Sellier AB, Seiler-Mußler S, Emrich IE, et al. - Polymorphisms of fibroblast growth factor receptor 4 (FGFR4) (rs351855) and Klotho (rs9536314) were not related to left-ventricular mass index (LVMI) or cardiac events in chronic kidney disease (CKD) patients. No evidence was generated in favor of a relevant clinical role of either FGFR4 stimulation or soluble form of Klotho deficiency in left-ventricular hypertrophy (LVH) development.

• According to experimental evidence, LVH is promoted by FGFR4 activation by fibroblast growth factor 23, and deficiency of the soluble form of its co-receptor Klotho.

• A Mendelian randomization study of CKD G2–G4 patients, of whom 519 agreed to SNP genotyping (FGFR4: rs351855; Klotho: rs9536314).

• LVMI changes between baseline and follow-up did not differ between carriers of the different alleles.

• Cardiac decompensation occurred in 104 patients, and atherosclerotic cardiovascular disease (ASCVD) in 144 patients.

• No difference was observed in time to cardiac decompensation and ASCVD between carriers of different alleles.