BRIEF OVERVIEW OF RENAL SPARING IMMUNOSUPPRESSIVE REGIMENS POST-HEART TRANSPLANTATION

Chronic kidney disease (CKD) is a common complication after heart transplantation1-4 increasing in incidence with time after transplant to 10.9 % at 5 years5. A number of risk factors have been identified, these include use of calcineurin inhibitors, increasing recipient age, female gender, diabetes mellitus, hypertension, positive hepatitis C virus, need for renal replacement therapy post-operatively, renal function pre-transplant and deteriorating renal function within the first 3 months post-transplantation2, 4, 6, 7. CKD is associated with increased mortality and morbidity with a relative risk for death with CKD of 4.555. A recent UK survey reported the highest mortality risk was associated with a CKD stage 5 without dialysis compared to patients receiving dialysis (RR 8.54 vs 4.07)7. Calcineurin inhibitors (CNIs) form the cornerstone of immunosuppressant regimens after heart transplantation8; however, they are associated with nephrotoxicity. The use of the newer ‘non-nephrotoxic ’ immunosuppressants such as the proliferation signal inhibitors (sirolimus and everolimus), mycophenolate mofetil and the anti-CD25 (interleukin-2 receptor) monoclonal antibodies (basiliximab and dacluzimab) have allowed for a number of strategies which have shown potential to improve renal function in heart transplant recipients by allowing for CNI minimisation and even elimination9, 10- not all of which will be discussed here. The ultimate goal for suc