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Angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria in diabetic and nondiabetic nephropathy. However, no studies have determined whether this antiproteinuric effect modifies the progression of renal insufficiency. We studied the evolution of 46 nondiabetic patients with nephrotic proteinuria treated with captopril for a minimum of 12 months. The follow-up period before captopril treatment was 12 to 18 months. At the end of follow-up, after captopril introduction (24.4 +/- 7.6 months), proteinuria had decreased from 6.3 +/- 2.5 to 3.9 +/- 3.1 g/24 h (P less than 0.001), with a mean decrease of 45% +/- 28%. The proteinuria decrease was higher in patients with reflux nephropathy, proteinuria associated with reduction of renal mass, inactive crescentic glomerulonephritis, nephroangiosclerosis, and IgA nephropathy, whereas patients with membranous glomerulonephritis and idiopathic focal glomerulosclerosis showed a poorer response. Patients were separated according to a proteinuria reduction greater (group A, 23 patients) or lower (group B, 23 patients) than 45% of the initial value. At the end of follow-up, renal function had not significantly changed in group A with respect to values at the start of treatment: serum creatinine (SCr) was 229 +/- 167 mumol/L (2.6 +/- 1.9 mg/dL) versus 203 +/- 97 mumol/L (2.3 +/- 1.1 mg/dL), and creatinine clearance (CrCl) was 0.80 +/- 0.52 mL/s (48 +/- 31 mL/min) versus 0.87 +/- 0.47 mL/s (52 +/- 28 mL/min). The slope of the reciprocal of Scr (1/SCr) showed a significantly beneficial change after captopril introduction.(ABSTRACT TRUNCATED AT 250 WORDS)

We report a 35-year-old man with adult polycystic kidney disease (APKD) that developed nephroptic syndrome accompanied by a rapid worsening of renal function. Histologic examination showed marked tubulointerstitial chronic abnormalities and focal glomerulosclerosis (FGS) lesions in 24% of the glomeruli. With captopril, an renal function continued to deteriorate. No other cases of nephrotic-range proteinuria were detected among 65 APKD patients with renal insufficiency. Histologic examination of an other 12 kidneys removed from patients with APKD showed striking interstitial lesions, most of the glomeruli being normal. However, those patients with higher amounts of proteinuria had more glomeruli (14-32%) with FGS lesions.

Although hypoalbuminemia is a fundamental characteristic of nephrotic syndrome (NS), there are many patients with massive proteinuria that do not develop hypoalbuminemia. We have studied the clinical and biochemical characteristics of 19 patients with persistent massive proteinuria (greater than 5 g/d) and normal serum albumin (group I) in comparison with 16 patients with similar proteinuria excretion, but persistent hypoalbuminemia (group II). Most of group I patients had diagnoses suggesting glomerular hyperfiltration (focal glomerulosclerosis [FGS] associated with vesicoureteral reflux [VUR], reduction of renal mass, proteinuria associated with obesity, sclerotic phase of idiopathic crescentic glomerulonephritis [GN] in contrast with those of group II, in which membranous GN was the most frequent diagnosis. We prospectively investigated differences in the antiproteinuric effect of captopril, an antiotensin-converting enzyme inhibitor (ACEI); after 6 months of treatment, proteinuria decreased clearly in group I (7.1 +/- 1.7 to 3.7 +/- 1.7 g/d; P less than 0.001), whereas no significant changes were observed in group II (8.1 +/- 2.4 to 8.8 +/- 4 g/d). Serum creatinine (Scr) remained stable during captopril treatment in group I, whereas three patients in group II showed a worsening of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)

A prospective study was made of 38 adult patients (15 male and 23 female, age 30.5 +/- 10.8 years) with isolated hematuria of unknown etiology in which presence of hypercalciuria and/or hyperuricosuria without lithiasis was observed. Eighteen patients also referred episodes of macroscopic hematuria. Twenty-six patients had hypercalciuria (5.1 +/- 1.4 mg/kg/day), 29 hyperuricosuria (1053 +/- 198 mg/day) and 17 presented both alterations. A four months treatment was instituted with thiazides in patients with hypercalciuria and allopurinol in those with hyperuricosuria. From the first months and throughout the whole therapy, urinary excretion of calcium an uric acid became normalized in all cases. In 22 patients (57.8%) (Group I: Respondents) hematuria disappeared coinciding with normalization of calcium and uric acid values in urine and was maintained during the follow-up months. In the remaining 16 patients (Group II: Non-Respondents) the hematuria condition persisted in spite of such normalization, in most cases other causes for hematuria becoming clear later. No differences with regard to age, relationship male/female nor basal calciuria and uricosuria values were seen between both Groups. Group I had a greater incidence of macroscopic hematuria episodes (64% vs 12% in Group II, p less than 0.01) and of family nephrolithiasis (64 vs 25% in Group II, p less than 0.05). We conclude that hypercalciuria and hyperuticosuria are potentially reversible causes of hematuria in adults. Therefore, urinary determination of calcium and uric acid should be included in urinary evaluation of patients with hematuria even though they do not present renal lithiasis.