Successful kidney transplantation for a dialysis patient with anthracycline-induced cardiomyopathy: a case report

Keywords Anthracycline-induced cardiomyopathy Hemodialysis Kidney transplantation UremiccardiomyopathyProgress in the field of anticancer agent development hasfacilitated the long-term survival of children with malig-nancies. Anthracycline is a widely used anticancer agentthat is well known to cause fatal cardiotoxicity, a conditiontermed anthracycline-induced cardiomyopathy (AIC).Routine use of angiotensin converting enzyme inhibitor(ACEi) is recommended as the first-line treatment for AIC.Although ACEi has a short-term beneficial effect on car-diac function [1], it cannot prevent the progression ofcardiac dysfunction associated with AIC, and its long-termeffectiveness is unclear [2]. Here we present a case ofsuccessful kidney transplantation that helped to preventaggravation of left ventricular (LV) function in AIC.A 22-year-old man was admitted because he complainedof cardiac symptoms equivalent to NYHA III. He under-went systemic anticancer chemotherapies, includinganthracycline, to treat Burkitt’s lymphoma 17 years ago.Although the Burkitt’s lymphoma was cured completely,he suffered from AIC and end-stage renal failure due to theadverse effects of the anticancer agents. He had startedperitoneal dialysis and was treated with b-blocker andACEi 12 years before. At the time of admission, anechocardiogram revealed a LV ejection fraction (LVEF) of0.23, severe diffuse LV hypokinesis, and an enlargedbilateral chamber. A coronary angiogram demonstratednormal coronary arteries and a heart biopsy revealedmyocardial interstitial fibrosis compatible with drug-induced cardiomyopathy (Fig. 1a). Appropriate hemodial-ysis management improved his cardiac symptoms andincreased his LVEF to 0.48. Because his cardiac functionafter hemodialysis was the same as that observed five yearsbefore, we believed that he would tolerate kidney trans-plantation surgery. Six months after admission, he under-went a living-related renal transplantation and producedurine soon after the transplantation. His LV functionimproved as his LVEF increased to 0.6, which has beenmaintained along with a favorable renal allograft functionfor four years (Fig. 1b).Early-onset AIC, which occurs during the year after thecompletion of chemotherapy, is largely irreversible [3].However, it has been reported that late-onset AIC can bereversed in almost two-thirds of cases [4]. The exact factorsresponsible for AIC irreversibility are unknown.It is widely accepted that the heart and kidney areaffected by each other, and chronic kidney disease mayalso cause heart failure in the absence of coronary arterydisease. Uremic cardiomyopathy is expressed as LV dila-tation and systolic dysfunction. Although the uremic toxinsare not yet to be clearly determined, the uremic milieu canaffect myocardial contractility and function. It has beenshown that LV function improves after successful kidneytransplantations [5]. We presume that the main reason forthe improvement in LV function in our patient wasrecovery from the uremic milieu associated with AIC, andthis recovery from the uremic state helped to stop theprogression of AIC itself.The present case indicates that kidney transplantationcan be safely performed in a dialysis patient with AIC, andthat successful kidney transplantation may even help toprevent aggravation of LV function.