4.6 Article

Switch from calcineurin inhibitors to sirolimus-induced renal recovery in heart transplant recipients in the midterm follow-up

Journal

TRANSPLANTATION
Volume 81, Issue 5, Pages 692-696

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.tp.0000177644.45192.a3

Keywords

heart transplantation; cyclosporine; nephrotoxicity; sirolimus; mycophenolate mofetil

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Background. Calcineurin inhibitor (CI)-based immunosuppression has prolonged the survival of heart transplant recipients. However, Cl-induced renal injury remains as a major problem in these patients. Sirolimus is an immunosuppressant with no significant impact on renal function. A limited number of recent papers have showed that the switch from CI to sirolimus improved renal function in late follow-up of heart transplant patients with CI-related nephrotoxicity. Methods. Ten heart transplant recipients with CI-induced nephrotoxicity (creatinine 3.9 +/- 1.8 mg/dl) at a median of 701 (465 to 1325) days posttransplant had CI switched to sirolimus (target though levels 10 to 14 ng/ml) while mycophenolate mofetil (MMF, 3g/day) was maintained and adjusted according to white blood cell count. Results. This maneuver caused a marked decrease in serum creatinine (P < 0.00001) at 30 (1.2 +/- 0.4 mg/dl), 90 (1.3 +/- 0.4 mg/dl) and 180 (1.3 0.4 mg/dl) days postconversion and a significant decrease in serum potassium levels (5.1 +/- 0.5 at baseline vs. 3.9 +/- 0.3 at 180 days, P < 0.00005). After the drugs switch no changes in hemoglobin levels, white blood cell count, platelets count, blood glucose and glutamic oxaloacetic transaminase plasma levels were observed. Total cholesterol increased from 242 28 to 290 117 mg/dl (P > 0.05) after 90 days and decreased to 216 58 mg/dl at day 180 (P > 0.05) after statins dose adjustment. Rejection and infection rates were not modified by sirolimus. Conclusions. Conversion to a sirolimus-based immunosuppression regimen associated with MMF allowed striking renal function recovery in heart transplant recipients with calcineurin inhibitor-induced renal impairment at midterm follow-up.

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