Impact of cardiac transplantation on kidney function: A single-center experience

Long-term follow-up of cardiac transplant recipients reveals a progressive decline in kidney function in a significant number of patients. This complication is one of the most important prognostic parameters for the outcome of cardiac transplantation. The risk factors implicated in the pathogenesis of renal dysfunction following cardiac transplantation are numerous, with the immunosuppressive drug cyclosporine (CsA) playing a major role. This case-control study was designed to evaluate the role of different risk factors among patients who had been transplanted at the Northern General Hospital Cardiothoracic Centre (CTC) with the possibility of identifying modifiable risk factors that mitigate the nephrotoxicity of CsA. Over a 10-year period, heart transplantation was performed in 205 patients at the CTC. Seventeen patients who experienced chronic renal failure (CRF) and were treated at the outpatient clinic of the Sheffield Kidney Institute were randomly selected from those who had >2-year graft survival and follow-up after cardiac transplantation. As controls, 15 cardiac transplant patients were randomly selected from 32 with comparable survival and follow-up after transplantation and without evidence of significant renal dysfunction (serum creatinine less than or equal to150 mumol/L). The putative risk factors for development of renal insufficiency were retrospectively studied as well as those affecting the rate of progression of CRF. Seventy-five percent of the progressors (cases) had ischemic cardiomyopathy compared with 10% of nonprogressors (controls) (P < .05). CsA trough levels during the follow-up period were higher among the nonprogressors compared with the progressors (P = .03). Follow-up systolic blood pressure revealed a statistically significant correlation with the slope of serum creatinine in the progressor group (r = -.515 and P < .05). At the time of transplantation, ischemic cardiomyopathy as an underlying diagnosis seems to be a detrimental factor, contributing to the pathogenesis of renal dysfunction after heart transplantation. CsA trough levels alone do not seem to discriminate between progressors and nonprogressors. A randomized controlled study may be required to evaluate the possibility of replacing or reducing CsA to the lowest possible dose in the early posttransplant period for the subset of patients with ischemic cardiornyopathy.