An integrated transcriptomic approach to identify molecular markers of calcineurin inhibitor nephrotoxicity in pediatric kidney transplant recipients

Calcineurin inhibitor nephrotoxicity (CNIT) has been associated with the development of chronic renal allograft dysfunction and decreased graft survival. This study evaluated 37 formalin-fixed paraffin-embedded biopsies from pediatric kidney transplant recipients using gene expression profiling. Oxidative phosphorylation and mitochondrial dysfunction were the top molecular pathways as-sociated with overexpressed genes in CNIT samples. Decreased ATP synthesis was identified as a significant biological function in CNIT, while key toxicology pathways included NRF2-mediated oxidative stress response and increased permeability transition of mitochondria. To identify a unique molecular signature for accurate pediatric CNIT diagnosis.