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Cytochrome c: potential as a noninvasive biomarker of drug-induced acute kidney injury

Introduction: Acute kidney injury (AKI) in critically ill patients is closely associated with increased morbidity and mortality, yet there remains continued reliance on increased serum creatinine and blood urea nitrogen to diagnose AKI. These biomarkers increase only after significant renal structural damage has occurred. Recent research efforts have focused on discovery and validation of novel serum and urine biomarkers to detect AKI prior to extensive structural damage. Cytochrome c is best known as an indicator of cell death burden in any organ or tissue. It is released during mitochondrial damage that is associated with processing of apoptosis, cell lysis during necrosis and even reversible mitochondrial and cell injury. Areas covered: This article reviews the current literature on the potential for cytochrome c as an early biomarker of AKI. The article is based on PubMed searches, using the terms ‘acute kidney injury,’ ‘renal failure,’ ‘biomarker,’ ‘toxicity’ and ‘cytochrome c’, with a focus on experimental and clinical data. Expert opinion: Cytochrome c, as a biomarker, has the potential to improve outcome for AKI patients. Its release indicates mitochondrial damage, one of the earliest changes in cell injury and death. New mitochondrial-targeted therapeutics may be designed around this molecule. Its disadvantages include only transient increase at expression levels that are easily measurable and nonspecificity for kidney injury. The appropriate and optimal utilization of cytochrome c as a biomarker for AKI will be realized only after its complete characterization in experimental and clinical arenas.