Comparative effects of losartan versus enalapril in renal transplant recipients treated for hypertension

Angiotension II inhibition decreases proteinuria, reduces histologic evidence of renal injury and slows progression to end stage renal failure. After renal transplantation, intraglomerular hypertension can occur and contribute to the progression towards renal failure. Although angiotensin II type 7 receptor antagonists have similar systemic antihypertensive effect to ACE-inhibitors they do not raise serum kinin levels and there is conflicting information on whether they have the same favourable effects on glomerular hemodynamics. In this study we compared the effects on blood pessure, graft function, proteinuria and hemoglobin concentration in renal transplant recipients, with hypertension and stable serum creatinine of < 2.5 mg/dl, of Losartan 50 mg/day in 12 patients and Enalapril 70 mg/day in 11 patients. Over 6 months there was a significant reduction in blood pressure with both therapies. The average fall;all (mmHg) in systolic blood pressue was 14 +/- 16.2 with Losartan and 11 +/- 10,4 with Enalapril, in mean blood pressure 8 +/- 9.7 vs 9 +/- 6.8 and in diastolic 4 +/- 11,1 VS 9 +/- 6.8; none of the differences between the groups was significant. Overal graft function remained stable and the slight rise inserum potassium in both groups (from 4.5 +/- 0.5 to 4.7 +/- 0.6 mmol/L with Losartan vs 4.6 +/- 0.4 to 4.8 +/- 0.4 mmol/L for Enalapril) was not significant. Proteinuria fell significantly after Losartan (0.5 +/- 0.4 to 0.1 +/- 0.1 g/L; p < 0.05) and Enalapril (0.9 +/- 0.9 to 0.3 +/- 0.3 g/L; p < 0.05); the difference between groups was not significant. Both therapies caused a significant fall in hemoglobin concentration (Losartan -0.6 +/- 0.9 vs Enalapril -1.2 +/- 1.8 g/dl; difference between groups not significant). In summary, in a preliminary retrospective analysis, antihypertensive therapy with either Losartan or Enalapril significant lowered blood pressure, proteinuria and hemoglobin. There were no significant differences between the two therapies. These results suggest that the clinical effects of angiotensin II inhibition by both drugs are mainly due to type I receptor blockage.