [2]. Furthermore, kidneys may be isoechoic to the liver even when no clinical or laboratory evidence of renal disease is documented.Since numerous renal parenchymal diseases may reveal similar appearance on gray scale US [1, 3], whereas a single renal parenchymal disease may present variable appearances on gray-scale US according to the stage, the correlation of the US pattern with patient’s clinical history and background is essential for a correct characterization.US presents a general sensitivity of 62–77 %, a specificity of 58-73% and a positive predictive value of 92 % for detecting microscopically confirmed renal parenchymal diseases [3 – 5]. In early clinical stages of renal parenchymal diseases, kidneys may appear normal on US, whereas as parenchymal diseases progress hyperechoic renal parenchyma may reesult also with increased or reduced corticomedullary differentiation. There is a correlation between cortical echogenicity and focal leukocytic infiltration, severity of global sclerosis, focal tubular atrophy, and number of hyaline casts per glomerulus [6]. However, lack of overlying fat such as in pediatric patients or abundant fat such as in obese patients, may make corticomedullary differentiation less evident.Decreased corticomedullary differentitation is observed when inflammatory infiltrates (glomerulonephritis and acute tubulointerstitial nephritis) and fibrous tissue (glomerulosclerosis, tubulointerstitial fibrosis) extend to renal medulla or when hyaline casts are present within collecting ducts. Reversed corticomedullary differentiation is observed in several specific diseases including medullary nephrocalcinosis [7] due to hyperparathyroidism, medullary sponge kidney, renal tubular acidosis (type 1), sarcoidosis, Tamm–Horsfall proteinuria, recessive polycystic disease, and haemoglobinuria.Renal sinus fat appears hyperechoic if compared with renal parenchyma, in the presence of hilar adipose tissue with fibrous septae, blood vessels and lymphatics. It may appear inhomogeneous at US due to septal thickness, fibrosis, atrophy, and loss of adipose tissue with a progressive lower renal sinus–renal parenchymal differentiation. With increasing age, amount of renal parenchyma decreases and renal sinus fat increases [1, 2]. Renal sinus fat may be increased also in renal sinus lipomatosis which can be seen in obesity and parenchymal atrophy as well as in normal variants [1, 2]. Assessment of renal size is important in the diagnosis, treatment and determination of prognosis in diffuse renal diseases even though renal volume correlates better with total body area and renal function [8, 9]. especially if the volume is obtained by using 3D ultrasound system instead of being length-based [10]. The length of both kidneys is considered normal between 10 and 12 cm with a kidney length <10 cm unusual in people younger than age 60 years [2]. Reduced kidney dimensions are typically found in chronic kidney disease, while increased renal dimensions may result from infiltrative diseases (e.g., multiple myeloma, amyloidosis, lymphoma), acute glomerulonephritis or tubulointerstitial nephritis due to edema and inflammation, and renal vein thrombosis due to obstruction of blood flow and subsequent edema. Normally, renal margins are smooth, except in some normal anatomical variants such as functional parenchymal defects and renal fetal lobulations. Mean normal value of renal cortical thickness, measured from the base of the medullary pyramid to the edge of the kidney, ranges from 7mm to 10 mm (being thicker at the renal poles), while renal parenchyma thickness including renal medulla ranges from 15mm to 20 mm [2]. Renal parenchymal arterial and venous vessels have to be evaluated by flow optimization for slow flows with low pulse repetition frequency, low wall filter, and by appropriate gain setting with the lowest possible level of noise [1, 2]. Increased sensitivity of color and power Doppler and ultrasensitive Doppler techniques (also called micro-Doppler imaging), based on ultrafast plane wave imaging, in which Doppler signals corresponding to all pixels are acquired at the same time continuously and simultaneously across the full image, and advanced clutter suppression algorithms [11] provided by the latest digital US equipments allows depiction and spectral Doppler interrogation of the renal parenchymal vessels up to the interlobular arteries [11] (Figure 1). Assessment of renal vascular resistances is obtained by spectral Doppler trace analysis and measurement of angle-corrected (<60°) peak systolic and diastolic velocities with calculation of the intrarenal resistive indices (RIs): (peak systolic velocity minus the end-diastolic velocity) divided by the peak systolic velocity). The mean reference value for normal renal RI in adults is 0.60 ± 0.10, with 0.70 as the upper limit of normal [2, 7, 12]. The RIs measured on segmental, interlobar and arcuate renal parenchymal arteries are normally below 0.70, and decrease progressively from segmental to interlobular vessels [2, 7, 12]. Intrarenal RIs do not reliably distinguish the different types of renal medical disorders [12]. While it has been shown that intrarenal RIs are related not only to intrarenal vascular resistance but also to vascular compliance, intersitial and venous pressure, heart rate, aortic stiffness, and pulse pressure [13 – 15]. However, RIs maintain an important diagnostic role and may increase in several many causes of acute renal diseases, including acute urinary tract obstruction, acute tubular necrosis, acute rejection, hepatorenal syndrome, and sepsis due to increases in down- stream resistance, while RIs remain normal in prerenal azotemia and glomerular diseases. Contrast-ehanced US (CEUS) with microbubble – based contrast agents is the method of choice for identification of parenchymal perfusion defects, such as renal infarction, cortical necrosis, and ischemia, with a sensitivity of over 90% [11, 16] but it is not frequently used for diffuse renal disease. Shear – wave US elastography (transient eleastography, acoustic radiation force impulse - ARFI -, or Supersonic shearwave imaging) generates an US force that propagates a shear wave through tissue to assess quantitatively the elastic properties of tissues. Shear – wave US elastography ARFI quantifies shearwave velocities which are related to renal tissue stiffness in kPa while normal renal cortical stiffness ranges from 2.15 to 2.54 m/s (13.9–19.3 kPak) and increases in chronic kidney disease or chronic renal allograft nephropathy due to renal interstitial fibrosis [2, 11, 17 – 19] even though poor correlation was found [20]. Unfortunately, ARFI is not standardized for kidneys and ARFI would be difficult to be employed in kidneys with thin renal cortex due to difficult ROI placement. Moreover, chronic kidney diseases are often present in obese patients and US elastrography doesn’t provide reliable results after 6cm depth. The appearance of renal parenchymal diseases on gray scale and Doppler US, with some reference to CEUS and US elastography, will be described. Bibliographic search was conducted on PubMed, Scopus, and Web of Science medical databases by using the terms “kidney”, “disease”, “ultrasound”, “Doppler”, and “contrast agents” as search criteria. Each cited study had IRB or IACUC approval. All ultrasound US images are original and not previoulsly published, and no permission to reprint was necessary.Renal Infections In acute renal infections bacteria may reach the kidney principally through the ascending route, while the haematogenous route represents a less common alternative pathway of infection. Acute renal infections correspond to active interstitial nephritis characterized by the presence of polymorphonuclear leukocytes within the lumen of the tubules. The most prevalent agents include E. Coli, Proteus Mirabilis, Klebsiella Pneumoniae, Staphilococcus Aureus, Pseudomonas Aeruginosa [21]. Renal involvment may also be observed in Even disseminated fungal infection, infective endocarditis, tuberculosis, and filariasis may affect the kidney. Predisponing Predisposing factors include vesicoureteral reflux, pre-existing urinary tract diseases, diabetes mellitus, stones, immunodeficiency, neurogenic bladder, and surgical complications. The diagnosis of acute pyelonephritis is based on clinical symptoms and laboratory findings. Classic symptoms include an abrupt onset of chills, fever, and unilateral or bilateral flank pain. Histologically, there is extensive focal destruction by inflammation, with relative preservation of vessels and glomeruli. Infiltrates mainly contain neutrophils , which are which even fill filling tubules and collecting ducts. Papillary necrosis may be present.US is frequently used as a first-line imaging tool to evaluate the urinary tract in patients with symptoms of pyelonephritis. Unfortunately, gray-scale US presents a sensitivity of only 20% in patients with pyelonephritis [21, 22] which can rise up to 70 - 90% with the use of power Doppler [23, 24] and to 80% with the additional application of tissue harmonic imaging and microbubble contrast agents [25]. At US and tissue harmonic imaging kidneys appear enlarged with increased parenchymal thickness, loss of renal sinus fat due to diffuse parenchymal edema, and changes in renal parenchymal echogenicity due to edema (hypoechoic) or hemorrhage (hyperechoic). The corticomedullary differentiation can also be reduced [21, 22]. Color and power Doppler and CEUS may reveal focal absence of renal parenchyma vascularity due to reactive vasoconstriction (Figure 2). Haematogenous abscesses are usually found in immunodepressed patients, in diabetic patients or in patients with i.v. drug abuse or with infection foci. At gray-scale US, the typical abscess appears as a wall thickenedthick-walled hypoechoic mass with through transmission, hypervascular wall and internal debris that lacks internal flow on color Doppler US [21 – 24]. The role of CEUS is limited in noncomplicated acute pyelonephritis due to the poor contrast ratio between the infected and noninfected parenchyma, but the detection of abscesses and even microabscesses can be easily achieved [11].Chronic recurrent pyelonephritis corresponds to a chronic interstitial nephritis with long-standing, recurrent infection and ongoing renal destruction and not to the residuum of inactive disease (reflux nephropathy). Chronic pyelonephritis is more frequent in diabetics, with an incidence of 20–40% compared to 2–6% in the normal population according to autopsy series [21]. The imaging findings are characterized by renal scarring, atrophy and cortical thinning, hypertrophy of residual normal tissue (which may mimic a mass lesion), calyceal clubbing secondary to retraction of the papilla from overlying scar, thickening and dilatation of the caliceal system, and overall renal asymmetry.Primary diffuse renal parenchymal diseasesPrimary diffuse renal parenchyma diseases (Figure 2) may be due to glomerual diseases [26] (Table 1) or tubulointerstitial diseases [27] (Table 2) even though primary glomerular diseases are often associated with prominent tubulointerstitial changes. Acute glomerulonephritis may manifest as acute nephritic syndrome (hematuria, proteinuria <3.5 g/dayie, red cell casts and decreased glomerular filtration rate [GFR]) (Figure 23) or as nephrotic syndrome (proteinuria ≥3 grams per day, ?low serum albumin level and edema) or as. Glomerulonephritis is often caused by antibody-induced inflammation through in situ immune complex formation due to anti-glomerular basement membrane (GBM) autoantibodies, deposition of circulating immune complexes, and antineutrophil cytoplasmatic autoantibodies (ANCA). Histologically, the main feature is cellular proliferation of mesangial or endothelial cells, leukocyte infiltration and GBM thickening due to subendothelial (e.g. membranoproliferative glomerulonephritis) or subepithelial immune complex deposition (e.g. postinfectious glomerulonephritis or membranous glomerulonephritis) or also immune complex deposition within GBM itself often with components of complement or within the mesangium (e.g. systemic lupus erythematosus or IgA nephropathy), and hyalinosis and sclerosis of the glomerulus. Those immune complexes activate complement and recruit inflammatory cells resulting in inflammatory injury. Rapidly progressive glomerulonephritis is a variant of the acute nephritic syndrome associated with a rapid loss of renal function and with capillary thrombosis and necrosis and/or capillary hypercellularity, mesangial hypercellularity, and subendothelial immune complex deposits characterized by extensive crescents (usually >50%). Nephrotic syndrome is also a rare manifestation of malignancy associated with paraneoplastic syndrome. It has been reported in various malignancies including malignant lymphoma, colon cancer, lung cancer and prostate cancer. Membranous glomerulonephritis represents the main cause of paraneoplastic nephrotic syndrome. In glomerulonephritis with a prevalent mesangial matrix and GBM involvement - minimal-change glomerulonephritis, IgA nephropathy, focal glomerulosclerosis, and membranous glomerulonephritis - cortical echogenicity is usually normal or slightly increased since glomerular component accounts only for 8% of renal parenchyma [6]. Increased echogenicity is more common in crescentic (Figure 4, Figure 5) and membranoproliferative glomerulonephritis (Figure 3), in diabetic glomerulosclerosis and tubulointerstitial renal diseases (Figure 46, Figure 57) which present glomerular, interstitial, and vascular involvement [6]. The renal parenchymal vascularity is reduced on color and power Doppler US while intrarenal RI values are significantly correlated to the amount of arteriolosclerosis, glomerular sclerosis, edema, and interstitial fibrosis. Frequently Doppler US reveals elevated RIs (>0.70) in kidneys with active disease involving the tubulointerstitial (Figure 46) or vascular compartment, whereas kidneys with glomerular diseases present more often normal RI values [1] except in crescentic and membranoproliferative glomerulonephritis where RI values are frequently increased. Doppler US is useful in the follow-up of renal parenchymal diseases to predict noninvasively the improvement or worsening of renal function according to progressive decrease or increase (>0.70 – 0.75) of RI values.Renal allograft The most common complications in renal allografts include renal vein thrombosis, arterial occlusion, acute tubular necrosis (ATN), interstitial fibrosis and tubular atrophy (previously called chronic allograft nephropathy), and acute or chronic allograft rejection.Acute renal allograft rejection (1 - 3 weeks after transplantation) consists of intimal arteritis (subendothelial infiltration by mononuclear cells) and tubulitis (renal intersitium infiltration by > 4 mononuclear cells / tubular cross-section). Histological specimen of the transplanted kidney is required to differentiate acute rejection from ATN since gray-scale US and Doppler US may reveal only aspecific non specific findings like increase in renal length, increased cortical echogenicity, reduction in corticomedullary differentiation, and increase in intrarenal RIs [28] (Figure 86). However, the evidence of lack of flow during diastole on Doppler US was found described as typical for ATN [29] and even for renal vein thrombosis. Micro-Doppler techniquesColor Doppler may depict a reduced parenchymal perfusion in acute renal transplant rejection [30]. Microbubble contrast agent arrival time after i.v. injection is increased in acute allograft rejection [31] while CEUS can identify improved parenchymal perfusion due to change in immunosuppressive therapy [32].The features suggestive of chronic allograft rejection consist in of GBM duplication and interstitial fibrosis and tubular atrophy, vascular changes, and glomerulosclerosis. Doppler US reveals an increase in the intrarenal RI values (>0.8) while real-time elastography can suggest the presence of progressive renal graft scarring [8, 11, 20, 33, 34, 35]. CEUS can monitor microvascular changes expressed by reduced parenchymal perfusion in the early diagnosis of chronic allograft nephropathy [32, 36] and may detect transplant renal artery stenosis with higher diagnostic accuracy than Doppler US [37]. Similar findings are described in renal transplant interstitial fibrosis and tubular atrophy also with evidence of increased renal tissue stiffness on US elastography [11]. Acute kidney injuryAcute kidney injury (AKI) represents an abrupt (within 48 hours) decrease in kidney function and is de?ned as any of the following: increase in serum creatinine by ≥ 0.3mg/dl (≥ 26.5 ?s de?ned as any of the following: increase in serum creatinine to ≥ 1.5 - 2 times baseline; or urine volume < 0.5 ml/kg/h for 6 hours (oliguria) according to Kidney Disease Improving Global Outcomes (KDIGO) [38, 39, 40, 41]. Kidney failure is a stage of AKI and it is de?ned as a GFR < 15ml/min per 1.73 m2 [40]. AKI is classified as prerenal if caused by reduced blood flow to kidneys, intrarenal if due to conditions that injure the glomerular capillaries (e.g. acute glomerulonephritis), vessels (e.g. vasculitides), renal tubular epithelium (e.g. ischemic or toxic ATN due to carbon tetrachloride, mercury, lead, ethylene glycol, tetracyclines, or cis-platinum), or renal interstitium (acute tubulointerstitial nephritis) - and postrenal if caused by urinary tract obstruction. The two leading causes of AKI that occur in the hospitals are prerenal and intrarenal due to ischemic or toxic ATN.Acute tubular necrosis (ATN). It can be due to ischemia or nephrotoxicity. Despite the intrinsic ability of the kidney to regulate renal blood flow and glomerular filtration rate, prerenal AKI can lead to ischemic ATN when renal blood flow falls below 20 - 25% of normal as in cardiocirculatory shock. Histologically, ATN consists in of destruction of tubular cells with rupture of GBM and tubular occlusion by casts. Although kidneys with ATN may appear normal on gray-scale US [42], usually kidneys appear enlarged with increased cortical echogenicity with decreased corticomedullary differentiation and with increased RI values (Figure 97). Proteinaceous casts are thought to cause the increased echogenicity associated with ATN [38, 43]. ATN may also occur in extremely ill individuals, often as a result of obstetric complications, hemorrhagic or septic shock, disseminated intravascular coagulation, severe trauma, sepsis, malaria or burns. Necrosis results from constriction of small intracortical blood vessels with preferential flow of blood away from the renal cortex. Usually, the involved kidney becomes shrunken and scarred and cortical nephrocalcinosis may then develop. ATN is not completely reversible in up to 25% of patients [28]. Differential diagnosis between different AKI forms. In patients with renal impairment gray-scale and color-Doppler US are the first imaging modalities to differentiate postrenal AKI due to urinary tract obstruction from prerenal and renal AKI and to assess renal vessels and parenchymal abnormalities without the use of nephrotoxic agents. The renal size is usually normal in prerenal AKI, while in renal AKI both kidneys may appear normal although they frequently appear enlarged and with increased cortical echogenicity and corticomedullary differentiation especially when related to tubulointerstitial nephritis, and acute glomerulonephritis. The finding of large, smooth kidneys with nondilated calyces should indicate that AKI is probably due to primary acute kidney disease and that the process is potentially reversible. On the other hand, detection of kidneys of reduced size suggests a complicated underlying chronic nephropathy and worse prognosis. In prerenal AKI RIs < 0.7 are related to complete recovery after fluid restoration, whereas in renal AKI RIs are often >0.7. The threshold values of renal RI for renal impairment and/or prognostic values of poor renal outcome range from 0.70 to 0.79 [44]. The clinical course of renal AKI may be monitored with Doppler US by using serial measurements of intrarenal RIs with a progressive decrease of RIs, which can precede the recovery of renal function, or with an increase of RIs in case of complications [45 - 48]. In patients with AKI CEUS can reflect renal perfusion reduction [49 – 52] and may detect renal parenchymal perfusion defects as non-enhancing areas even in globally hypoperfused kidneys [16, 53, 54].In postrenal AKI, accounting for 5-25% of AKIs, gray-scale US is accurate in detecting hydronephrosis, consisting in a dilation of the urinary collecting system (renal calyces, infundibula, and pelvis), even though it may reveal false-negative results, such as obstructive AKI with nondilated urinary tract (due to dehydration or renal parenchyma tissue stiffness such as in chronic kidney diseases), or false-positive results such as dilation of the urinary tract in nonobstructed patients. Doppler US may provide unique data not available from gray-scale US in postrenal AKI. A mean RI >0.7 is considered a significant diagnostic clue for postrenal AKI [55 – 57]. Chronic kidney diseaseChronic kidney disease is defined as GFR <60?ml/min per 1.73?m2 for > 3 months. In chronic kidney disease gray-scale US reveals reduced renal length and cortical thickness, an hyperechoic renal parenchyma with a poor visibility of renal pyramids, and an increased evidence amount of renal sinus fat (Figure 810). Renal length does not correlate with renal reduced function, whereas it correlates, as does cortical echogenicity, with severity of pathological changes, including global sclerosis, focal tubular atrophy and hyaline cast number per glomerulus [6, 58, 59]. In patients with chronic kidney disease increased renal RIs (≥0.8) [58 – 60] and the mean splenic RI subtracted from the mean renal RI [61] are related toindicate progression towards AKI. Disease progression with reduced renal parenchyma perfusion and increased stiffness in renal parenchyma can be assessed by CEUS [62] and real-time US elastography [63]. Patientswith chronic kidney disease treated with dialysis or renal transplantation oftendevelop acquired cystic kidney disease in end-stage renal disease with a significantly increased risk of solid and cystic malignancies [64].Systemic vasculitidesIn systemic vasculitides glomerulonephritis represent a local form of vasculitis that involves glomerular capillaries. On histology the major finding consists in of inflammation with leucocyte infiltration within and around vessel walls. Systemic vasculitides affecting the kidney comprise Antineutrophil Cytoplasmic Antibody (ANCA) positive vasculitides, rheumatoid vasculitis, cryoglobulinemia-related vasculitis, hypersensitivity vasculitides (leukocytoclastic vasculitis angiitis), Beh?et's disease, and IgA vasculitis (Henoch–Sch?nlein purpura). ANCA-associated vasculitides are a group of small and medium sized vessel vasculitides which are characterized by the presence of ANCA in the peripheral circulation directed against leukocyte myeloperoxidase or proteinase-3 and causing inflammation by activating leukocytes by direct binding [Table 3] [21, 65]. ANCA-associated vasculitides are characterized by glomerular necrosis with crescents accompanied by extracapillary proliferation, inflammatory cell infiltration, and often rupture of the Bowman’s capsule [66].US may reveal early involvement in renal vasculitis since vascular and interstitial components are both involved in renal vasculitides. On gray-scale US renal vasculitides manifest as an increased cortical echogenicity with reduced corticomedullary differentiation (Figure 911). US may reveal also multiple cortical hypoechoic areas of variable size and shapes with cortical distortion, expressing regions of parenchymal edema [2, 6]. The intrarenal RI values are significantly correlated with creatinine level and presence of interstitial disease. Multiple intra-renal arterial aneurysms may be identified (Figure 120).Vascular diseases This category includes all those pathologies which may affect the large and/or small renal arteries [Table 4].Renal artery stenosis. Atherosclerotic renal artery disease can lead to renovascular hypertension and ischemic renal disease with progressive decreased inof renal size and function up to end-stage renal disease. In haemodynamically significant renal artery stenosis accelerated flow is detected at the site of stenosis with high systolic peak velocity (>200 cm/s), renal-aortic ratio greater than 3.5, and post-stenotic turbulent flow with spectral broadening and reversed flow. A decreased RIs with increased side-by-side difference higher than 5%, prolonged acceleration time (higher than 0.05–0.08 secs) with loss of early systolic peak and decreased acceleration (lower than 370–470 cm/sec2) may be observed in interlobar–arcuate renal cortical arteries in severe significant renal artery stenosis (>70%) (Figure 13). In stenosis higher than 70% of renal artery branches or of accessory renal arteries, a similar pattern may be observed in a portion of the kidney [67]. Renal cortical necrosis. Renal cortical necrosis can complicate any condition associated with hypovolemic or endotoxic shock as in premature placental separation late in pregnancy. The most typical finding corresponds tois an hypoechoic band, corresponding to the renal cortex, which surrounds the kidney. CEUS shows no enhancement within the renal cortex due to tissue necrosis with homogenous enhancement of the renal medullary tissue and adjacent renal parenchyma [68] (Figure 141). Atheroembolic renal disease. Renal cholesterol microembolization may be caused by renal angioplasty, atrial fibrillation and cardiac valvular defects. In patients with severe aortic atherosclerosis, atheromatous debris may embolize into the renal arteries up to glomerular capillaries causing AKI. Even though large renal infarcts may be hypoechoic in comparison with the viable renal parenchyma segmental renal infarcts are usually isoechoic or rarely hyperechoic if haemorrhagic component is present [68 – 70]. Both color and power Doppler US may increase diagnostic capabilities of US, especially in elderly or obese patients and in patients with renal diseases, by depting depicting renal infarcts as avascular regions. Howerver, CEUS is more sensitive than color or power Doppler US for the identification of the non-enhancing parenchyma [69].Renal vein thrombosis. Diagnosis of renal vein thrombosis relies on visualization of an echogenica thrombus within a dilated renal vein devoid of flow signals on color Doppler evaluation. Both kidneys areThe affected kidney is usually enlarged with reduced cortical–medullary differentiation since even the renal cortex becomes hypoechoic. Doppler spectral analysis of renal arteries may reveal slightly increased RIs with absent or reversed holo-diastolic flow in renal interlobar–arcuate arteries and normal parenchymal venous flows, since collateral venous supplies open after renal vein thrombosis. However, even though absent or reversed diastolic signals on Doppler US could be suggestive of renal vein thrombosis,their absence should not prevent further diagnostic work-up [68]. Diabetic Nephropathy. Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects roughly 40% of type 1 and type 2 diabetic patients [71 – 74]. Diabetic nephropathy typically manifests with gradual progression of disease from microalbuminuria to proteinuria, usually about 15 years after onset of diabetes. The diabetic patient is also prone to pyelonephritis, papillary necrosis, and obstructive nephropathy which lead to renal failure. At histologic analysis diabetic nephropathy presents diffuse expansion of collagenous component of the glomerulus with accumulation of extracellular matrix, progressive thickening of GBM (diffuse intercapillary glomerulosclerosis) and expansion of mesangium up to nodular glomerulosclerosis with associated hyaline in arterioles and occasionally in Bowman’s capsule (Kimmelstiel–Wilson nodules). On gray-scale US diabetic nephropathy manifests with enlarged kidneys due to hyperfiltration and hypertrophy, increased parenchymal thickness, and increase of the renal parenchymal echogenicity with increased visibility of renal pyramids and corticomedullary differentiation (Figure 152). In advanced diabetic nephropathy, kidneys become smaller, renal parenchymal echogenicity may appear increased or normal according to vascular and interstitial compartment involvement, whereas renal margins are usually diffusely irregular [75]. The RIs are typically elevated in advanced diabetic nephropathy, whereas RIs are often normal in the early stage of disease [76]. The RIs are highly correlated with serum creatinine concentration and creatinine clearance rate, whereas an elevated RI (≥0.70) is associated with impaired renal function, increased proteinuria, and poor prognosis [77]. CEUS can be used for the diagnosis of the renal cortical perfusion reduction in early and late stage diabetic patients expressed by a reduced area under time-intensity curve obtained after microbubble injection [78, 79].Hypertensive nephrosclerosis. Sustained Systemic hypertension causes hypertensive nephrosclerosis (benign nephrosclerosis) which represents the second most common diseases that result in chronic kindey disease and patient referral for transplantation. Hypertensive nephrosclerosis corresponds to the macroscopic renal change related to hypertension and consists in the granularity of renal cortical surfaces with evidence of coarse scars due to arteriolosclerosis of the interlobar, arcuate and interlobular renal arteries with thickening and collapse of GBM. Glomerular tufts are obliterated by scar and collagen and matrix material are deposited within the Bowman space with tubular atrophy and interstitial fibrosis with chronic inflammation. Malignant hypertensive nephrosclerosis is often superimposed on hypertensive nephrosclerosis with intimal thickening in arteries and fibrinoid necrosis and hyaline sclerosis of arterioles. On gray-scale US both kidneys are usually symmetrically reduced in their diameters with cortical scars, irregularities of renal margins and reduction in renal parenchymal thickness in most of patients [75] although these findings are not specific. Color and power Doppler US reveal nonspecific reduction of vascularization while renal RIs are typicallycan be increased (>0.7 and frequently around 0.8). Antiphospholipid syndrome is a common autoimmune disease caused by pathogenic antiphospholipid antibodies causing recurrent vascular thrombosis in arterial, venous or small vessels and pregnancy complications. It is classified as primitive when antiphospholipid syndrome occurs in the absence of other autoimmune diseases or a secondary when it occurs in association with a number of autoimmune disorders and mostly systemic lupus erytematosus. Antiphospholipid antibodies are associated with various renal manifestations including large renal vessel thrombosis, renal artery stenosis, and antiphospholipid nephropathy consisting in acute thrombotic microangiopathy, proliferative and fibrotic lesions of the intrarenal vessels, and ischemic lesions of the renal parenchyma which can lead to AKI and manifest with increased RIs (>0.7) on Doppler US [80] (Figure 1316) Hepatorenal syndrome represents a functional renal impairment which occurs in 20% - 40% of patients with advanced liver disease. The pathophysiological hallmark is portal hypertension leading to splanchnic arterial vasodilation, which leads to vasoconstriction of the renal renal arteries, and reduced renal perfusion and GFR [81]. At Doppler US RI values are markedly elevated in patients with clinically overt hepatorenal failure and represent independent predictors of kidney dysfunction [81]. CEUS may detect improvement in renal parenchyma perfusion in response to pharmacologic treatment in patients with hepatorenal syndrome [82].Thrombotic microangiopathy with thrombocytopenia and microangiopathic hemolytic anemia represents the most severe form of vascular endothelial cell injury leading to AKI and it may be caused by hemolytic uremic syndrome and thrombotic thrombocytopenic purpura or also it may be drug-induced [Table 4]. Thrombotic thrombocytopenic purpura is caused by a genetic or acquired deficiency of a protease creating microvascular thrombosis. Renal involvement is often absent. Hemolytic uremic syndrome is a microangiopathic hemolytic anemia that causes thrombocytopenia, renal failure, and hypertension and occurs principally in children about 3–10 days following episodes of gastroenteritis due to enterohemorrhagic E. Coli or viral upper respiratory tract infections.It is A similar syndrome occurs less frequently in adults, often associated with complications of pregnancy or during the postpartum period but can be associated with the use of oral contraceptives or may occur following treatment with antineoplastic agents. Histologically there is a wide band of subendothelial expansion due to insudation of plasma protein and endothelial cell swelling with narrowing of the capillary lumen promoting thrombosis and ischemic necrosis. Thrombotic microangiopathy determinesClinically manifests with microangiopathic hemolytic anemia, thrombocytopenia, and, in certain conditions, AKI due toplatelet or platelet-fibrin thrombi in the interlobular renal arteries, arterioles, and glomeruli. Gray-scale US reveals enlarged kidneys, enhanced echogenicity of the renal cortex and increased corticomedullary differentiation with sharp delineation of swollen hypoechoic pyramids [83 – 85]. RIs are markedly increased, often over 0.9. Pre-eclamptic nephropathy. In pre-eclamptic nephropathy (pregnancy-induced nephropathy) glomeruli are uniformly enlarged and endothelial and mesangial cells are swollen with narrowing of the lumen of glomerular capillaries. Doppler US may reveal reduced venous flow [86].Systemic and hematological diseases Systemic lupus erythematosus is a multisystem autoimmune disease characterized by the development of autoantibodies to ubiquitous self-antigens (e.g., antinuclear antibodies and antidouble-stranded DNA antibodies) and widespread deposition of immune complexes in affected tissues. In 90% of cases patients are women especially in the age range between 20 and 40 years. Commonly affected organs are kidneys, joints, skin, central nervous system, blood vessels, gastrointestinal tract, lymph nodes, and pleura. The kidneys are the most commonly affected organs. Lupus nephritis follows the classification proposed by the International Society of Nephrology/Renal Pathology Society (ISN/RPS) [Table 5] [21, 66, 87]. Gray-scale US has been reported to have a sensitivity of 95 % in lupus nephritis detection [88]. In lupus nephritis, kidneys may present reduced or increased dimensions and an increased cortical echogenicity with increased or even reduced corticomedullary differentiation. Gray-scale US may also reveal regions of parenchymal edema manifesting as multiple cortical hypoechoic areas of variable size and shapes with cortical distortion. The intrarenal RI values are significantly correlated with creatinine level and severity of lupus nephritis [89, 90] and also with systemic vascular changes [91], whereas normal intrarenal RI values are considered as a good prognostic factor.Renal sarcoidosis is characterized by granulomatous interstitial nephritis with randomly distributed, distinct granulomas or infiltrative pattern with or without areas of central necrosis [27]. Renal involvement is seen in 7-22% of patients [92]. Clinical manifestations include nephrolithiasis and nephrocalcinosis [93] due to the increased absorption of calcium, nephrogenic diabetes insipidus, renal insufficiency, and acute tubulointerstitial nephritis with or without granuloma. Kidneys may appear increased in dimensions or atrophic depending on the extent and duration ofinvolvement. On gray scale US kidneys may appear normal or, rarely, may manifest multiple tumorlike nodules that can mimic lymphoma or metastatic tumors [94].In gout nephropathy hyperechoic papillary foci or a diffuse hyperechoic medulla may be observed [93]. Renal stones are usually present, while kidneys present normal or reduced dimensions with smooth margins. In hyperoxaluria, and particularly in enteric hyperoxaluria due to enhanced absorption of dietary oxalate in patients with ileal disease, kidneys present normal or reduced dimensions with smooth margins and a hyperechoic renal cortex and medulla. Glycogenosis results in liver and kidney involvement, with increased liver and kidney dimensions owing to massive accumulation of glycogen in these organs, hypoglycemia, and hyperuricemia. Kidney manifestations of leukemia and lymphomas encompass a broad spectrum of disease: prerenal AKI, ATN, renovascular disease, renal parenchyma cell infiltration, urinary tract obstruction, glomerulopathies, and electrolyte and acid-base abnormalities [95]. In leukemia one or both kidneys are increased in size due to diffuse leukemic cell infiltration, with/without single or multiple hypoechoic nodules, wedge-shaped lesions or geographic areas. In general, when renal involvement is detected at imaging, there is also evidence of extramedullary involvement. In lymphoma renal involvement is most often observed in patients with non-Hodgkin disease, typically, diffuse large B cell lymphoma or Burkitt lymphoma, who also have evidence of advanced-stage extranodal disease. Gray-scale US reveals renal enlargement without disruption of the renal contour, a solitary mass or multiple parenchymal lesions , and/or perirenal or renal sinus lesions [96]. Renal function is usually preserved in patients with renal lymphoma, but it can be affected by diffuse cell parenchyma infiltration and by obstructive uropathy secondary to infiltration and obstruction of the renal pelvis and ureters by retroperitoneal lymphadenopathy. Multiple myeloma is an hematologic malignancy involving the pathologic proliferation of terminally differentiated plasma cells. Light chain deposition disease, or so-called myeloma cast nephropathy, consisting of Bence Jones or light chain proteins combined with Tamm–Horsfall protein, is seen in approximately half of patients with multiple myeloma who have renal disease. Renal failure is caused either by blockage of the tubules by protein casts or by hypercalcemia and hyperuricemia. Intratubular obstruction results in interstitial fibrosis and a lymphocytic infiltration associated with tubular atrophy [27]. When the kidney is affected by monoclonal immunoglobulin deposition [Table 1] and patients do not meet criteria for a diagnosis of multiple myeloma, the term monoclonal gammopathy of renal significance is used including light chain cast nephropathy, amyloid light chain (AL) amyloidosis, cryoglobulinemia (type I and II) and monoclonal immunoglobulin deposition diseases with light chain, light and heavy chain or even heavy chain deposition disease. All these disorders involving the kidneys manifest with nephrotic syndrome. Amyloid nephropathy - both in the AL (associated with a monoclonal plasma cell dyscrasia) and AA types (associated with a chronic inflammatory disease[97] - consists in accumulation of fibrillary deposits in the mesangium extending along the inner surface of GBM frequently obstructing the capillary lumen occasionally also with tubulointerstitial amyloid deposition [27]. Both onIn multiple myeloma and renal amyloidosis both kidneys appear enlarged and hyperechoic with increased, normal or even reduced corticomedullary differentiation on gray scale US (Figure 174) . Other findings consist in of diffusely infiltrative soft tissue encasing the kidneys with/without calcifications (acute form), renal atrophy with cortical thinning (chronic form), or focal renal parenchymal mass or hypoenhancing lesions resulting from amyloid deposition. The RI values at Doppler US are usually increased. HIV-associated nephropathyHIV-associated nephropathy is seen in 12% of AIDS patients at histology,is more frequent in patients with a CD4 cell count <200 cells/mm3 [98] and consists of a focal segmental glomerulosclerosis with increased mesangial sclerosis and a proliferative cap of visceral epithelial cells with dilatation of the Bowman ’s space and interstitial fibrosis and infiltration by mononuclear leukocytes. Clinically, HIV-associated nephropathy should be suspected in the HIV patient with AKI in the absence of hypertension (Figure 185). AKI in the HIV population may be due also to ATN secondary to nephrotoxic agents used to treat opportunistic infections (pentamidine, amphotericin B, and foscarnet) or to antiretroviral therapy (tenofovir or didanosine). Nephrolithiasis represents a recognized side effect of indinavir and nelfinavir. US reveals normal-sized or enlarged kidneys, with increased parenchymal echogenicity and reduced or loss corticomedullary differentiation on grayscale US with a reduced visibility of renal pyramids related to focal and segmental glomerulosclerosis and to dilated renal tubules filled by proteinaceous material [99, 100]. Drug - induced kidney diseaseNephrotoxic drugs contribute towards AKI in 20–30% of patients [101]. Most drug nephropathies involve mainly the tubulointerstitial compartment by a cell-mediated immune response. International Serious Adverse Event Consortium classifies drug-induced kidney diseases [102] into four clinical phenotypes: AKI (further classified in acute vascular disease, acute glomerual disease, ATN, acute interstitial nephritis) [103], glomerular disease (mainly membranous GN), nephrolithiasis/crystalluria, and tubular dysfunction. Beta-lactam antibiotics, sulfonamides, antituberculous drugs, nonsteroidal anti-inflammatory drugs, diuretics, anticonvulsants, proton pump inhibitors, allopurinol, captopril, phenytoin, penicillamin, and interferon are among the most important drugs involved in acute interstitial nephritis. Gray-scale US may be completely normal or may show non-specific findings in drug toxicity. Grayscale US may show renal swelling, increased or decreased renal echogenicity, renal parenchyma calcifications, effacement of the renal sinus or loss of corticomedullary differentiation (Figure 1619). In analgesic nephropathy kidneys may reveal hyperechoic foci on renal pyramids due to papillary calcifications, which can also be observed also in sarcoidosis, primary hyperparathyroidism, diabetes mellitus, medullary sponge kidney, and prolonged dialysis treatment. Renal papillary necrosis, appearing as an hyperechoic filling defect without acoustic shadowing within renal calyx, occurs in 70–80 % of patients with analgesic nephropathy but may be observed also in diabetes mellitus, obstructive uropathy, sickle cell disease, acute or chronic pyelonephritis, ATN, and renal vein thrombosis. Diffuse incrementation of renal RIs may be observed. Contrast medium–induced nephropathy (accounting for 12% of all cases of hospital-acquired AKI) originates from the kidney medulla's unique hyperosmolar environment. Highly concentrated iodinated contrast media in the tubules and vessels increases fluid viscosity determining a flow reduction through medullary tubules, glomerual capillaries and vessels and thereby damage cells creating medullary vasoconstriction and then hypoxia [104]. US reveals normal kidneys with increased RIs at Doppler US which reduce progressively after medical treatment.Pediatric Renal Parenchymal DiseasesAlthough hyperechogenicity of renal parenchyma is a nonspecific parameter even in pediatric patients, there is a proven relationship between the degree of cortical echogenicity and histopathological changes on renal biopsy [105].The more frequent renal parenchymal disease in children is acute glomerulonephritis, where kidneys may appear normal or enlarged, with or without hyperechoic renal cortex, with normal or increased RIs, and with a normal or reduced renal parenchymal perfusion on Color and power Doppler. Other pediatric renal parenchymal diseases associated with increased renal echogenicity are type I glycogenosis, glomerulosclerosis, oculocerebral syndrome, renal dysplasia, oxalosis, renal amyloidosis, acute multifocal pyelonephritis, sickle cell anemia, primary polycythemia, and acute lymphatic leukemia .Nephrotic syndrome is uncommon in pediatric patients and may be related to acute glomerulonephritis, collagen vascular diseases, and amyloidoses. In nephrotic syndrome, kidneys may appear normal on US or may be enlarged with increased parenchymal echogenicity. Hemolytic uremic syndrome is a microangiopathic hemolytic anemia that causes thrombocytopenia, renal failure, and hypertension and occurs principally in children about 3–10 days following episodes of gastroenteritis due to enterohemorrhagic E. Coli or viral upper respiratory tract infections. A similar syndrome (named thrombotic thrombocytopenic purpura) occurs less frequently in adults (see above). Renal cortex appears typically hyperechoic with increased corticomedullary differentiation, probably related to platelet aggregates and fibrin thrombi in the lumen of glomerular capillaries. Markedly elevated RIs are found. Nephrocalcinosis is rare in children and associated mainly with hypercalcemic status, renal tubular diseases, enzymatic disorders, prolonged furosemide therapy, and Tamm–Horsfall proteinuria.ConclusionDiffuse renal parenchymal diseases manifest with increased parenchymal echogenicity and maintenance or loss of corticomedullary differentiation on gray scale US. correlation of the US pattern with patient’s clinical history and background is essential for a correct characterization. Gray-scale US and spetral Doppler US may be used in the follow-up of renal parenchyma diseases especially during pharmacologic medical treatment. 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Utrasensitive Color Doppler MicroDoppler US allows visualization of renal cortical vessels up to the capsule with distinct identification of the interlobular arteries (straight arrows).Figure 2: Right focal acute pyelonephritis in a 25-year-old woman. There is an hyperechoic focus (arrow) in the upper pole of the right kidney with reduced vascularity on Color Doppler US related to acute bacterial pyelonephritis.Figure 32 (a – h): Scheme representing the different patterns of glomerular diseases. (a) The normal glomerulus with the endothelium surrounding the glomerular vessel lumen (red) and the Bowman's capsule - visceral layer, namely podocytes (orange) separated by a thin glomerular basement membrane (yellow) which derives both from endothelial and epithelial cells, the Bowman's capsule - parietal layer (blue), and the Bowman's space (green). (b) Focal glomerulosclerosis. Glomerular consolidation affects some, but not all, glomeruli and initially involves only part (gray) of an affected glomerular tuft. (c) Membranous nephropathy. There is no evident proliferation by light microscopy, with global scattered subepithelial accumulation of immunocomplexes, between podocytes and glomerular basement mambranemembrane, with projections which are called spikes (black spots) of basement membrane adjacent to the deposits. (d) Membranoproliferative glomerulonephritis, with endocapillary and mesangial hypercellularity and glomerular basement membrane double contours due to mesangial and subendothelial deposits (gray) also with monocyte/macrophages and mesangial cells cell vascular infiltration, (e) IgA glomerulonephritis. Mesangioproliferative glomerulonephritis with IgA deposits, predominantly in the mesangium (gray). (f) Crescentic rapidly progressive glomerulonephritis. There is capillary thrombosis (violet) and necrosis and/or capillary hypercellularity, mesangial hypercellularity, subendothelial immune complex deposits (gray) with cellular crescent due to proliferation of parietal epithelial cells and influx of macrophages (gray). (g) Multiple myeloma / Amyloid nephropathy are characterized by varying degrees of mesangial proliferation (dark red) and, in its advanced form, by nodular glomerulosclerosis. Amyloidosis is characterized by accumulation of fibrillary deposits in the mesangium extending along the inner surface of GBM (h) Diabetic nephropathy. There is mesangial increase or nodular sclerosis (violet), accompanied by hyalinosis of both afferent and efferent arterioles and thickening of the glomerular basement membrane lamina densa without deposits.Figure 43a, b.Images in 56-year-old man with crescentic glomerulonephritis. (a) Grayscale US, longitudinal plane. Kidneys appear increased in dimensions and present parenchymal thickening with compressed renal sinus and hyperechoic renal parenchyma with reduced corticomedullary differentiation. Figure 5a-c.Images in 45-year-old man with rapidly progressive glomerulonephritis due to crescentic glomerulonephritis. (a) Grayscale US, longitudinal plane. Kidneys present parenchymal thickening with compressed renal sinus and hyperechoic renal parenchyma with reduced corticomedullary differentiation. (b) Color Doppler US. Longitudinal plane. Renal parechyma vascularity appears reduced. (c) Increased resistive index (0.73) is revealed on spectral Doppler US.Figure 4a6a, b: Images in 45-year-old man with tubulointerstitial nephritis. (a) Grayscale US, longitudinal plane. Kidneys present parenchymal thickening, hyperechoic renal parenchyma and reduced corticomedullary differentiation. (b) Spectral Doppler US interrogation of interlobar arteries visualized on color Doppler US reveals increased resistive index value (0.77). Figure 57(a, b): Images in 45-year-old woman with IgG4-related tubulointerstitial nephritis. (a) Grayscale US, longitudinal plane. Kidneys appear increased in dimensions withpresent increased parenchymal thickeness, renal sinus compression and reduced corticomedullary differentiation on grayscale ultrasound. (b) Color Doppler reveals reduced renal parenchyma vascularity. Figure 68: Acute transplant rejection in a 55-year-old man with treated diabetes mellitus. Spectral Doppler US interrogation of interlobar arteries reveals increased resistive index values with inverted diastolic flow.Figure 79(a, b): Images in 45-year-old woman with acute tubular necrosis. (a) Grayscale US, longitudinal plane. Kidneys appear enlarged with increased parenchymal thickeness, and increased parenchyma echogenicity with reduced corticomedullary differentiation on grayscale ultrasound. (b) Spectral Doppler US interrogation of interlobar arteries reveals increased resistive index values (0.77). Figure 810. Images in 75-year-old man with chronic kidney disease. Gray-scale US, longitudinal plane. Kidneys reveals diffusely irregular margins, reduced cortical thickness and increased cortical echogenicity with increased volume of renal sinus fat. Figure 911(a, b): 50-year-old man referred for acute renal failure due to ANCA positive vasculitis at renal pathology. (a) At gray scale US the size of the kidneys and the cortical thickness were normal but the corticomedullary differentiation was lost. (b) At color Doppler and spectral Doppler US, the cortical vascularization was reduced but the resistive index was normal measured at 0.67. Figure 10 12 (a, b)Patient presenting with fever and renal failure, referred for the drainage of multiple renal abscesses. (a) Gray scale and Color Doppler US confirmed the presence of multiple anechoic to hypoechoic round nodules (arrows) inside the renal parenchyma of both kidneys. (b) At CEUS performed immediately before the drainage, these areas enhanced strongly during the arterial phase, and were corresponding to multiple aneuryisms (arrows). The histologic diagnosis of Behcet like disease was established afterwards. Aneurysms were not indentified on color Doppler due to high flow optimization.Figure 13(a, b) 35-year-old mam with systemic hypertension secondary to renal artery stenosis. (a) At color Doppler US a tight stenosis is revealed at the right renal artery with increased peak systolic velocity and spectral broadening. (b) On spectral Doppler US the Doppler waveforms at the level of the interlobar arteries, downstream to the site of stenosis, revealed a normal resistive index (0.62) but a tardus - parvus pattern with prolonged systolic acceleration and small systolic amplitude with rounding of systolic peak. Figure 1114(a, b) 36-year-old man, second transplantation due to loss of the first renal graft after severe acute rejection. At day 13, the patient was presenting with poor recovery of renal function and fever. (a) At gray scale US and color Doppler US, the renal transplant exhibited a complete loss of the cortico-medullary differentiation with diffuse hyperechoic pattern of the renal cortex, a hypoechoic area at the upper pole corresponding to a known infarct and poor renal cortical vascularization. However, the Doppler waveforms at the level of the interlobar arteries were normal with a resistive index measured at 0.62. (b) CEUS revealed the presence of cortical necrosis (thin arrows) combined with medullary necrosis (thick arrows), as this frame is acquired at 60 sec after injection. Some cortical areas remained perfused (arrow head).Figure 1215: 72-year-old man presenting with chronic kidney disease due to diabetic nephropathy. Kidneys were enlarged presenting with irregular margins, increased echogenicity and corticomedullary difference. At spectral Doppler US, the resistive index measured at the foot origin of the interlobar arteries are increased at 0.81.Figure 1316(a - c) 61-year-old woman referred for acute renal failure due to antiphospholipid syndrome. (a) At gray scale US the size and the echostructure of both kidneys were normal. (b) Color Doppler US revealed a decrease in the intra-renal blood vessels but the resistive index recorded at the level of the interlobar arteries was normal. (c) Contrast-enhanced US was performed due to the discordance between the clinical status of the patient and the US findings. It revealed the presence of patchy cortical necrosis at the lower pole (arrows) that explained the presence of acute renal failure.Figure 1417(a, b) 53-year-old woman presenting with renal amyloidosis and chronic kidney disease. Note that the examination was performed after biopsy complicated with gross hematuria. (a) At gray scale US the kidney was enlarged and the pelvi-caliceal tree was enlarged and filled with echoic materials corresponding to clots (arrows). The renal parenchyma was hyperechoic and the differentiation between the cortex and the medulla was reduced. (b) Color Doppler US revealed the reduction of intra parenchymal vascularity but the resistive index recorded at the level of the interlobar arteries was normal (0.70). Figure 1518(a, b) 50-year-old woman presenting with HIV – associated nephropathy without hypertension. Note that the examination was performed after biopsy complicated with gross hematuria. (a) Gray scale US shows renal swelling, increased renal echogenicity, and loss of corticomedullary differentiation. (b) Color Doppler US reveals reduced parenchymal vascularity.Figure 196: 73-year-old woman presenting with lithium nephropathy and mild chronic kidney disease. Gray scale US reveals reduced corticomedullary differentiation, multiple hyperechoic cortical micro-calcifications and multiple cysts. ................
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