Clinical and pathologic findings in the kidneys of 30 consecutive acquired immunodeficiency syndrome (AIDS) autopsies and in 34 consecutive renal biopsies performed on HIV infected patients at our institution between 1983 and 1987 were studied. To determine if the lesions of HIV-associated nephropathy have morphologic specificity, a subgroup of 13 biopsies with a diagnosis of HIV-associated nephropathy (HIVN) were compared to 13 biopsies each of heroin-associated nephropathy (HAN) and of idiopathic focal segmental glomerulosclerosis (IFSGS) matched for patient age, proteinuria and serum creatinine. A diagnosis of HIVN was made in 1 of 30 (3.3%) AIDS autopsies and 26 of 34 (76.5%) renal biopsies. When compared to HAN and IFSGS, HIVN had more globally "collapsed" glomeruli (P less than 0.001), less glomerular hyalinosis (P less than 0.02), more severe visceral epithelial cell swelling (P less than 0.05), more numerous visceral epithelial cell droplets (P less than 0.002), more prevalent and severe tubular microcystic dilatation (P less than 0.02), and tubular cell degenerative changes (P less than 0.001). Focal glomerular electron-dense deposits were present in 14 of 26 cases. Tubuloreticular inclusions were extremely numerous in glomerular and interstitial capillary endothelial cells as well as in interstitial leukocytes (P less than 0.001). Granular degeneration of nuclear chromatin was present in 10 of 26 cases. Nuclear bodies were more numerous in tubular and interstitial cells of HIVN (P less than 0.01), particularly type 3 (P less than 0.001). Reversal of tissue T4/T8 ratio was observed. We conclude that while no single morphologic feature of HIVN is specific, the combination of clinical and pathologic findings is quite distinctive and permits a presumptive diagnosis of HIVN in otherwise asymptomatic carriers.

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Two groups of rats received amphotericin-B (Amp). One group (AA) received a single acute dose of 1 mg/kg i.v. The second (CA) received 10 mg/kg i.p. daily for 4 days. In AA rats, measurements 1 to 5 hr after Amp were compared with their own preinfusion values. Inulin clearance, (CIn, 4.5 ml X min-1 X kg-1 per kidney pre vs. 1.3 post), renal plasma flow (RPF, 12.0 ml X min-1 X kg-1 vs. 7.4), and the estimated pressure in the glomerular capillaries (Pgc, 52 mm Hg vs. 40), were all significantly decreased while renal vascular resistance (5.2 mm Hg/ml vs. 12.0) was increased. Only 45% of the 3H-inulin injected into surface tubules was recovered in the urine as contrasted with 100% recovery before injection. This suggests that tubule permeability was increased, but there was no histologic evidence of renal tubule necrosis. Twenty-four hours after intravenous Amp, CIn and RPF returned to normal. Data from CA rats were compared with values from sham-treated pairfed (PF) control rats. Again, CIn (4.22 ml X min-1 X kg-1 in PF vs. 2.69 in CA), RPF (16.1 ml X min-1 X kg-1 vs. 8.3), and Pgc (48 mm Hg vs. 38) were decreased, and renal vascular resistance (4.9 mm Hg/ml vs. 8.0) was increased. The recovery of 3H-inulin in the urine was slightly, but significantly, decreased (96% vs. 83%). These findings demonstrate that Amp decreases renal function by at least two mechanisms. An increase in renal vascular resistance is most important, although increased tubule permeability with a "backleak" of tubule fluid also contributes to renal dysfunction, particularly after intravenous Amp.

CASE PRESENTATIONA 41-year-old woman was admitted to Harlem Hospital Center for the evaluation of nephrotic-range proteinuria, microhematuria, hypoalbuminemia, and edema. The patient was born in the Dominican Republic and came to the United States 10 years ago. She gave a history of episodic cloudy urine for the past 28 years. Five years before admission during her last pregnancy, she was noted to have proteinuria (2 g/24 h). Two years before admission, she was treated for filariasis at another hospital, and after 1 year, she was admitted to the same hospital for edema and was found to have chronic active hepatitis C infection with incipient cirrhosis by liver biopsy. For the past 3 months, the patient noted progressive swelling of both lower extremities associated with episodic passage of cloudy urine and flank pain. There was no history of diabetes mellitus, hypertension, renal stones, or gross hematuria. She was on no medications and denied alcohol, illicit drug, and tobacco use.Physical examination revealed a thin and malnourished woman weighing 55.5 kg with a temperature of 371C, pulse 92/min, and blood pressure 104/60 mmHg. There was no skin rash. The heart and lung examinations were normal. The abdomen was soft with the liver palpable 3 cm below the right costal margin. The spleen was not palpable and there was no shifting dullness. There was 3 þ pitting bilateral pedal edema.Laboratory data on the current admission included hematocrit 46% (reference interval, 42-52%), white blood count 6.6 Â 10 9 /l (reference interval, 4.0-10.5 Â 10 9 /l) with normal differential, platelet count 381 Â 10 9 /l (reference interval, 150-500 Â 10 9 /l), blood urea nitrogen 7 mg/dl (2.5 mmol/l) (reference interval, 7-18 mg/dl, 2.5-6.4 mmol/l), serum creatinine 0.7 mg/dl (63 lmol/l), total protein 4.1 g/ dl (41 g/l) (reference interval 6.0-7.8 g/dl, 60-78 g/l), albumin 1.9 g/dl (19 g/l) (reference interval 3.5-5.0 g/ dl,35-50 g/l), bilirubin 0.