Fibroblast Growth Factor 23 and Pro-B-Type Natriuretic Peptide as a Risk factor of Cardiac Hypertrophy in Chronic Kidney Disease

Abstract

Cardiac hypertrophy is a life-threatening disorder and is frequently observed in patients with chronic kidney disease (CKD). Much attention has been focused on the derangement in hormonal factors, including FGF23, as a novel cause of cardiac hypertrophy in CKD. Recently, FGF23 is shown to be elevated as CKD progresses and may be responsible for the development of cardiac hypertrophy and heart failure. Furthermore, FGF23 not only inhibits the renal expression of angiotensin converting enzyme 2 but also enhances renin gene transcription, both of which could accelerate renin-angiotensin-aldosterone system. Although the increase in serum phosphate concentrations is a pivotal stimulus for FGF23 production, recent studies suggest that reduced iron status and elevated aldosterone levels, frequently seen in patients with CKD or on dialysis, might also contribute to the elevation in serum FGF23 levels. Conversely, phosphate binders and appropriate iron status could reduce serum FGF23, potentially leading to the alleviation of cardiac hypertrophy and heart failure. Also, it was hypothesized that N-terminal pro–B-type natriuretic peptide (NT–pro-BNP) and B-type natriuretic peptide (BNP) levels could identify CAD and LVH in asymptomatic patients with CKD. In conclusion, novel therapeutic strategies associated with FGF23 may confer a benefit in the management of cardiac disorders in CKD.