China
Africa
Explore chapters and articles related to this topic
Answers
Published in John D Firth, Professor Ian Gilmore, MRCP Part 2 Self-Assessment, 2018
John D Firth, Professor Ian Gilmore
The major abnormalities are hypocalcaemia and hyper-phosphataemia secondary to chronic renal failure. In chronic renal failure there is failure of the renal 1-alpha hydroxylase enzyme, preventing vitamin D from being converted to 1-alpha hydroxycholecalciferol, an intermediary on the way to the main active metabolite, 1,25-dihydroxycholecalciferol. Hypercalcaemia can therefore be corrected with 1-alpha hydroxycholecalciferol, which should be done to prevent/retard the development of secondary hyperparathyroidism that has long-term adverse consequences, particularly on bone. In chronic renal failure there is also phosphate retention that can be ameliorated by the consumption of phosphate binders before/at the same time as food. Calcium carbonate is commonly used. Aluminium hydroxide is also effective, but is no longer used (except in rare circumstances) because of the adverse consequences of aluminium intoxication. Sevelamer is an effective alternative.
Meta-analysis of the efficacy and safety of sevelamer as hyperphosphatemia therapy for hemodialysis patients
Published in Renal Failure, 2023
Qian Zeng, Yuanlong Zhong, Xiqiu Yu
The results of this study suggest that sevelamer can readily reduce serum levels of phosphorus, Ca, iPTH, and Ca × P, doing so more effectively in CKD5D patients undergoing dialysis than CC treatments, with similar superiority to LC treatment albeit with comparable efficacy in the overall reduction of Ca × P levels. Just one of the included studies compared sevelamer-associated changes in serum biomarkers to those of patients treated with a placebo and showed that the sevelamer group had lower blood phosphorus levels. A French study in patients with CKD stages 3D and 4 also tested the effect of placebo versus sevelamer carbonate (4.8 g daily) [51]. After 12 weeks of treatment with sevelamer, urinary phosphorus was reduced but serum FGF23, α-klotho, or P levels were essentially unchanged.
In vitro cytogenetic analysis of two different anti-phosphates (sevelamer hydrochloride and calcium carbonate) agents used by patients with hyperphosphatemia
Published in Drug and Chemical Toxicology, 2023
Goulzar Ulaya, Hasan Basri İla
Sevelamer appears to be the first choice in the treatment of people with the end-stage renal disease with high levels of phosphorus and calcium in the serum, prevention of hypercalcemia, regulation of parathyroid hormone, low density lipoprotein (LDL), cholesterol levels, and improvement of mortality (Block et al.2007). Previous studies have shown increased levels of DNA damage and genomic instability in patients with chronic kidney disease (Sandoval et al.2010, 2012, Stoyanova et al.2010, 2014, Rodriguez-Ribera 2014, Pastor et al.2018). In this context, it was reported that there was no increase in DNA damage levels observed in comet assay or micronucleus tests of patients receiving the drug to determine whether the increased level of DNA damage observed in such patients was associated with the use of common pharmacological treatments, including sevelamer (Pastor et al.2018).
An update on phosphate binders for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis: a review of safety profiles
Published in Expert Opinion on Drug Safety, 2022
Hiroaki Ogata, Akiko Takeshima, Hidetoshi Ito
Sevelamer hydrochloride was first approved for clinical use as a non-calcium-based phosphate binder [13]. Sevelamer hydrochloride use is associated with hyperchloridemic acidosis in some cases. Therefore, sevelamer carbonate, which exchanges carbonate for phosphate in the gastrointestinal tract, was developed and is now available for use in clinical practice [24]. In addition, sevelamers have been reported to have off-target actions. Their use is associated with a reduction in inflammatory cytokine levels [25] and advanced glycation end products [26] and an improvement of endothelial function [27]. Sevelamer can also bind bile salts in the gastrointestinal tract and can, consequently, reduce serum levels of total and low-density lipoprotein cholesterol [28]. However, its use is likely to also suppress fat absorption and fat-soluble vitamins (A, D, E, and K) [29]. In an observational study, sevelamer use was associated with vitamin K deficiency and an unfavorable gut microbial metabolism pattern [30]. It remains unclear whether sevelamer causes malabsorption of fat-soluble vitamins. Concomitant use of ciprofloxacin [31], thyroxine [32], or cyclosporine [33] with sevelamer has been reported to lower the bioavailability of these drugs. Although all phosphate binders are likely to interfere with gastrointestinal levothyroxine absorption to varying degrees, sevelamer has been suggested to have a higher degree of interference compared with other phosphate binders [34]. It should be noted that these drugs are often administered within several hours of sevelamer administration.