Mechanism of decreased albuminuria caused by angiotensin converting enzyme inhibitor in early diabetic nephropathy

Abstract

The mechanism of decreased albuminuria caused by an inhibitor of angiotensin converting enzyme (ACE) was investigated in patients with early diabetic nephropathy. The subjects were 10 patients with non-insulin-dependent diabetes mellitus without azotemia but with albuminuria (less than 650 mg/day). First, a two-week study was done: one week with a diet with ordinary sodium levels and one week with a sodium-restricted diet, in random order. The systemic blood pressure and urinary excretion of sodium and albumin were measured daily. Intrarenal hemodynamics, in terms of the resistance of afferent and efferent arterioles (RA and RE) and glomerular capillary pressure (PGC), were calculated from renal clearance, the plasma total protein concentration, and the pressure-natriuresis relationship. Results obtained before and two weeks after starting the ACE inhibitor cilazapril (2 mg/day) were compared. Urinary excretion of albumin was decreased by cilazapril in 8 of the 10 patients. Cilazapril decreased the RE [6830 (3680, 14,750) to 4660 (1750, 10,790) dynes.sec.cm-5, P < 0.05, mean (minimum, maximum)] and PGC (53 +/- 5 to 43 +/- 9 mm Hg, P < 0.02, mean +/- SD) in these 8 patients, but not in the two other patients. The RA was not significantly changed in any patient. The percent change caused by cilazapril in the urinary excretion of albumin was significantly correlated with the change in PGC (N = 10, r = 0.875, P < 0.01), but not with changes in the systemic blood pressure. In conclusion, the mechanism by which an ACE inhibitor caused a short-term decrease in albuminuria in early diabetic nephropathy involved a glomerular hemodynamic change, namely, a decrease in PGC.