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FGF23 and Klotho Handling by Kidneys

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Dr Ashish Nandwani, New Delhi    09 January 2018

Also, impaired bone remodeling is associated with occurrence of fractures, and extraskeletal calcification in soft tissues and arteries. FGF23 is a recently identified hormone involved in the regulation of mineral homeostasis. It is a 251-amino-acid protein that is synthesized and secreted by bone cells mainly osteoblasts and osteocytes. Klotho is a 130-kDa transmembrane β-glucuronidase that catalyzes the hydrolysis of steroid β-glucuronides. The Klotho gene is expressed mainly in the kidney and mutations have been associated with abnormal mineral metabolism, characterized by increased blood calcium, phosphorous and vitamin D levels. FGF23 and Klotho are, mutually and independently, important regulators of mineral metabolism in health and disease. With deteriorating renal function, CKD becomes a state of excess FGF23 and Klotho deficiency. FGF23 has become an important prognostic marker for CKD-related complications and CV mortality. Increased FGF23 levels are associated with increased CV mortality in CKD patients. FGF23 has direct pathogenic effect in causing left ventricular hypertrophy and sodium and calcium reabsorption in the distal tubules, causing renal sodium retention, volume overload, hypertension and cardiac hypertrophy. FGF23 and Klotho are recently recognized contributors to ectopic calcification in soft tissues, including cardiac valves and the aorta. Increased FGF23 levels have been shown to increase CV mortality, progression of renal disease and resistance to vitamin D analogs.

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