title: Antihypertensive treatment of patients with proteinuric renal diseases: risks or benefits of calcium channel blockers?
abstract: In patients with proteinuric renal diseases the rate of progression of renal insufficiency is determined by the level of blood pressure and proteinuria. It has been demonstrated that strict blood pressure control with angiotensin converting enzyme (ACE)-inhibitors or beta-blockers, aimed at reaching values below 130/80 mm Hg, attenuates the deterioration of renal function. In general, the beneficial effects of these drugs are reflected in a parallel lowering of proteinuria. Calcium channel blockers are effective antihypertensive drugs, however, their safety in patients with proteinuric renal diseases and renal insufficiency may be questioned because of reported untoward effects on urinary protein excretion. The present review discusses the potential benefits and risks of calcium channel blockers (CCBs) in the treatment of patients with renal diseases. To this end we have evaluated the effects of these drugs in animal models of progressive renal injury. In these animal models adverse effects of CCBs have been reported which are attributed to an impairment of autoregulation. In patients with proteinuria, the dihydropyridine CCBs do not lower proteinuria despite a reduction of blood pressure. Studies on the effects on the course of renal function are limited, however, the available data do suggest that this class of CCBs may be less advantageous than other antihypertensive drugs, thus arguing against the use of these agents as first-line drugs in patients with proteinuric renal diseases. Information on the effects of the non-dihydropyridine CCBs is limited to a small number of studies in patients with diabetic renal disease. Although the data suggest that these classes of CCBs might be more beneficial, more studies are needed, particularly in patients with non-diabetic renal diseases, before founded conclusions can be reached.
authors.affiliation: Department of Medicine, University Hospital Nijmegen, The Netherlands.
authors.forename: H J
authors.initials: HJ
authors.lastname: Kloke
authors.forename: A J
authors.initials: AJ
authors.lastname: Branten
authors.forename: F T
authors.initials: FT
authors.lastname: Huysmans
authors.forename: J F
authors.initials: JF
authors.lastname: Wetzels
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000502:physiology; D002121:Calcium Channel Blockers / Q000009:adverse effects / Q000627:therapeutic use*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D007674:Kidney Diseases / Q000188:drug therapy* / Q000503:physiopathology; D011507:Proteinuria / Q000188:drug therapy*; D012307:Risk Factors
chemical_list: D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers