Abstract
Recent evidence has indicated that fibroblast growth factor 21 (FGF21) regulates longitudinal bone growth, with increased FGF21 levels leading to bone loss. The present study evaluated the relationship between bone mineral density (BMD) and serum FGF21 levels in patients undergoing hemodialysis (HD). We analyzed blood samples from 95 patients undergoing HD and measured BMD using dual-energy X-ray absorptiometry of the lumbar vertebrae (L2–L4). Serum FGF21 concentrations were determined using a commercially available enzyme-linked immunosorbent assay kit. Thirteen (11.6%) patients were found to have osteoporosis, 27 (28.4%) osteopenia, and 57 patients had normal BMD. Advanced age and decreased body mass index, height, body weight, waist circumference, and triglyceride level were associated with lower lumbar T-scores, as were increased alkaline phosphatase, urea reduction rate, fractional clearance index for urea, and FGF21 levels. Low log-FGF21, increased body mass index, increased pre-HD body weight, and increased logarithmically transformed triglycerides (log-TG) were found to be significantly and independently associated with lumbar BMD by multivariate forward stepwise linear regression analysis with adjustment for significant confounders. We conclude that high serum FGF21 level is negatively associated with BMD in patients undergoing HD.
Highlights
Chronic kidney disease–mineral bone disorder (CKD-MBD) is a common systemic disorder which occurs in the context of end-stage renal disease (ESRD) and manifests as mineral metabolism dysregulation, damage to bone structure, and vascular calcification [1]
Given that Fibroblast growth factor 21 (FGF21) might influence bone mineral density (BMD), our study aimed to identify the association between FGF21 with BMD in patients undergoing hemodialysis (HD)
Lumbar BMD did not differ statistically according to presence of diabetes mellitus (DM) or hypertension or the use of ACEi, angiotensin receptor blockers, β-blockers, calcium-channel blockers, statins, or fibrates
Summary
Chronic kidney disease–mineral bone disorder (CKD-MBD) is a common systemic disorder which occurs in the context of end-stage renal disease (ESRD) and manifests as mineral metabolism dysregulation, damage to bone structure, and vascular calcification [1]. As CKD progresses, the elevation of serum fibroblast growth factor 23 (FGF23) leads to suppression calcitriol production, inducing hypocalcaemia and stimulating parathyroid hormone (PTH) secretion, resulting in decreased bone mineral density (BMD) [2]. This is associated with severe complications such as fracture, stroke, cardiovascular disease, and mortality [1,2].
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