FGF23 from Bench to Bedside.

FGF23 from Bench to Bedside.
Am J Physiol Renal Physiol. 2016 Feb 10;:ajprenal.00606.2015
Authors: Kovesdy CP, Quarles LD
Abstract
There is a strong association between elevated circulating Fibroblast Growth Factor-23 (FGF23) levels and adverse outcomes in patients with chronic kidney disease (CKD) of all stages. Initially discovered as a regulator of phosphate and vitamin D homeostasis, FGF23 has now been implicated in several pathophysiological mechanisms that may negatively impact the cardiovascular and renal systems. FGF23 is purported to have direct (off-target) effects in the myocardium, as well as canonical effects on FGF receptor/ -klotho receptor complexes in the kidney to activate the renin-angiotensin-aldosterone system, modulate soluble α-klotho levels, and increase sodium retention, to cause left ventricular hypertrophy (LVH). Conversely, FGF23 could be an innocent bystander produced in response to chronic inflammation or other processes associated with CKD that cause LVH and adverse cardiovascular outcomes. Further exploration of these complex mechanisms is needed before modulation of FGF23 can become a legitimate clinical target in CKD.
PMID: 26864938 [PubMed - as supplied by publisher]

Source: Am J Physiol Renal P... - February 10, 2016 Category: Urology & Nephrology Authors: Kovesdy CP, Quarles LD Tags: Am J Physiol Renal Physiol Source Type: research