| dc.description.abstract | Captopril's short-term effects on clinical and biochemical parameters were studied in 21 diabetic nephropathic patients. Their mean age was 57.50 +/- 2.28 years; 16 of them were women and 5 were men. Eleven patients had been regulated with insulin and 10 of them had been regulated with oral antidiabetics. Fifteen patients were microalbuminuric (200 mg/daily and below albuminuria) and their mean diabetes mellitus history was 14.86 +/- 1.44 years. Six patients had advanced diabetic nephropathy (400 mg/daily and above albuminuria). Their mean diabetes mellitus history was 4.50 /- 2.87 years. Captopril in a low dose (37.5 mg/daily p.o., three separated doses) was given during 20 days. In the microalbuminuria group there were insignificant alterations in renal function, blood glucose levels, and systolic blood pressure. Diastolic blood pressure decreased significantly in this group (p < .05). Microalbuminuria increased significantly after the therapy in this group (p < .05). In the advanced diabetic nephropathy group, blood glucose and systemic blood pressure levels did not change significantly (p > .05), while serum BUN and creatinine levels increased significantly (p < .05), and GFR decreased significantly in this group (p < .05). Albuminuria decreased after the therapy in this group (p < .05). In all study groups, serum potassium levels increased significantly while serum total protein and albumin levels did not change significantly. We concluded that in the microalbuminuria group, increasing microalbuminuria may be related to a captopril-induced increase in renal plasma flow rate and single nephron glomerular filtration rate. This increase in microalbuminuria cannot be related with blood glucose levels, renal functions, and systemic blood pressure alterations. The decrease in albuminuria in the advanced diabetic nephropathy group may be related to a captopril-induced decrease in single nephron glomerular filtration rate due to nephrotoxic, or to unknown, effects of captopril, especially in patients with renal dysfunction. This decrease cannot be related with blood glucose levels and systemic blood pressure factors. | en_US |
