Renal failure following cardiac transplantation

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Abstract
The clinical outcome of cardiac transplantation has markedly improved over the last two decades due to the introduction of cyclosporin therapy. However, the renal side-effects of cyclosporin appear to be a major drawback to its use. The early studies by Myers et al. [1] described the renal structural and functional changes in the native kidneys of heart transplant recipients. Repeated haemodynamic investigations revealed a progressive decrease in glomerular filtration rate (GFR), a concomitant drop in renal plasma flow, and an increase in renal vascular resistance associated with systemic hypertension. Renal biopsies in a subset of patients disclosed glomerulosclerosis, striped interstitial fibrosis, and afferent arteriolopathy. In the original study a high starting dose of cyclosporin was used (17 mg/kg), which was later decreased to 10 mg/kg. However, when these two groups were compared, both of them had developed hypertension and a decreased GFR. Even with a low dose of cyclosporin the decline in GFR was approximately 45% from baseline, as compared with historical controls treated with azathioprine and prednisone without cyclosporin. Patients treated with low doses of cyclosporin had slightly lower mean serum (s-) creatinine concentrations, but similar pathological changes according to renal biopsies, than those treated with higher doses [2,3]. In addition, it was demonstrated that sequential biopsies of the native kidney in the two cyclosporin groups revealed progressive histopathological changes. Furthermore there was an approximately 10% cumulative incidence of end-stage renal disease during 10 years. The renal dysfunction could not be explained by the differences in cardiac function among the groups.