Additives in packaged meat, poultry, and fish can contribute significantly to the dietary phosphorus and potassium loads in CKD patients, researchers say.
The use of phosphate binders to manage hyperphosphatemia in maintenance hemodialysis patients might allow diets less restricted in protein and calories, according to a study.
Serum phosphorus fell to similar levels in two-thirds of peritoneal dialysis patients, but sucroferric oxyhdroxide recipients had a lower pill burden.
In a study of patients with chronic kidney disease and cardiovascular disease, niacin therapy lowered serum phosphate by just 0.25 mg/dL over 3 years compared with placebo.
Phosphate binder use is associated with a 25% and 37% decreased risk of death from infection-related causes and all-causes, respectively, compared with non-users.
Achieving a phosphate value of 1.4 mmol/L seemed optimal.
Patients with non-dialysis chronic kidney disease and iron deficiency anemia treated with ferric citrate experienced significant declines in FGF23 regardless of change in serum phosphorus.
Admission serum phosphorus levels below 2.5 and 4.9 mg/dL and above are associated with increased odds of dying in the hospital.
After switching to sucroferric oxyhydroxide, a higher proportion of patients achieved in-range serum phosphorus levels.
A randomized controlled pilot study demonstrated the feasibility and safety of performing a large clinical trial that is powered to establish whether phosphate lowering reduces fatal and nonfatal cardiovascular events.
Each 1-mg/dL increase in serum phosphorus among kidney transplant recipients is associated with 36% and 21% increased risk in graft failure and death, respectively.
Phase 2 randomized placebo-controlled trial demonstrated the safety and efficacy of sevelamer in lowering serum phosphorus levels in children and adolescents.
Creatinine, phosphorus, and electrolyte levels were not significantly different for exposed and unexposed hospitalized patients.
New findings suggest that nutritional index should be considered in the management of phosphorus level in HD patients, researchers conclude.
Of 7 phosphate binders, iron-based agents were optimal when efficacy and safety are considered.
Almost 40% of pre-dialysis patients with stage 4-5 CKD patients and type 2 diabetes had lab results suggesting low turnover bone disease.
Serum phosphorus and intact parathyroid hormone levels were not reduced with 12 weeks of rilonacept therapy.
CKD patients with and without diastolic dysfunction had average serum phosphate levels of 7.3 and 5.5 mg/dL, respectively.
The proportion of patients with serum phosphorus levels within target range rose from 22% to 65% within 6 months of starting ferric citrate treatment.
Use of sevelamer was associated with a 14% decreased risk of death compared with non-use.
Among other changes, the new KDIGO guidelines highlight the potential dangers of hypercalcemia.
From 2003 to 2011 there was a 26.7% decrease in in-hospital mortality rate after hip fracture.
Patients receiving educational or behavioral interventions aimed at controlling hyperphosphatemia had an average reduction in phosphate of 0.23 mmol/L more than standard care patients.
Converting hemodialysis patient to sucroferric oxyhydroxide from a previous binder increased the proportion of patients achieving target serum phosphorus levels.
Survival improved by 12% when serum phosphate levels approached a safer target range.
In a study of hemodialysis patients, mortality risk increased along with phosphorus level, particularly among patients with higher residual renal urea clearance.
At 18 months, PTH levels were within target for 67% and 68% of participants who initiated etelcalcetide at 2.5 mg and 5 mg, respectively.
Nearly twice as many patients achieved the target phosphorus range after a year of taking the phosphate binder, regardless of iPTH level.
Replacing foods containing phosphorus-based additives with similar foods not containing these additives can control hyperphospatemia without interfering with nutritional status.
Alkaline phosphatase was more strongly linked to mortality compared with other biomarkers of chronic kidney disease-mineral and bone disorder.
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