Abstract
BackgroundFetuin-A is known as a circulating inhibitor of vascular calcification. Factors associated with serum fetuin-A concentrations after long-term use of different phosphate binders in hemodialysis patients is still uncertain.MethodsIn the post-hoc study, we analyzed serum fetuin-A and biochemical factors (Ca, P, i-PTH, hsCRP, TG, LDL-C) in 50 hemodialysis patients, who completed a 48-week, open-Label, controlled randomized parallel-group study. 23 patients received sevelamer and 27 patients received calcium carbonate.ResultsAfter the 48-week treatment, the sevelamer group had less serum calcium increment, less iPTH decrement, more ALK-P increment, more hsCRP decrement and more LDL-C decrement. There was no significant difference in the serum fetuin-A decrement between two groups. Decreased serum fetuin-A levels were found after 48-week treatment in both groups: from 210.61 (104.73) to 153.85 (38.64) ug/dl, P = 0.003 in sevelamer group, from 203.95 (107.87) to 170.90 (58.02) ug/mL, P =0.002 in calcium group. The decrement in serum fetuin-A (Δfetuin-A) levels was associated with ΔCa (ρ = - 0.230, P = 0.040), ΔiPTH (ρ = 0.306, P = 0.031) and Δalbumin (ρ = 0.408, P = 0.003), not associated with sevelamer use, ΔP and ΔhsCRP.ConclusionAfter long-term sevelamer or calcium carbonate treatment, both groups of maintenance HD patients had lower serum fetuin-A levels. Serum levels of increased calcium, decreased iPTH and decreased albumin were associated with the serum fetuin-A decrement.
Highlights
Fetuin-A is known as a circulating inhibitor of vascular calcification
Chronic kidney diseases - mineral and bone disorders (CKD - MBD) including hyperparathyroidism, hypercalcaemia and hyperphosphataemia contribute to the development of vascular calcification and cardiovascular disease (CVD) [1,2,3]
Fetuin-A binds to serum calcium and phosphate, forming small calciprotein particles that are presumably removed through the reticuloendothelial system and normal kidney [10]
Summary
Fetuin-A is known as a circulating inhibitor of vascular calcification. Factors associated with serum fetuin-A concentrations after long-term use of different phosphate binders in hemodialysis patients is still uncertain. Chronic kidney diseases - mineral and bone disorders (CKD - MBD) including hyperparathyroidism, hypercalcaemia and hyperphosphataemia contribute to the development of vascular calcification and cardiovascular disease (CVD) [1,2,3]. Fetuin-A, a circulating inhibitor of vascular calcification, is associated with lower cardiovascular calcification and mortality in hemodialysis (HD) patients [4,5,6,7]. The non-calcium phosphate binder, sevelamer hydrochloride, has been shown to reduce progression of vascular calcification and mortality in CKD or end-stage renal disease (ESRD) patients in comparison with calcium-based. The longterm effect of different phosphate binders on serum fetuin-A levels has not been published before
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