NEPHROTIC PROTEINURIA WITHOUT HYPOALBUMINEMIA - CLINICAL CHARACTERISTICS AND RESPONSE TO ANGIOTENSIN-CONVERTING ENZYME-INHIBITION

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 (〉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 < 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. Finally, since several lines of evidence suggest a role of tubular protein catabolism in the pathogenesis of nephrotic hypoalbuminemia, we have studied the urinary excretion of β2-microglobulin and N-acetyl-β-glucosaminidase (NAG) and the presence of renal glycosuria in 13 patients of group I and 12 of group II; group I patients had a significantly lower fractional excretion of β2-microglobulin (FEβ2M; 0.8% ± 1.6%) than those of group II (9.8% ± 12.9%; P < 0.05) and a lower excretion of NAG. Renal glycosuria was not detected in group I patients, whereas seven of 12 patients in group II (58%) showed glycosuria ranging from 2.5 to 12 g/d. In conclusion, the patients with massive proteinuria and normal serum albumin have distinctive clinical characteristics; the absence of hypoalbuminemia could be a predictor of the antiproteinuric response to ACEI. © 1991, National Kidney Foundation, Inc.. All rights reserved.