Urinary ATP synthase subunit β is a novel biomarker of renal mitochondrial dysfunction in acute kidney injury

摘要: Although the importance of mitochondrial dysfunction in acute kidney injury (AKI) has been documented, noninvasive early biomarkers damage are needed. We examined urinary ATP synthase subunit β (ATPSβ) as a biomarker renal during AKI. Mice underwent sham surgery or varying degrees (5, 10, 15 min ischemia) ischemia/reperfusion (I/R)-induced Serum creatinine, BUN, and neutrophil gelatinase-associated lipocalin were elevated only I/R group at 24 h. Immunoblot analysis ATPSβ revealed two bands (full length ∼52 kDa cleaved ∼25 kDa), both confirmed by LC-MS/MS, that increased 24 h 10- 15-min groups. These changes associated with evidenced reduced cortical expression proteins, COX1, proximal tubular oxygen consumption, ATP. Furthermore, group, was until 72 h before returning to baseline 144 h after reperfusion recovery function. Evaluation nonalcoholic steatohepatitis model liver ATPSβ, suggesting specificity full-length for injury. analyses patient urine samples collected 36 h cardiac levels patients postcardiac surgery-induced LC-MS/MS urinalysis human subjects AKI ATPSβ. translational studies provide evidence may be novel sensitive could serve valuable tool testing potential therapies chemical-induced nephrotoxicity.