Background and objectives: Fibroblast growth factor-23 (FGF23) regulates mineral metabolism. Circulatory FGF23 levels are increased and predict outcomes in CKD. However, the relation of FGF23 to albuminuria and disease progression in patients with CKD and one underlying diagnosis is unknown.
Design, setting, participants, & measurements: Prospective, observational study in 180 patients with IgA nephropathy (IgAN), CKD stage 1-4, and median 55-month follow-up (range, 12-177 months). Primary outcomes were (1) time-averaged albuminuria, (2A) progression to CKD stage 5 or ≥50% loss of estimated GFR, (2B) progression to CKD stage 5 or ≥25% loss of estimated GFR within 10 years, and (3) annual loss of estimated GFR.
Results: FGF23 was independently associated with baseline and time-averaged albuminuria (change in 1 g/24 hour albuminuria per increase in log FGF23: β = 0.26; P=0.02). Log FGF23 predicted CKD progression in crude models and after adjustment for mineral metabolites (endpoints 2A and 2B). It remained significant after adjustments for age, sex, serum albumin, calcium, phosphate, parathyroid hormone, 25-hydroxyvitamin D, baseline albuminuria, baseline estimated GFR, mean arterial BP, body mass index, and angiotensin-converting enzyme inhibitors/angiotensin-receptor blocker use in endpoint 2B (hazard ratio, 2.53; P=0.02) but not endpoint 2A (hazard ratio, 2.01; P=0.43). Log FGF23 predicted annual loss of estimated GFR in the same model (change in ml/min per 1.73 m(2) per increase in log FGF23, 1.50; P=0.008).
Conclusions: In patients with CKD and IgAN, FGF23 was associated with albuminuria and CKD progression, a finding that suggests its role as a potential biomarker in IgAN.