Given the same level of arterial pressure control, studies in diabetic animal models have demonstrated certain classes of antihypertensive medication to confer better overall preservation of renal histologic features and function as well as reduced albuminuria when compared with other agents. The present study was designed to assess whether any differences exist among antihypertensive agents with regard to progression of diabetic renal disease and albuminuria in human subjects.
The study was a randomized, prospective, parallel group design that evaluated the effects of a converting enzyme inhibitor (lisinopril; group 1), a calcium antagonist (diltiazem hydrochloride; group 2), and a combination of a loop diuretic and a β-blocker (furosemide and atenolol; group 3) in 30 subjects. All subjects received a low-salt, low-protein diet. Metabolic (blood glucose, cholesterol profiles, and urine urea nitrogen and sodium levels) as well as renal hemodynamic (renal blood flow and glomerular filtration rate) profiles and arterial pressure measurements were performed at various intervals during an 18-month period.
Both groups 1 and 2 had significantly slower rates of decline in glomerular filtration rate compared with group 3. No significant differences were observed in renal hemodynamics between groups 1 and 2 at 18 months. Group 3 had the worst metabolic, lipid, and side-effect profile of any group. Reductions in albuminuria were not different between groups 1 and 2, but both were significantly reduced compared with group 3.
Given a similar level of arterial pressure control, both lisinopril and diltiazem slow progression of diabetic renal disease and reduce albuminuria to a greater extent than does the combination of a loop diuretic and β-adrenoreceptor antagonist. These drugs were also better tolerated and produced no adverse metabolic effects.(Arch Intern Med. 1993;153:973-980)
Slataper R, Vicknair N, Sadler R, Bakris GL. Comparative Effects of Different Antihypertensive Treatments on Progression of Diabetic Renal Disease. Arch Intern Med. 1993;153(8):973-980. doi:10.1001/archinte.1993.00410080037006