RENAL KALLIKREIN IN DIABETIC-PATIENTS WITH HYPERTENSION ACCOMPANIED BY NEPHROPATHY

We measured the 24-h excretion of urinary kallikrein in 27 patients with Type 2 (non-insulin-dependent) diabetes and in 10 normal control subjects. Mean (.+-. SD) kallikrein excretion in diabetic patients with nephropathy (6.2 .+-. 2.4 naphthyl units (NU)/day, n = 13) was significantly lower than in control subjects (12.8 .+-. 3.4 NU/day, p < 0.01) and in diabetic patients without nephropathy (9.4 .+-. 3.4 NU/day, n = 14, p < 0.05). Kallikrein excretion in hypertensive diabetic patients with nephropathy (5.1 .+-. 1.6 NU/day, n = 8) was significantly lower (p < 0.05) than in normotensive patients with nephropathy (8.3 .+-. 2.1 NU/day, n = 5). There were no significant differences in kallikrein excretion rate (24-h excretion of urinary kallikrein/24-h creatinine clearance) among control subjects (9.9 .+-. 4.3 NU/ml), diabetic patients with (9.0 .+-. 3.2 NU/ml) and without (9.3 .+-. 3.5 NU/ml) nephropathy. However, kallikrein excretion rate in hypertensive diabetic patients with nephropathy (7.7 .+-. 3.3 NU/ml) was significantly lower (p < 0.05) than in normotensive diabetic patients with nephropathy (11.8 .+-. 2.0 NU/ml, n = 10). Respectively basal and post-stimulated (with intravenous furosemide 40 mg plus 60 min ambulation) plasma aldosteorne concentrations measured in control subjects and in hypertensive diabetic patients with neprhopathy were similar and increased to the same extent in the 2 groups (5.5 .+-. 3.2 versus 5.3 .+-. 3.2 and 9.3 .+-. 2.6 versus 10.5 .+-. 3.4 ng/ml), although the respective plasma renin activity tended to be lower in diabetic patients than in control subjects (0.7 .+-. 0.6 versus 1.3 .+-. 0.9 and 1.8 .+-. 1.8 versus 3.0 .+-. 2.6 ng-1 .cntdot. ml-1 .cntdot. h-1). The results indicate that urinary kallikrein excretion is decreased in hypertensive diabetic patients with nephropathy, and that the decrease might not be attributable to an altered renin-aldosterone system.