RENIN-ALDOSTERONE AXIS IN NORMOALBUMINURIC INSULIN-DEPENDENT DIABETES-MELLITUS PATIENTS WITH GLOMERULAR HYPERFILTRATION

The renin-aldosterone axis was evaluated by captopril test in 22 normotensive normoalbuminuric insulin-dependent diabetes mellitus (IDDM) patients with and without glomerular hyperfiltration. Patients were divided into those with glomerular hyperfiltration (Hf-IDDM) and with normal glomerular filtration rate (GFR; Nf-IDDM) according to the upper limit of GFR (134.7 ml/min per 1.73 m(2)). sixteen normal individuals were also studied. GFR was measured by the Cr-51-EDTA single injection method, extracellular fluid volume as the distribution volume of Cr-51-EDTA, and blood volume using Cr-51-sodium chromate-labelled red blood cells. Twenty-five mg of captopril were administered per os and plasma renin activity (PRA; RIA), plasma aldosterone (RIA) and blood pressure were measured at 0 and 120 min post-captopril. PRA at time zero (Hf-IDDM = 2.4 +/- 1.7; Nf-IDDM = 2.5 +/- 1.9; controls = 1.0 +/- 0.6 ng/ml/h) and at 120 min (Hf-IDDM = 9.9 +/- 8.3; Nf-IDDM = 11.2 +/- 8.9; controls = 5.4 +/- 5.7 ng/ml/h) was higher in IDDM patients than in controls (P = 0.01). The increase of PRA was similar in patients (Hf-IDDM = 7.5 +/- 7.3, and Nf-IDDM = 8.7 +/- 7.2 ng/ml/h) and controls (4.4 +/- 5.3 ng/ml/h). There was no difference in PRA levels between Hf-IDDM and Nf-IDDM patients. PRA did not correlate with GFR, aldosterone, blood pressure, blood volume, duration of diabetes, 24-h urinary sodium and metabolic control indexes. Plasma aldosterone and the magnitude of its decrease after captopril was similar among patients and controls. Captopril induced a greater reduction of systolic blood pressure in patients (Hf-IDDM = 12.3 +/- 6.9 mmHg; Nf-IDDM = 11.1 +/- 7.3 mmHg) than in controls (5.4 +/- 5.2 mmHg) (P = 0.01). No difference was found between Hf-IDDM and Nf-IDDM patients. In conclusion, normoalburninuric IDDM patients, irrespective of glomerular hyperfiltration, presented increased levels of PRA and larger blood pressure response to captopril as compared to normal individuals.