Lessons from effect of etelcalcetide on left ventricular hypertrophy in patients with end-stage kidney disease. Issue 4 (10th July 2022)

• Record Type: Journal Article
• Authors: Dörr, Katharina; Kainz, Alexander; Oberbauer, Rainer
• Is Part Of: Current opinion in nephrology and hypertension. Volume 31:Issue 4(2022)
• Page Start: 339
• Page End: 343
• Publication Date: 2022-07-10
• Subjects: etelcalcetide -- fibroblast growth factor 23 -- haemodialysis -- myocardial hypertrophy; Hypertension -- Periodicals; Nephrology -- Periodicals; Hypertension -- Indexes; Hypertension -- Periodicals; Kidney Diseases -- Indexes; Kidney Diseases -- Periodicals; Nephrology -- Periodicals; 616.132
• DOI: 10.1097/MNH.0000000000000799
• Languages: English
• ISSNs: 1062-4821

Abstract

Abstract : Purpose of review: Patients with end-stage kidney disease (ESKD) frequently develop left ventricular hypertrophy (LVH), which is associated with an exceptionally high risk of cardiovascular events and mortality. This review focuses on interventional studies that modify levels of fibroblast growth factor 23 (FGF23) and examine effects on myocardial hypertrophy, cardiovascular events and mortality. Recent findings: Quantitative evaluations of trials of calcimimetics found no effects on cardiovascular events and cardiovascular and all-cause mortality when compared with placebo. However, a recent randomized, controlled trial of etelcalcetide versus alfacalcidol showed that etelcalcetide effectively inhibited the progression of LVH in comparison to vitamin D in patients on haemodialysis after 1 year of treatment. Prior to that, oral calcimimetic treatment has already been shown to reduce left ventricular mass in patients on haemodialysis, whereas treatment with active vitamin D or mineralocorticoids was ineffective in patients with ESKD. Summary: Data from a recent trial of etelcalcetide on LVH suggest that FGF23 may be a possible therapeutic target for cardiac risk reduction in patients on haemodialysis. If these findings are confirmed by further research, it might be speculated that a treatment shift from active vitamin D towards FGF23-lowering therapy may occur in patients on haemodialysis.