Klotho deficiency is an early biomarker of renal ischemia–reperfusion injury and its replacement is protective - Hu, Ming-Chang; Shi, Mingjun; Zhang, Jianning; Quiñones, Henry; Kuro-o, Makoto; Moe, Orson W. (Kidney international, 2010)
Keywords: acute kidney injury; Acute Kidney Injury - etiology; Acute Kidney Injury - metabolism; Acute Kidney Injury - prevention & control; Acute-Phase Proteins - metabolism; Adult; Aged; Animals; biomarker; Biomarkers - metabolism; Case-Control Studies; Creatinine - blood; Glucuronidase - deficiency; Glucuronidase - genetics; Glucuronidase - therapeutic use; Humans; ischemia–reperfusion injury; Kidney Tubules - metabolism; Klotho; Klotho Proteins; Lipocalin-2; Lipocalins - metabolism; Male; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Mice, Transgenic; Middle Aged; Models, Animal; neutrophil gelatinase-associated lipocalin; Oncogene Proteins - metabolism; Oxidative Stress; Proto-Oncogene Proteins - metabolism; Rats; Rats, Sprague-Dawley; Reperfusion Injury - complications; Reperfusion Injury - metabolism; Reperfusion Injury - prevention & control; therapy; acute kidney injury; biomarker; ischemia–reperfusion injury; Klotho; neutrophil gelatinase-associated lipocalin; therapy