Klotho deficiency is an early biomarker of renal ischemia–reperfusion injury and its replacement is protective

• Published in: Kidney international Vol. 78; no. 12; pp. 1240 - 1251
• Main Authors: Hu, Ming-Chang, Shi, Mingjun, Zhang, Jianning, Quiñones, Henry, Kuro-o, Makoto, Moe, Orson W.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2010; Elsevier Limited
• Subjects: 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

Klotho is an antiaging substance with pleiotropic actions including regulation of mineral metabolism. It is highly expressed in the kidney and is present in the circulation and urine but its role in acute kidney injury (AKI) is unknown. We found that ischemia–reperfusion injury (IRI) in rodents redu...