Kidney Week Educational Symposia-Hyperphosphatemia Management in Adults Treated with Dialysis for Kidney Failure: Old Lessons, New Directions

Video Transcription

Video Summary

The symposium focuses on hyperphosphatemia as a common, persistent complication of chronic kidney disease (CKD), especially in end-stage kidney disease (ESKD), and its links to cardiovascular and all-cause mortality. Management is described as “three-pronged”: phosphate binders, dietary phosphorus restriction, and dialysis, though adherence is difficult and influenced by patient-centered, psychosocial, and provider factors.<br /><br />Dr. Sagar Nigwekar reviews the burden and biology of hyperphosphatemia in hemodialysis and peritoneal dialysis. Registry data suggest ~35–40% of patients remain persistently hyperphosphatemic. Consequences include secondary hyperparathyroidism, altered FGF23/vitamin D pathways, inflammation and oxidative stress, vascular calcification, fractures, pruritus, calciphylaxis, hospitalization, and mortality; observational data also associate higher phosphate with sudden cardiac death. Dialysis removes limited phosphate unless intensity/time increases (e.g., nocturnal dialysis). He reviews binder classes (aluminum, calcium, sevelamer, lanthanum, iron-based) and notes trials/cohort studies showing unclear superiority of non-calcium binders for hard outcomes, though some data suggest stricter phosphate targets may reduce coronary calcification. Ongoing trials (e.g., Hi-Lo) aim to clarify optimal targets. A novel non-binder approach, tenapanor, may reduce intestinal phosphate absorption by affecting paracellular transport.<br /><br />Dr. Kathleen Hill-Gallant addresses dietary strategies. Guidelines suggest limiting dietary phosphorus, but evidence quality is low and clinical outcome data are lacking. Intestinal absorption is largely paracellular and may remain high in CKD despite low calcitriol, supporting interventions to reduce absorbed load. She emphasizes focusing on highly bioaccessible inorganic phosphate additives, while cautioning that overly restrictive diets can reduce protein intake and may worsen outcomes; healthier dietary patterns (e.g., Mediterranean) correlate with better survival despite higher phosphorus intake. Education should be individualized and practical, using small “swap” strategies to avoid additives.

Asset Subtitle

Moderators: Ebele Umeukeje

Introduction - Ebele Umeukeje
Phosphorus Metabolism in Kidney Failure: How Biology Informs Medication Therapy - Sagar Nigwekar
Diet Strategies to Improve Hyperphosphatemia Independent of and Integrated with Medication Therapy - Kathleen Hill Gallant

Support is provided by an educational grant from Akebia Therapeutics, Inc.

Meta Tag

Date 11/4/2022

Pathway 1 Fluid, Electrolyte, and Acid-Base Disorders

Pathway 2 Bones, Stones, and Mineral Metabolism

Session ID 439795

Session Type ES - Educational Symposium

Keywords

hyperphosphatemia

chronic kidney disease (CKD)

end-stage kidney disease (ESKD)

phosphate binders

dietary phosphorus restriction

dialysis phosphate removal

vascular calcification

FGF23 and vitamin D pathways

tenapanor

phosphate additives