Linkage of Fibroblast Growth Factor 23 and Phosphate in Serum: Phosphate and Fibroblast Growth Factor 23 Reduction by Increasing Dose of Sevelamer

BACKGROUND: High serum phosphate and fibroblast growth factor-23 (FGF-23) levels are well-recognized independent risk factors of mortality and morbidity in patients with chronic kidney diseases (CKDs). Sevelamer, as a phosphate chelating agent, reduces serum phosphate and FGF-23 levels produced by bone osteocytes. This study aimed to determine the best dose at which sevelamer could successfully reduce serum phosphate and FGF-23 levels in rat models of adenine-induced CKD. METHODS: CKD was induced using adenine. Healthy and CKD-induced rats were divided into 6 groups as follows: healthy controls; CKD controls; rats treated with 1%, 2%, and 3% sevelamer for CKDs; and healthy rats administered 3% sevelamer. Biochemical factors and serum FGF-23 levels were measured using spectrophotometry and enzyme-linked immunosorbent assay methods. RESULTS: Serum phosphate levels were best decreased in rats receiving 3% sevelamer in their diet (5.91±1.48 mg/dL vs. 8.09±1.70 mg/dL, P < 0.05) compared with the CKD control rats. A dose-dependent decrease in serum FGF-23 levels was observed, and the most significant results were obtained in rats receiving 3% sevelamer compared with the CKD control rats (142.60±83.95 pg/mL vs. 297.15±131.10 pg/mL, P < 0.01). CONCLUSIONS: Higher sevelamer doses significantly reduced serum phosphate and FGF-23 levels in adenine-induced CKD rats.

[Effect of common paraoxonase 1 polymorphism [Q192R] on atherosclerosis risk in referred diabetic patients to Tabriz Shahid Madani heart hospital in 2010]

Paraoxonase is a HDL-associated enzyme implicated in the pathogeneses of atherosclerosis by protecting lipoproteins against peroxidition in numerous studies. Its biallelic gene polymorphism at codon 192Q>R has been associated with coronary artery disease [CAD]. Therefore, in the present study the role of polymorphism paraoxonase 1 gene was evaluated for CAD in diabetic patients. In this case- control study, peripheral blood was taken from 105 CAD patients diagnosed with angioplastically and 95 CAD individuals with no history of diabetes from Northwest of Iranian population. The abundance of mutant alleles of the 192Q>R paraoxonase were determined by PCR-RFLP. The abundance of RR allele in diabetic group was significantly higher than in selected group with no diabetic history [41.1% in diabetic vs. 24.5% in non-diabetic individuals]. Regarding significant prevalence of RR allele and considering ethnic diversities like Turk, Kurd, Lore and others living in Iran, it appears that other polymorphism of this gene like 163T>A and 55L>M is needed to be studied in diabetic patients, which their relations to atherosclerotic problem has been already determined.