Renal Vascular Lesions Research Articles

Ischemic renal diseases: New insights into old entities

Vascular nephropathies are a steadily increasing cause of end-stage renal failure. Arterionephrosclerosis and arteriolonephrosclerosis are common features in the hypertensive patient. This is especially true for blacks of African descent, in whom hypertension and nephrovasculopathies are a major cause of renal insufficiency. That primary hypertension leads to renal vascular lesions, glomerular obsolescence and interstitial fibrosis has long been established. It should not, however, obscure the fact that renal vascular lesions can be observed in animal models as well as in some humans, especially young blacks, in the absence of, or anticipating the onset of hypertension. This leads to considering the hypothesis that nephroangiosclerosis might stem from a genetic defect in the renal vascular bed and that this defect is strongly associated with the hypertensive trait. Atherosclerotic renal disease is a major, potentially treatable cause of chronic renal disease is a major, potentially treatable cause of chronic renal failure, especially in whites. It leads to renal atrophy, but the ischemic kidney retains a vigorous potential for tubular cell regeneration, which pleads for early recognition and treatment. Recent data suggest that renal ischemia, be it due to renal artery stenosis or to cholesterol crystal embolism, ranks among the multiple causes of secondary focal segmental glomerulosclerosis. Irrespective of its initial mechanism, ischemia induces renal fibrosis, the pathophysiology of which is centered on increased generation of angiotensin II. Finally, renal vascular lesions are commonly observed in the course of various nephropathies, even in the absence of hypertension, and the relationship between these lesions and the unfavorable prognosis of glomerulopathies, especially primary focal-segmental glomerulosclerosis, membranous glomerulopathy and IgA glomerulonephritis, remains to be elucidated. Expanding knowledge of the spectrum of nephrovasculopathies opens perspectives for investigating, understanding and treating a major mechanism of progressive renal insufficiency.

Renal growth and development in mice lacking AT1A receptors for angiotensin II.

To examine the role of the type 1A (AT1A) angiotensin receptor in renal growth and development, we analyzed F2 progeny from a series of crosses between F1 mice that were heterozygous for a targeted disruption of the AT1A receptor gene [Agtr1A-(+/-)]. Among 21-day-old weanling F2 mice, we found that 194 (32%) were homozygous for the wild-type allele Agtr1A-(+/+), 299 (49%) were Agtr1A-(+/-), and 119 (19%) were Agtr1A-(-/-). This differed significantly from the proportions predicted by Mendelian genetics (P = 0.01), suggesting that the complete absence of AT1A receptors is associated with a mild survival disadvantage. Agtr1A-(-/-) mice grew normally, and we found no significant differences in body weight or heart and kidney weights in Agtr1A-(+/+) and Agtr1A-(-/-) mice examined at 21, 60, and 100 days. Protein and DNA content of kidneys and hearts were also similar in weanling or adult Agtr1A-(+/+) and Agtr1A-(-/-) mice. By light microscopy with immunohistochemistry, kidneys from Agtr1A-(-/-) were essentially normal, with two exceptions: 1) there was marked hypertrophy of the juxtaglomerular apparatus (JGA) and proximal expansion of renin-producing cells along the afferent arterioles, and 2) some glomeruli showed evidence of mesangial expansion. We did not find the severe renal vascular lesions or papillary atrophy that have been observed in angiotensinogen- or angiotensin converting enzyme-deficient animals. We conclude that the AT1A receptor is not essential for the normal organogenesis of the kidney; however, its absence is associated with mild mesangial expansion and JGA hypertrophy.

Renal vascular lesions in lupus nephritis.

We retrospectively studied the prevalence, histologic features, clinical correlations, and long-term outcome of the intrarenal vascular lesions of lupus nephritis (LN) in a series of 169 renal biopsies performed between 1980 and 1994 in 132 patients with systemic lupus erythematosus. The most common vascular lesions were nonspecific sclerotic changes, found in 37% of the biopsies (24% if only the cases with moderate to severe changes are considered). The other common vascular lesions were "immunoglobulin microvascular casts," found in 24% of the biopsies. Vasculitis and thrombotic microangiopathy were rare lesions and were seen in only 4 (2.4%) and 1 (0.6%) cases, respectively. Isolated sclerotic vascular changes were present in biopsies from older patients with a longer duration of LN, compared with the group with no vascular lesions, and were associated with a significantly higher prevalence of hypertension. Overall, however, the long-term renal and patient survival of this group did not differ significantly from that of the patients without vascular changes. Immunoglobulin microvascular casts (IMCs) ("lupus vasculopathy") were characterized by the presence of immunoglobulin deposition within the glomerular capillaries and small arterioles. In the present study we extensively investigated the morphologic and immunologic features of this lesion. The lesions were notable for the absence of endothelial or parietal vascular lesions and of fibrin, platelets, and leukocytes, which indicates that thrombosis is not involved in the vascular obstruction. According to our data immunoglobulin precipitation in the microvasculature seems to play a central role in the pathogenesis of this lesion, which is why we propose the term "immunoglobulin microvascular casts." In general, IMCs were associated with the most severe and active forms of diffuse proliferative lupus nephritis (World Health Organization [WHO] class IV). However our data show that, in contrast to previous studies, the long-term outcome of patients with IMCs is not worse than that of other patients with class IV LN. It may even be somewhat better, suggesting that this type of lesion may reverse with immunosuppressive therapy. In addition, we did not find any association between the presence of IMCs and the lupus anticoagulant, IgG anticardiolipin antibodies, or extrarenal vascular manifestations. Concerning vasculitis and thrombotic microangiopathy, our results confirm that their occurrence is quite rare in-lupus nephritis. The outcome of our 4 patients with vasculitis was not particularly poor, which could be related to early and/or aggressive treatment. Taken as a whole, our data confirm that the presence of active and severe forms of diffuse proliferative LN (WHO class IV) carries a worse prognosis compared with the other forms of LN. In our study, and in agreement with previous reports (23), the long-term renal survival of patients with class IV LN was significantly worse than that of patients with other forms of LN, with a 10-year renal survival of 70% compared with 85%, respectively. However our data do not support the conclusions of some previous studies that the presence of intrarenal vascular lesions is a marker of poor renal prognosis in lupus nephritis. More precisely, our data show that the somewhat poorer renal outcome observed in patients with IMCs is related to the fact that in most cases these lesions are associated with class IV lupus nephritis, and not related to the presence of the vascular lesion per se.

The significance of arterial hypertension at the onset of clinical lupus nephritis.

The prognostic importance of hypertension at the onset of clinical lupus nephritis is not well established. We studied retrospectively 44 patients with lupus nephritis in order to ascertain the prevalence...

Accuracy of the diagnosis of hypertensive nephrosclerosis in African Americans: A report from the African American Study of Kidney Disease (AASK) Trial

African Americans have excess hypertension and end-stage renal disease presumed due to hypertension compared to Caucasians. The AASK was designed to examine the impact of antihypertensive therapies and two levels of blood pressure control on the rate of decline of GFR in African Americans with presumed hypertensive renal disease. During the pilot phase of the trial, eligible participants were requested to undergo renal biopsy to assess the underlying lesions in this population. Eighty-eight hypertensive (diastolic BP > 95 mm Hg) non-diabetic African American patients between the ages of 18 to 70 years, with GFR between 25 to 70 ml/min/1.73 m2 and without marked proteinuria were assessed for possible renal biopsy. Forty-three patients did not undergo renal biopsy due to refusal or contraindications. Adequate renal biopsies were obtained in 39 of the remaining 46 patients. Biopsy findings were analyzed and then compared to clinical parameters. The 39 patients studied, 29 men and 10 women, were on average 53.0 +/- 11.0 years old, and had a MAP of 109 +/- 15 mm Hg and GFR 51.7 +/- 13.6 ml/min/1.73 m2 (not significantly different from nonbiopsied patients). Thirty-eight of these 39 biopsies showed arteriosclerosis and/or arteriolosclerosis, severity on average 1.5 +/- 0.9 and 1.5 +/- 0.8, respectively on a 0 to 3+ scale. Interstitial fibrosis was moderate, 1.3 +/- 0.9 (0 to 3+ scale). Segmental glomerulosclerosis was present in five biopsies, and in one patient, biopsy and clinical findings were consistent with idiopathic focal segmental glomerulosclerosis. Additional lesions included mesangiopathic glomerulonephritis in one patient, basement membrane thickening suggestive of diabetic nephropathy in one, and cholesterol emboli in two cases. Arteriolar and arterial sclerosis were tightly linked, and correlated with interstitial fibrosis and the reciprocal of serum creatinine. Global glomerulosclerosis was extensive, involving on average 43 +/- 26% of glomeruli. The extent of this lesion did not correlate with degree of arteriolar or arterial thickening, but did correlate with systolic blood pressure (P = 0.0174), the reciprocal of serum creatinine (P = 0.0009), serum cholesterol (P = 0.0129) and interstitial fibrosis (P < 0.0001). These data underscore that renal biopsies in non-diabetic hypertensive African-Americans with mild to moderate renal insufficiency in the absence of marked proteinuria are overwhelmingly likely to show renal vascular lesions consistent with the clinical diagnosis of hypertensive nephrosclerosis.

The significance of anticardiolipin antibodies in patients with lupus nephritis.

The objective of this study was to determine whether anticardiolipin antibodies (ACL) in SLE patients are associated with a specific pattern of lupus nephritis and/or with renal microvascular changes. Patients with SLE, followed prospectively between June 1991-May 1994 at The Wellesley Hospital Lupus Clinic, who underwent a renal biopsy were included. The ACL was measured by the ELISA according to international standardized method. Renal biopsy morphology was assessed using the WHO criteria for the classification of lupus nephritis. Renal vascular changes included glomerular hyaline thrombi, intimal fibrosis and intraluminal thrombi of renal arterioles. There were 23 SLE patients. The mean age at diagnosis of SLE was 28.2 years and the mean disease duration was 6.3 years. Of these 10 (43%) had high levels of ACL. No difference in the frequency of severe nephritis (Class III and IV) was identified amongst patients with and without ACL. Mesangial nephritis was more common in patients with ACL 40% vs 0, p = 0.02). Glomerular hyaline thrombi occurred in 3 (13%) patients. None of them had positive ACL. Renal vascular lesions included intimal proliferation in 4 (ACL + , 1) occluded lumens by thrombi in 2 (ACL + 1). Our data indicate that the development of glomerular and/or microvascular changes is not related to the presence of ACL.

P-915 - Chronic effect of lemildipine(NB-818), a new dihydropyridine calcium antagonist, on renal vascular lesion in conscious spontaneously hypertensive rat.

P-915 - Chronic effect of lemildipine(NB-818), a new dihydropyridine calcium antagonist, on renal vascular lesion in conscious spontaneously hypertensive rat.

Renal vascular lesions in the elderly: nephrosclerosis or atheromatous renal disease?

In white Europeans, renal size and function decline with age. This phenomenon has long been attributed to nephrosclerosis, i.e. primary vascular lesions associated with glomerular obsolescence, tubulointerstitial lesions and fibrosis. The part played by ageing and by pre-existing hypertension is still a matter of debate. Nephrosclerosis is a diagnosis of exclusion when no renal histology is available. As renal biopsy is rarely carried out in an elderly patient with atrophic kidneys, a long history of hypertension and only microalbuminuria or no proteinuria, the diagnosis of nephrosclerosis is generally overestimated. Even when renal histology is available, only subtle differences in vascular lesions have been claimed to distinguish those due to ageing from those due to hypertension. At any rate, meticulous control of blood pressure is certainly the most efficient means of protecting the renal vessels from further deterioration. Atheromatous renal disease has more recently been recognized as a major cause of progressive renal failure in the elderly. Renal artery stenoses due to atheromatous plaques might well be the cause of 10-15% of end-stage renal failure in whites aged > 50 and be the fourth cause of uraemia in this age group. Such stenoses are usually bilateral and developing. Present imaging methods, such as duplex ultrasound scanning and renal scintigraphy, are valuable means of diagnosis. Renal angioplasty can halt the the pace of renal insufficiency, or even durably improve it in nearly half of the cases. Finally, aorto-renal atheroma is a common and underestimated cause of cholesterol embolism. Minor, spontaneous forms thereof are indistinguishable from nephrosclerosis. Massive embolism entails a dismal prognosis, in terms of both renal function and patient survival. In conclusion, renal vascular lesions in the elderly remain a major concern. Improving non-invasive diagnostic procedures and applying preventative as well as curative measures should significantly reduce the incidence of end-stage renal disease is such patients.

Superselective Endo-Vascular Treatment of Renal Vascular Lesions

Embolization with platinum micro-coils delivered through the Tracker-18 micro-catheter was performed in 6 patients when peripheral selective catheterization with standard angiographic catheters was not possible. The patients had a total of 7 peripheral renal vascular lesions (3 arteriovenous fistulas, 2 false aneurysms, 1 direct vascular trauma and 1 arteriovenous malformation). In all patients we initially used platinum micro-coils as the embolic agent. Two patients required repeat embolization with glue. Endo-vascular treatment was technically successful in all cases and no complications were encountered. There was no renal parenchyma infarction in 3 patients and small peripheral infarctions (10 to 15% of the renal parenchyma) occurred in 3. Super selective endo-vascular treatment with a variable stiffness catheter is safe and useful technique when classical methods of embolization are not possible.

EFFECT OF DIETARY CALCIUM ON THE DEVELOPMENT OF HYPERTENSION AND HYPERTENSIVE VASCULAR LESIONS IN DOCA-SALT AND TWO-KIDNEY, ONE CLIP HYPERTENSIVE RATS

To examine the effect of modest changes in dietary calcium on systolic blood pressure (SBP) and myocardial and renal vascular lesions in Sprague-Dawley rats. Regular- (0.4%, by weight), high- (0.8%) or low-calcium (0.24%) diets were fed to normotensive control, deoxycorticosterone acetate (DOCA)-salt and two-kidney, one clip (2-K, 1C) hypertensive rats for 8 weeks. Tail-cuff SBP and metabolic balance were measured once a week. At the end of the study the kidneys and hearts were collected for histological study. Dietary calcium had no effect on SBP in the DOCA-salt rats, but loading with calcium accelerated the rise in SBP in 2-K,1C rats (P < 0.01, high- versus regular-calcium diet). The high-calcium diet reduced the percentage medial area of intramyocardial arteries in the DOCA-salt and 2-K,1C hypertensive rats. The DOCA-salt rats on the low-calcium diet had a higher renal vascular lesions score than those on the regular- or high-calcium diet (P < 0.05). A high-calcium diet appears to prevent intramyocardial vascular wall thickening in DOCA-salt and 2-K,1C hypertensive rats, and a low-calcium diet aggravates renal vascular lesions in DOCA-salt hypertensive rats. These effects are not related simply to changes in blood pressure.

EFFECT OF DIETARY SODIUM CHLORIDE ON THE DEVELOPMENT OF RENAL GLOMERULAR AND VASCULAR LESIONS IN HYPERTENSIVE RATS

1. The hypothesis that high levels of NaCl in the diet aggravates hypertension-associated renal vascular lesions was examined in unilaterally nephrectomized deoxycorticosterone acetate treated (DOCA) and two kidney one clip (2K1C) hypertensive rats, as well as normotensive controls. 2. High NaCl diet significantly increased systolic blood pressure (SBP) in DOCA rats, but had little effect on SBP in normal control rats, and did not affect the rise of SBP in 2K1C rats. 3. High NaCl diet was associated with a higher percentage of glomerular lesions and renal arterial and arteriolar lesions in DOCA and 2K1C rats (P < 0.05). 4. Thus high NaCl intake exacerbated renal arterial and arteriolar and glomerular lesions in both DOCA and 2K1C hypertensive rats. In 2K1C rats this effect may be in part independent of blood pressure.

Embolization of renal vascular lesions: clinical experience with microcoils and tracker catheters.

After biopsy (n = 6) and nephrostomy (n = 1) of three native and four transplanted kidneys, gross hematuria, hypertension, and deterioration of function necessitated performance of transarterial embolization. Angiography revealed five arteriovenous fistulas (AVFs), one pseudoaneurysm, and one arteriocaliceal fistula. Superselective catheterization was accomplished using 5 Fr standard diagnostic catheters and 3 Fr coaxial Tracker catheters. Four of five AVFs were embolized successfully by inserting unfibered (2 patients) and fibered (2 patients) platinum coils (diameters 2 mm and 4 mm, respectively). For one AVF, additional injection of butylcyanoacrylate was necessary. The pseudoaneurysm was embolized successfully by such injection, and the arteriocaliceal fistula was occluded using one unfibered 2-mm coil. Embolization stopped the bleeding in all patients. One week after treatment, renal function was improved in 5 patients and remained unaffected in 2. Superselective embolization using Tracker catheters and fibered microcoils is an effective, safe treatment of renal vascular lesions.

Renovascular hypertension.

Renovascular disease, particularly when associated with atherosclerosis, is a common cofactor in accelerating hypertension and deteriorating renal function. With increased longevity and effective antihypertensive medications, the prevalence of vascular lesions affecting renal viability is increasing, possibly accounting for 15% of end-stage renal disease. Renal vascular lesions alter renin release and multiple associated mechanisms related to adrenergic and vascular regulation. Several new diagnostic modalities, including captopril renography, duplex ultrasonography, and magnetic resonance angiography, are being applied for noninvasive diagnosis. Advances in interventional radiologic procedures, including endovascular stents and surgical revascularization, offer the potential for both improved blood pressure management and salvage of renal function. Optimal management of renovascular disease depends on careful assessment of the progression of each patient and associated risk of intervention.

Iatrogenic renal vascular lesions: treatment by arterial catheter embolisation

Five patients, four male and one female aged 17–65 years (mean 41 years), with iatrogenic renal vascular lesions were treated by percutaneous artenial embolisation. Vascular trauma was caused by percutaneous biopsy (two cases), percutaneous nephrolithotomy (one case), partial nephrectomy (one case) and total nephrectomy (one case). Recurrent macroscopic haematuria was present in four cases and congestive cardiac failure due to reno-caval shunt in one case. Selective renal arteriography revealed false aneurysm in all cases, associated with arteriovenous fistula in four cases. Treatment was performed by selective embolisation of the injured artery. Coils and n-butyl-2-cyanoacrylate mixed with iodised oil or tantalum powder were used as embolic agents. Two patients required two embolisation procedures for definitive treatment. No complication was observed.

The dissociation of arterial hypertension and lupus glomerulonephritis in systemic lupus erythematosus.

In spite of several articles questioning the general opinion that arterial hypertension in patients with systemic lupus erythematosus (SLE) is only the consequence of lupus glomerulonephritis (LGN), this still remains the usual pathophysiologic explanation. The purpose of this study was to explore the correlations between hypertension and LGN and to assess the importance of hypertension control for the prognosis of patients. A retrospective analysis of 173 patients with SLE over a period of 14 years was performed. For most of the patients, data were available from regular follow-up visits over an average of 6 years. Our results show a dissociation of hypertension and LGN and an association of hypertension and renal dysfunction. Severe hypertensive renal vascular lesions correlated well with a decrease of renal function. Successful treatment of hypertension is therefore essential in order to prevent deterioration of renal function in patients with LGN.

Hypertension artérielle maligne au cours du syndrome des antiphospholipides, en l'absence d'atteinte rénale lupique spécifique

We retrospectively analyzed the records of 5 patients with antiphospholipid syndrome, primary (n = 1) or secondary to systemic lupus erythematotus (n = 4), who developped a malignant systemic hypertension with renal insufficiency and biopsy-proven intra-renal vascular lesions, in the absence of lupus nephritis.

Renal Thrombotic Microangiopathy in Patients With Systemic Lupus Erythematosus and the Antiphospholipid Syndrome

Current studies indicate that a thrombotic microangiopathy (TMA) identifies patients with systemic lupus erythematosus (SLE) who are at high risk of progressing to end-stage renal disease. We have observed two patients with SLE and one patient with a primary antiphospholipid syndrome (APS) who developed acute renal insufficiency with thrombocytopenia. Renal biopsies showed a TMA characterized by thrombi or by cellular and mucoid intimal hyperplasia of small arteries and arterioles. No arterial or arteriolar immune-complex deposits were detected by immunofluorescent or electron microscopy. Biopsies from one SLE patient and the APS patient showed no immune-complex glomerular disease. Both had serum antiphospholipid antibodies (aPL). aPL were not detected in the serum of the other SLE patient who had an active lupus nephritis. Acute renal failure and thrombocytopenia resolved in each case following treatment by plasmapheresis or prednisone and heparin. None of the patients were initially treated with cytotoxic drugs. As more knowledge is gained, the accurate identification of renal vascular lesions in SLE or related diseases could influence renal prognosis and choice of therapy. The cases reported here provide further evidence that a TMA can cause acute renal failure independent of lupus nephritis. TMA should be distinguished from other forms of renal vascular disease, particularly a noninflammatory lupus microangiopathy, which is probably mediated by subendothelial immune-complex deposits. The absence of immunoglobulin deposits in vessels involved by a TMA indicates that microvascular thrombosis is promoted by mechanisms other than those usually attributed to immune-complex disease. Phospholipid reactive antibodies may be pathogenetic in some cases.

Renal Vascular Lesions as a Marker of Poor Prognosis in Patients With Lupus Nephritis

The frequency of renal vascular lesions (RVL) and their relevance in the progression of renal damage were evaluated by the Pathology Group of the "Gruppo Italiano per lo Studio della Nefrite Lupica" (GISNEL). Of 285 patients with lupus nephritis collected from 20 nephrology centers in Italy and classified according to World Health Organization (WHO) criteria, 79 cases (27.7%) with RVL were identified and classified as follows: (1) lupus vasculopathy (n = 27); (2) hemolytic-uremic syndrome/thrombotic thrombocytopenic purpura (HUS/TTP) malignant hypertension-like lesions (n = 24); (3) vasculitis (n = 8); (4) arterio-arteriosclerosis (n = 20). At the time of renal biopsy, patients with RVL had mean serum creatinine levels significantly higher than patients without RVL (201.8 +/- 195.9 mumol/L [2.2 +/- 2.2 mg/dL] v 108.1 +/- 108.0 mumol/L [1.2 +/- 1.2 mg/dL]; P less than 0.01). Hypertension was more frequent in patients with RVL than in those without (68.4% v 30.5%; P less than 0.01). The probability of kidney survival assessed according to the Kaplan-Meier method at 5 and 10 years was, respectively, 74.3% +/- 5.9% and 58.0% +/- 8.9% in patients with RVL, compared with 89.6% +/- 2.7% and 85.9% +/- 3.7% in patients without RVL. However, the two groups did not differ significantly as regards overall survival, the probability of survival at 5 and 10 years being 86.5% +/- 4.5% and 78.8% +/- 6.6% in patients with RVL and 92.2% +/- 2.2% and 83.3% +/- 4.4% in patients without RVL.(ABSTRACT TRUNCATED AT 250 WORDS)

Therapeutic Benefit of Captopril in Salt-Loaded Stroke-Prone Spontaneously Hypertensive Rats Is Independent of Hypotensive Effect

In the present study we examined whether the angiotensin I converting enzyme inhibitor, captopril, would protect stroke-prone spontaneously hypertensive rats (SHRSP) from stroke and renal pathology over a 26-week period. In the control group of six untreated SHRSP fed Stroke-Prone Rodent Diet and 1% NaCl drinking solution, all animals developed severe hypertension and stroke by 16.1 weeks of age. In eight salt-loaded SHRSP treated with oral captopril (50 mg/kg/day) beginning at 8.4 weeks of age, systolic blood pressure was slightly but temporarily suppressed and then continued to rise; by 12 weeks of age systolic blood pressure reached levels of severe hypertension, 240 +/- 8 mm Hg, and did not differ from that of untreated SHRSP. No deaths or brain lesions were noted in captopril-treated SHRSP despite severe hypertension maintained through 26 weeks of age when the study ended. Captopril treatment prevented increases in urinary protein excretion (14 +/- 2 v 63 +/- 16 mg/day at 11.7 weeks of age, P less than .01) and the severe brain, renal, and cardiac vascular lesions observed in untreated SHRSP. When maintained on Stroke-Prone Rodent Diet and saline, plasma renin activity of untreated SHRSP surviving until 14.5 weeks of age was markedly increased (29.1 +/- 9.4 ng Ang I/mL/h) compared with either untreated SHRSP (9.2 +/- 2.5 ng Ang I/mL/h, P less than .01) or Wistar-Kyoto rats (3.5 +/- 1.0 ng Ang I/mL/h, P less than .01) maintained on standard diet and water.(ABSTRACT TRUNCATED AT 250 WORDS)

Color Doppler sonographic findings in renal vascular lesions.

Three patients with renal vascular lesions, one congenital arteriovenous (AV) fistula and two renal pseudoaneurysms, were assessed with color Doppler sonography. The AV fistula was detected initially by color Doppler after having been missed by both real-time sonography and computed tomography. High frequency shift blood flow within a hypoechoic lesion noted by color Doppler characterized the AV communication. Both renal pseudoaneurysms had detectable bidirectional swirling blood flow within an anechoic portion of a complex mass. Findings in all three cases were confirmed by angiography or pathology. Color Doppler sonography seems potentially useful in the evaluation of renal vascular pathology.