Renal effects of amlodipine in normotensive renal transplant recipients

Abstract

Renal effects of amlodipine in normotensive renal transplant recipients. The use of cyclosporin A (CsA) has improved the success of renal transplantation, but is associated with hypertension and significant renal toxicity. Previous reports suggest that calcium channel blockers may be useful in opposing the adverse effects of CsA. We have evaluated the effects of amlodipine (5 mg, once daily for 8 weeks) on renal function in 27 normotensive renal transplant recipients with stable renal function, in a double-blind, placebo-controlled, multicentre, cross over study. Amlodipine significantly reduced serum creatinine concentration relative to placebo (mean+/-SD: 168+/-65 vs 177+/-66 micromol/l; P=0.002) and there was a strong trend towards an increase in effective renal plasma flow on amlodipine relative to placebo (238+/-92 vs 217+/-87 ml/min; P=0.055). Glomerular filtration rate and lithium clearance were unaffected. Trough CsA blood concentration was unaffected. Amlodipine was well tolerated, with a low incidence of adverse events, and did not affect blood pressure or heart rate. In conclusion, amlodipine reduced serum creatinine in normotensive renal transplant recipients after only 8 weeks treatment, and was well tolerated in concomitant administration with CsA.

Amlodipine‐induced photodistributed telangiectasia and acquired dermal melanocytosis: A pediatric case report

“…Concomitant treatment with amlodipine has been suggested to ameliorate these adverse effects due to the vasodilating action. 2 CCBs are divided into two major categories based on their physiological effects: dihydropyridines and nondihydropyridines. Currently, there are only a few adult reports of photodistributed telangiectasia after CCB treatment, including amlodipine, nifedipine, and felodipine, 1,[3][4][5][6] and they all belong to the dihydropyridine group.…”

“…The second hypothesis is the generation of reactive oxygen species, including pyridine, nitrosopyridine, and nitropyridine, which can be induced by dihydropyridines on ultraviolet exposure, as shown in an in vitro experiment. 2 This generation activates the mitogenactivated protein kinases pathway, resulting in the expression of matrix metalloproteinases in the skin, which are responsible for extracellular matrix degradation and render the vasodilation. 7 The process is reversible under normal skin condition after discontinuing CCBs.…”

“…Jeng-Daw Tsai 2,3 Yu-Hung Wu 1,3 1 Department of Dermatology, MacKay Memorial Hospital, Taipei, Taiwan…”

Use of calcium antagonists in renal patients: Therapeutic benefit or medical malpractice?

“…CCBs, particularly the dihydropyridines, cause afferent arteriolar dilatation and thus may counteract these deleterious effects. Several studies have shown that, compared with placebo, renal transplant patients have lower serum creatinine concentrations if they are treated with dihydropyridine CCBs [48][49][50]. A separate study found that nifedipine-treated subjects had significantly higher GFRs and lower serum creatinine concentrations 2 years post-transplantation than subjects treated with lisinopril.…”

Importance of Proximal Tubular Fluid Output in Regulating Long-Term Urinary Sodium Excretion in Health and Disease

“…V prox has been reported to be unaltered during administration of Ca 2+ entry blockers in about half of the chronic clinical studies; in the remaining studies, it was elevated [47, 48, 49]. However, in the latter cases, the drug was given in the morning immediately before the clearance measurements, which makes it uncertain whether the Ca 2+ entry blocker did in fact increase V prox chronically or whether the observed increase merely reflected the well-known acute effect of the drug [50].…”