Abstract
Kidney is an excretion organ with influx transporters on the basolateral membrane of proximal tubular cells and efflux transporters on the apical membrane of proximal tubular cells. Cross-species differences in the expression, function, localization, and homology of kidney transporters are important considerations. Drug-indued kidney injury (DIKI) is mainly due to the intracellular drug accumulation or their metabolites and is associated with kidney histopathological changes and increase in serum creatinine (Scr). It is important to distinguish if an increase in Scr is related to DIKI or indirect inhibition of transporters leading to reversible and transient drug-induced Scr increase [DICI] without histopathological lesions. Finally, in vitro and in vivo animal models can predict unexpected changes in systemic exposure and kidney transporter-mediated effect.
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