IDENTIFYING factors predictive of postoperative kidney graft function is difficult owing to the many biologic variables contributing to transplantation outcome, among which drug nephrotoxicity is not negligible. The determination of urinary enzymes is a well-documented noninvasive test for the detection of renal diseases, valuable in the monitoring of kidney transplant and recognition of side effects of drugs. Although cyclosporine (CsA) is currently one of the cornerstones of posttransplant antirejection prophylaxis, acute and chronic nephrotoxicity reactions that may induce a decrease in renal flow secondary to vasoconstriction; direct tubular cell damage has been extensively documented. Diuretics increase cyclosporine toxicity. Antibiotics usually administered on the first 3 postoperative days may have additive side effects. Cilastatin, an inhibitor of the enzyme dehydropeptidase I, inhibits the tubular cells’ uptake of several organic substances, such as CsA, thereby preventing its intracellular accumulation and reducing the risk of direct parenchymal nephrotoxicity. Previous studies reported that the administration of Imipenem/Cilastatin reduces the the entity of acute CsA-induced nephrotoxicity in patients receiving a kidney, heart, or heart–lung transplant; but they did not clearly show a significant reduction of N-acetil-beta-d-glucosaminidase (Nag) urinary excretion, a parameter that correlates directly with tubular damage. The objective of this prospective randomized study was to evaluate whether Cilastatin reduces CsA-induced acute tubular damage and the contribution of the antibiotic treatment to kidney graft damage and outcome.
|Autori:||Carmellini M; Matteucci E; Boggi U; Cecconi S; Giampietro O; Mosca F|
|Titolo:||Imipenem/cilastatin reduces cyclosporin-induced tubular damage in kidney transplant recipients|
|Anno del prodotto:||1998|
|Appare nelle tipologie:||1.1 Articolo in rivista|