Abstract
A low response of the renin-angiotensin-aldosteone (RAA) system was reported by Christlieb and co-workers in patients with diabetic nephropathy. However, their clinical studies were based on observations of long-duration juvenile diabetic patients who revealed established hypertension and renal dysfunction. The present investigation was therefore designed to establish the kinetics of the RAA system in the compensated phase of diabetic nephropathy.
Plasma renin activity (PRA) and plasma aldosterone (PA) were measured at bed rest and after stimulation with furosemide in 27 adult-onset diabetics and 15 age-matched controls. Seventeen of the diabetics did not suffer from proteinuria (non-proteinuria group) but the other subjects suffered from persistent proteinuria, but from no hypertension or renal dysfunction (proteinuria group). They were kept on a diet containing 86 mEq of sodium as NaCl In the non-proteinuria group, the PRA levels from bed rest time to the post-stimulation period did not significantly differ from those in the control group. In the proteinuria group, the PRA levels were significantly lower than in the other two groups. The PA levels were slightly higher in the non-proteinuria group than in the control group (p: N.S.). In the proteinuria group, the PA levels were significantly lower than those in the other two groups at bed rest time and after stimulation. These findings suggest that (1) the renin-aldosterone system generally responds normally in diabetics without proteinuria but responds subnormally in diabetics with persistent proteinuria, even when there is no complicating hypertension or decreased renal function, and (2) the phenomen a are more closely related with renal disease itself than elevated blood pressure and renal dysfunction. The results for adult-onset diabetics are consistent with the suggestion that hyporeninemic-hypoaldosteronism is found in juvenile-onset diabetics with nephropathy.
