Renal Effects of Antihypertensive Medications: An Overview

Abstract

A variety of antihypertensive agents are available for management of elevated arterial pressure. Although these agents all effectively lower arterial pressure, they have somewhat diverse renal hemodynamic profiles. This report reviews the various similarities and differences in renal hemodynamic profiles among the different antihypertensive agents.

Evaluation of the incidence and risk factors for development of fenofibrate-associated nephrotoxicity

“…18,22,29 Diabetic patients treated with dihydropyridine calcium channel blockers still have histologic progression of renal disease despite adequate blood pressure control. 21,27 The clinical relevance of significantly greater use in the group with nephrotoxicity is unknown. The use of high-dose fenofibrate also seems to predispose the patient to risk of nephrotoxicity.…”

“…Review of animal and human data show conflicting results as to the effects of dihydropyridine calcium channel blockers on renal hemodynamics. [21][22][23][24][25] In general, although dihydropyridine calcium channel blockers decrease afferent arteriole resistance, they also fully impair renal autoregulation, resulting in glomerular hypertension. 22,23,[26][27][28] The class has variable effects on progression of proteinuria or renal disease, with no clear benefit.…”

Beneficial Effect of the Long-Term Treatment with the Combination of an ACE Inhibitor and a Calcium Channel Blocker on Renal Injury in Rats with 5/6 Nephrectomy

“…These growth factors play a major role in the development of glomerular sclerosis [36, 37, 38]. In addition, these peptides stimulate proliferation of mesangial cells in culture [19, 39]. Thus, it is possible that mesangial cell proliferation and matrix accumulation which culminates in glomerular sclerosis may result from permanent stimulation of mesangial cell proliferation and secretion of ECM by these and other growth factors.…”

“…Some of these differences relate to their effects on renal microcirculation. Dihydropyridine agents appear to act only on the afferent arteriole, increasing intraglomerular pressure and albumin excretion rate [19]. In contrast, nondihydropyridine agents like verapamil, may dilate efferent arterioles in addition to afferent arterioles [19] and with normalization of the systemic blood pressure, verapamil may reduce intraglomerular pressure and proteinuria.…”

“…Dihydropyridine agents appear to act only on the afferent arteriole, increasing intraglomerular pressure and albumin excretion rate [19]. In contrast, nondihydropyridine agents like verapamil, may dilate efferent arterioles in addition to afferent arterioles [19] and with normalization of the systemic blood pressure, verapamil may reduce intraglomerular pressure and proteinuria. However, some other nonhaemodynamic protective effects of CCB could be explained by their capacity to inhibit the influx of extracellular calcium, an important signal for the proliferative effect of mesangial cells’ mitogens [20], decrease the mesangial entrapment of macromolecules and, possibly, its effect as free radical scavenger [21, 22].…”