Effects of the angiotensin-1 receptor blocker valsartan compared with amlodipine on renal hemodynamics

Delles et al1 investigated the effects of the angiotensin-1 (AT1) receptor blocker valsartan compared with those of the calcium antagonist amlodipine on renal hemodynamics and the renal microcirculation using inferences derived from Gomez’ formulas2 assessing renal hemodynamics. They concluded that at similar blood pressure (BP) control, valsartan maintained glomerular filtration rate and glomerular pressure, whereas amlodipine led to glomerular hyperfiltration and an increase in PGlo. They proposed that these results might explain the favorable renal outcome with AT1 receptor blocker therapy. They then imply that the observed hemodynamic profiles may support the adverse effect of amlodipine on albuminuria in patients with type 2 diabetes mellitus. Regretfully, their report is confounded by both the lack of rigor of inferences of Gomez’ formulas and the discrepancies between the current isolated renal hemodynamic findings and clinical outcomes. “Therapeutic decisions” are based on a number of considerations. Early in the course of the development of a therapeutic pathway, decisions are often made on the basis of pathophysiologic considerations. Most physicians prefer a later stage, in which therapeutic decisions can be made on the basis of the outcome of well-designed, randomized controlled clinical trials. In the arena of renal injury and progressive renal disease, surely we have reached this advanced stage.