Plasma renin activity and hypertension in diabetes mellitus

• Published in: Diabetes (New York, N.Y.) Vol. 25; no. 10; pp. 969 - 974
• Main Authors: Christlieb, A R, Kaldany, A, D'Elia, J A
• Format: Journal Article
• Language: English
• Published: United States 01-10-1976
• Subjects: Adult; Diabetes Complications; Diabetes Mellitus - metabolism; Diabetes Mellitus - physiopathology; Diabetic Nephropathies - complications; Diabetic Nephropathies - drug therapy; Diabetic Nephropathies - metabolism; Female; Furosemide - therapeutic use; Humans; Hypertension - complications; Hypertension - drug therapy; Hypertension - metabolism; Male; Middle Aged; Posture; Potassium - metabolism; Renin - blood; Sodium - metabolism
• ISSN: 0012-1797; 1939-327X
• DOI: 10.2337/diab.25.10.969

Plasma renin activity (PRA) was determined in 48 patients with diabetes mellitus in sodium balance on a 10-20 mEq. Na diet. Nine were normotensive (group I), 11 11 were hypertensive without diabetic nephropathy (group III). Results were compared with those in 16 normal subjects and 49 nondiabetic patients with essential hypertension in similar Na balance. Mean supine PRA did not differ significantly among groups I and II, normal subjects, and patients with essential hypertension. Group III diabetics had a supine PRA of 2.4 +/- 0.4 ng./ml./hr. (x +/- S.E.M.), significantly lower than the other diabetic groups (P less than 0.005) and normal subjects (P less than 0.05). Upright PRA was 12.8 +/- 2.2 in group I diabetics, similar to that in normal subjects (13.3 +/- 2.3), and 8.1 +/- 1.4 in group II diabetics, similar to that in essential hypertensives (6.8 +/- 0.8). In group III diabetics, upright PRA was 4.0 +/- 0.5, significantly lower than that in any other group. These results suggest that (1) PRA is normal in normotensive diabetics, (2) upright PRA in diabetics with hypertension but no nephropathy is similar to that in essential hypertension, and (3) patients with diabetes, hypertension, and nephropathy have "low renin hypertension," explaining the virtual absence of malignant hypertension in this group. Although the major mechanism for this low PRA may be volume expansion, indicating the need for potent diuretics, other mechanisms include hyalinization of the afferent arteriole, decreased cathecholamine stimulation of renin release, and inadequate conversion of prorenin to renin.