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Response to "Sustained improvement of renal graft function for two years in hypertensive renal transplant recipients treated with nifedipine as compared with lisinopril".

This letter is in response to the article by Midtvedt et al. (1) published in the December 15, 2001 issue of Transplantation. In addition, we are concerned about the broad therapeutic recommendations that were stated in the accompanying editorial based on such incomplete data (2). The primary finding of this study was a superior improvement in glomerular filtration rate (GFR) in the nifedipine arm as compared with the lisinopril arm. Although the study reports 2-year results, these results are uninterpretable because of the large number of unevaluable patients at this endpoint. In addition, because of the imbalance in acute rejection episodes between the two arms of the study, only the subset analysis of patients without rejection truly can reflect the drugs’ impact. Thus, this study is limited to those patients without rejection at an endpoint of 1 year. At this endpoint, the difference between the dihydropyridine and angiotensin-converting enzyme (ACE) inhibitors was a mean change of 5 mL/min of GFR at 1 year (nifedipine group: 48 mL/min to 58 mL/min; lisinopril group: 46 mL/min to 51 mL/min). This is hardly an unexpected difference. In renal transplant recipients, dihydropyridines (and other calcium channel blockers) have long been known to improve cyclosporine-medicated renal vasoconstriction and improve GFR. However, to date, no study has demonstrated an effect of calcium channel blockers on the vascular or fibrogenic effects of cyclosporine, whereas an enormous literature is present on the effect of ACE inhibitors and angiotensin II receptor blockers and the prevention of cyclosporine-mediated fibrosis (3). We feel strongly that any recommendations regarding the choice of an antihypertensive agent in renal transplant patients must consider both preservation of the renal allograft and consideration of the patients’ cardiovascular risk. On both accounts, the literature strongly supports the utilization of agents that interrupt the renin-angiotensin system, with little evidence supporting the use of the dihydropyridine class of antihypertensive agents (3, 4). Dihydropyridines have been associated with higher cardiovascular death and cardiovascular risk in both hypertensive patients and in renal transplant recipients when compared with blockers or ACE inhibitors (4, 5). In terms of progression of renal disease, numerous studies in both animal and clinical models have documented a slowing of progression of renal disease with ACE inhibitors, with far fewer studies documenting the same ameliorative effect of dihydropyridine calcium channel blockers. In summary, we believe that the study of Midtvedt et al. (1) shows a slight advantage of nifedipine versus lisinopril in GFR at 1 year, a finding of doubtful relevance in view of the large literature regarding the use of ACE inhibitors in terms of cardiovascular protection and long-term renal protection. This flawed data certainly should not be used as evidence to support the use of dihydropyridines as the first-line antihypertensive treatment of choice in renal transplant recipients.