RA MUZASTI1,2, N LUBIS2, HR LUBIS1
1University of Sumatera Utara, Medan, Indonesia, 2Adam Malik Hospital, Medan, Indonesia
Background: Fibroblast growth factor 23 (FGF23) is an important hormone in the regulation of phosphate metabolism.The relationship between FGF23 and vascular calcification is still controversial. It is unclear whether FGF23 is a stimulator or inhibitor to abdominal aortic calcification (AAC) in chronic kidney disease (CKD) patients with regular hemodialysis.
Aim: To investigate the relationship between FGF23 and AAC in regular hemodialysis patients.
Method: Seventy-five regular hemodialysis patients were enrolled in this cross-sectional study. Serum levels of intact FGF23 was determined using an enzyme-linked immunosorbent assay (ELISA) and AAC was detected with lateral lumbal X-ray. The risk factors for AAC were evaluated using a logistic regression model.
Result: Of 75 patients, 51 (68.0%) had AAC. Median (min-max) intact serum FGF23 was 328 (217-950) pg/ml. Serum FGF23 levels of patients with AAC were significantly higher than those without AAC (p<0.001). Age at initiation of hemodialysis, and FGF23 levels were independent risk factors for AAC. Receiver-operating characteristic curves showed that the sensitivity and specificity of FGF23 for diagnosing AAC were 94.0% and 84.0%, respectively, with area of under the curve was 0.959 (p<0.001).
Conclusion: Elevated serum FGF23 concentrations are independently predicts AAC in CKD patients with regular hemodialysis. Further studies are needed to elucidate the potential biological mechanisms by which FGF23 may be involved in the pathogenesis of AAC.
Fellow of Nephrology and Hypertension. Internist, 2011. Lecturer
in Division of Nephrology-Hypertension, Department of Internal Medicine, College of Medicine, Sumatera Utara University. Staff in Adam Malik Hospital, Medan.