ABSTRACT
The effects of the angiotensin converting enzyme inhibitor captopril on blood pressure, proteinuria, creatinine clearance and metabolic control in diabetic nephropathy have been evaluated. Captopril 144 mg per day was given to 8 longstanding, insulin-dependent, diabetic females with nephropathy. The blood pressure was significantly reduced (systolic 45.4, diastolic pressure 30.6 and mean arterial pressure 33.8 mm Hg after 24 weeks of treatment). Plasma renin activity rose significantly from a basal value of 1.60 to 6.71 ng.ml-1.h-1, and so did serum potassium (from 4.57 to 4.83 mEq.1-1). Serum aldosterone fell from 161 to 70.9 pgm.ml-1 and from 27.3 to 15.3 micrograms.24 h-1 in plasma and urine, respectively, after 6 months on captopril therapy. Urinary protein excretion was decreased by about 48% and creatinine clearance remained unchanged throughout the study. Plasma triglycerides and cholesterol also remained unchanged, and glycosylated haemoglobin was significantly reduced from 13.8 to 10.2% after captopril. The results suggest that captopril is a useful drug to treat hypertension in patients suffering from diabetic nephropathy, as the decline in kidney function can be reduced without impairing glucose tolerance or the lipid profile.
Subject(s)
Captopril/therapeutic use , Diabetic Nephropathies/physiopathology , Hypertension/drug therapy , Adult , Blood Pressure/drug effects , Captopril/pharmacology , Diabetic Nephropathies/drug therapy , Female , Humans , Hypertension/physiopathology , Middle Aged , Renin/bloodABSTRACT
Renal uric acid handling in 62 insulin dependent diabetic (IDD) patients of both sexes, without clinical or biochemical signs of nephropathy or hypertension was studied and compared to healthy age matched control groups. IDD adults (n = 38, age 45-64) presented uremia similar to controls (n = 9 age 45-64). Neither, the tubular charge or filtration charge (CFU) or the uric acid excretion fraction showed statistically significant differences. Young IDD (n = 24, age 13-37) presented levels uric acid than significantly (p less than 0.001) lowers to young controls (n = 10, age 13-38) and adults IDD (p less than 0.001). The CFU is lower in both, young and adult IDD when compared to young controls (p less than 0.02). Nevertheless, the CFU is higher in young IDD than in controls of the same age (p less than 0.001) or in adult IDD (p less than 0.001). In summary, we conclude the existence of an abnormal (uric acid) renal management caused by a tubular defect probably lying on the proximal tubular segment where the uric acid secretion is carried out.
