[Skip to Navigation]
June 1992

Proteinuria, Renal Impairment, Metabolic Control, and Blood Pressure in Type 2 Diabetes Mellitus: A 14-Year Follow-up Report on 195 Patients

Author Affiliations

From the Department of Medicine, Sackler Faculty of Medicine, Tel Aviv University and Meir Hospital, Kfar-Saba, Israel.

Arch Intern Med. 1992;152(6):1225-1229. doi:10.1001/archinte.1992.00400180085013

Background. —  The deleterious effect of hypertension on the course of diabetic retinopathy and the protective influence of antihypertensive therapy are well known. There is, however, little information about the long-term effect of different levels of blood pressure within the normal range on the evolution of renal function in type II diabetes.

Methods. —  One hundred ninety-five young normotensive patients with recent-onset type II diabetes, normal renal function, and no proteinuria were followed up for 14 years. Plasma glucose, creatinine, and urinary protein levels and blood pressure were determined periodically.

Results.—  Thirty patients developed hypertension; among them, 18 developed proteinuria (0.3 g/L). Among 144 patients who remained normotensive, 30 developed proteinuria. The mean decline in renal function (decline in reciprocal creatinine [100/creatinine level], expressed as a percentage of the initial value) was 26% for normotensive patients, 43% for normotensive patients with nephropathy, 39% for hypertensive patients, and 52% for hypertensive patients with nephropathy. The degree of metabolic control was not associated with the presence of proteinuria or with the severity of renal impairment. There was a significant association between the mean blood pressure over the whole observation period and the degree of impairment in renal function. This association was significant also in the patients who remained normotensive with and without proteinuria.

Conclusion.—  Minor elevation of blood pressure as well as values in the upper normal range may be associated with acceleration of renal damage in type II diabetes.(Arch Intern Med. 1992;152:1225-1229)

Add or change institution