According to preliminary research, phosphate binders may bind to helpful substances such as vitamin K, but also to harmful ones, such as lipopolysaccharides and advanced glycation end products.
In a small study, vitamin K antagonist use and liver dysfunction emerged as the most important factors in the development of calciphylaxis.
Researchers estimate that half of calcium channel blockers, for example, contain phosphorus as an excipient.
In meta-analyses, elevated FGF23 correlated with 25% and 22% increased risks for all-cause mortality and cardiovascular events, respectively, among patients on maintenance hemodialysis.
In a phase 3 trial, tenapanor, which reduces paracellular phosphate transport in the intestine, lowered elevated serum phosphorus in patients on hemodialysis.
In a new study, patients with serum phosphate levels above 1.78 mmol/L at the start of peritoneal dialysis had a nearly 2-fold increased risk of death.
In a 2-phased trial, hyperphosphatemia and is sequelae developed in a smaller proportion of patients taking activated charcoal compared with placebo recipients.
Study supports the hypothesis that altered tubular phosphate handling drives the increase in serum phosphate during SGLT2 inhibition.
In 2 studies, roughly a third of hemodialysis patients achieved within-range serum phosphate levels after converting to sucroferric oxyhydroxide from another phosphate binder.
In a small study of hemodialysis patients, substituting egg white for meat and fish in 3 meals per week resulted in a significant decrease in serum phosphate.