In a recent publication in Kidney Medicine, authors indicated that elevated levels of fibroblast growth factor 23 (FGF23) may be correlated with an augmented risk of developing HF in adults diagnosed with chronic kidney disease (CKD).

The authors wrote, “Heart failure (HF) is an important cause of morbidity and mortality among individuals with chronic kidney disease (CKD). A large body of evidence from preclinical and clinical studies implicates fibroblast growth factor 23 (FGF23) excess in HF pathogenesis in CKD. It remains unclear whether the relationship of elevated FGF23 to HF risk among individuals with CKD varies by HF subtype.”

The researchers conducted an observational study that included 3,502 patients utilizing data from the longitudinal prospective Chronic Renal Insufficiency Cohort (CRIC) study. The CRIC Study examined the risk factors for cardiovascular and kidney-related outcomes in patients with mild-to-moderate CKD. The researchers sought to explore the correlation between FGF23 and the risk of HF in CKD patients and examine potential correlations between FGF23 and incident hospitalization for HF by subtype.

The primary outcome was defined as an incident HF event substratified as HF with preserved ejection fraction (HFpEF), HF with reduced ejection fraction (HFrEF), and HF with unknown ejection fraction (HFuEF). For the secondary analyses, researchers investigated correlations of FGF23 and HF burden defined as any HF event after enrollment, including individuals with a history of HF.

The results revealed that during an average follow-up period of 10.8 years, there were 295 HFpEF, 242 HFrEF, and 156 HFuEF hospitalizations, and the rate of total HF events augmented with FGF23 quartile.

The authors wrote, “Our findings highlight the need for additional research into the relationships between FGF23 and HF in individuals with CKD as a possible mechanism to reduce the risk of HF. The presented analysis confirms prior data linking elevated FGF23 with risk of HF and extends the literature by reporting on risks with HF subtypes in a large multicenter prospective CKD cohort.”

Based on their findings, the authors concluded that in this large multicenter prospective cohort study, elevated FGF23 was linked with boosted risks of all HF subtypes. The authors also indicated that their findings support ongoing research investigating elevated FGF23 as a possible therapeutic target for preventing and treating HF among CKD patients.

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