ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: TH-PO463

Association of SNPs on FGFR4 and Klotho Genes with LVH and Cardiovascular Outcome in CKD Patients

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 303 CKD: Epidemiology, Outcomes - Cardiovascular


  • Sellier, Alexander, Saarland University Medical Center, Homburg (Saar), Germany
  • Seiler, Sarah, Saarland University Hospital, Homburg, Germany
  • Emrich, Insa E., None, Haschbach, RP, Germany
  • Fliser, Danilo, Saarland University Medical Centre, Homburg/Saar, Germany
  • Zawada, Adam M., Saarland University Medical Center, Homburg (Saar), Germany
  • Heine, Gunnar H., Saarland University Faculty of Medicine, Homburg, Germany

High circulating levels of fibroblast growth factor 23 (FGF23) predict future cardiovascular events in CKD patients even after adjustment for baseline GFR. Recent rodent studies suggest that FGF23 may directly induce left ventricular hypertrophy by activating FGF-receptor 4 (FGFR4) independently from its co-receptor klotho. Opposing studies however reported a deficiency of soluble klotho, rather than high serum FGF23, to aggravate LVH. To compare the clinical relevance of these pathophysiological pathways, we examined whether SNPs within the FGFR4 and klotho gene affect the risk of prevalent LVH and incident cardiac events in our prospective CARE FOR HOMe study.


The ongoing CARE FOR HOMe study recruits chronic kidney disease G2-G4 patients, of whom 519 patients consented to DNA isolation and genotyping using qualitative real-time PCR (Gly388Arg for FGFR4 and Phe352Val for klotho). Echocardiography was conducted at baseline by one single physician following American Society of Echocardiography guidelines. All patients were followed for the occurrence of the primary endpoint cardiac decompensation for 4,2 ± 2,1 years.


Carriers of the different alleles of Gly388Arg and Phe352Val did not differ significantly in their left ventricular mass index (Gly388Arg: Gly/Gly: 91.7 ± 28.5 g/m2, Gly/Arg: 91.4 ± 24.4 g/m2, Arg/Arg: 93.9 ± 28.7 g/m2, p = 0.861; Phe352Val: Phe/Phe: 91.1 ± 25.4 g/m2, Phe/Val: 92.8 ± 28.2 g/m2, Val/Val: 100.9 ± 48.0 g/m2, p = 0.379). During follow up, cardiovascular events occurred in 104 patients. Neither Gly388Arg nor Phe352Val was significantly associated with risk of cardiac decompensation in univariate analysis (log rank test: Gly388Arg: p = 0.241; Phe352Val: p = 0.817).


In CKD patients, SNPs of FGFR4 and Klotho are neither associated with LV mass, nor with the risk of future cardiac decompensation. We suggest to analyze the association between SNPs, LV hypertrophy and incident cardiac events in independent large CKD collectives before findings from rodent studies should be transferred to clinical nephrology.