RENAL STRUCTURE AND FUNCTION IN NON-INSULIN-DEPENDENT DIABETIC-PATIENTS WITH MICROALBUMINURIA

We have recently described heterogeneity in renal structure in non-ins ulin-dependent diabetic patients (NIDDM) with microalbuminuria (MA, de fined as albumin excretion rate from 20 to 200 mu g/min). Thus, at var iance with IDDM patients, ''typical'' diabetic glomerulopathy by light microscopy is observed only in a third of NIDDM with MA (Category II, CII). Further, despite persistent MA, 30% of NIDDM have normal or nea r normal renal structure (Category I, CI). Another one-third shows ''a typical'' patterns of renal injury with absent or mild diabetic glomer ular changes, associated with disproportionately severe tubulointersti tial lesions and/or arteriolar hyalinosis and global glomerular sclero sis (Category III, CIII). The aims of this study were to evaluate whet her similar patterns of renal lesions could be confirmed in a larger g roup of NIDDM with MA and to investigate tubular function in order to understand the mechanisms underlying MA in NIDDM patients. Renal biops ies were performed in 53 NIDDM with MA Categories I, II and III were f ound in 41%, 26% and 33% of NIDDM with MA, respectively. All 8 patient s with proliferative diabetic retinopathy were in CII. We also studied the urinary daily excretion rate of alpha(1)-microglobulin (alpha(1)m ), a low molecular weight protein, which is a useful indicator of tubu lar function. alpha(1)m was markedly increased only in CII patients (C I vs. CII vs. CIII: 6.2 +/- 1.2 vs. 13.7 +/- 2.1 vs. 7.3 +/- 0.9 mg/da y, ANOVA, P < 0.01). In conclusion, we confirm that there is heterogen eity in renal structure in NIDDM patients with MA. This heterogeneity is not due to renal diseases other than diabetes. Increased alpha(1)m and proliferative retinopathy are useful indicators of the subgroup of MA NIDDM patients with typical diabetic glomerulopathy. It is suggest ed that diabetic microangiopathy explains the simultaneous occurrence of typical diabetic glomerulopathy, proliferative retinopathy and tubu lar dysfunction in a subgroup of NIDDM patients with MA.