Abstract
Chronic kidney disease (CKD), common after liver transplantation (LT), is associated with significant morbidity and mortality (1). Although multiple factors are implicated in the development of post-LT CKD, calcineurin inhibitor (CNI) induced nephrotoxicity has been considered to be the major culprit (1). CNI enhances TGF-β expression in tubular epithelial cells, which increases production of the extracellular matrix proteins and induces epithelial mesenchymal transformation with subsequent development of tubulointerstial fibrosis (2).
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