Author/Authors :
Briguori, Carlo Department of Cardiology - Clinica Mediterranea - Naples, Italy , Condorelli, Gerolama Department of Cellular and Molecular Biology and Pathology - Federico II University of Naples - Naples, Italy
Abstract :
Drugs and exogenous toxins, including aminoglycosides,
amphotericin B, cisplatin, and radiocontrast media,
may cause acute kidney injury (1). The manifestations
which indicate that damage is occurring are a sudden
increase in kidney injury biomarkers (NGAl [neutrophil
gelatinase-associated lipocalin], KIM-1 [kidney injury
molecule-1], etc.) and kidney failure (creatinine, cystatin
C). This implies a requirement for close monitoring of
kidney function with eventual dose reduction or even
the interruption of drug administration. however, it
may eventuate that, even if the source of the damage is
stopped, it could still result in permanent kidney failure.
one of the major causes of kidney injury driven by different
compounds is an increase in the production of reactive
oxygen species (RoS), activation of stress kinases and
thus apoptosis (2, 3).