TUBULAR DAMAGE IN MICROALBUMINURIC PATIENTS WITH PRIMARY GLOMERULONEPHRITIS AND DIABETIC NEPHROPATHY

Tubular damage as suggested by enzymuria and tubular proteinuria is a recognized feature of glomerulonephritis (GN) with clinical proteinuri a and both incipient and overt diabetic nephropathy (DN). However, lit tle is known about the presence of tubulopathy in patients with primar y GN, microalbuminuria [albumin excretion (AER) 30-300 mg/d] and micro hematuria. Three groups were studied. The GN group comprised 17 (2 F) patients with biopsy-proven GN with microalbuminuria. The DN group com prised 35 (14 F) patients with incipient diabetic nephropathy with AER 30-300 mg/d, and controls comprised 38 (15 F) normal subjects with no rmal AER < 30 mg/d. Serum creatinine, albuminurinuria, transferrinuria , and markers of tubular damage such as urinary excretion of N-acetyl- glucosaminidase (NAG), leucine aminopeptidase (LAP), gamma-glutamyl tr ansferase (gGT), and retinol binding protein (RBP) were measured. GN a nd DN had comparable degrees of albuminuria, transferrinuria, and LAP excretion, and these were significantly higher than controls. Serum cr eatinine was significantly higher in GN than DN and controls. DN had s ignificantly higher NAG and RBP and lower gGT than GN and controls. In both GN and DN groups, both glomerular proteins correlated,vith each other and NAG correlated significantly to LAP and gGT. Albuminuria cor related to tubular enzymuria in GN group but not in patients with DN. The results suggest that tubular damage is less marked in microalbumin uric patients with GN than those with DN despite similar degree of glo merular proteinuria. The pattern of tubulopathy is also different in t he two groups, indicating differences in the pathogenesis of tubular d amage in these two clinical settings.