Kidney Week 2025 Annual Meeting-Prevention of CKD-Associated Hyperphosphatemia in 2025: What Are the Risks and Benefits?

Video Transcription

Video Summary

The session reviewed 50 years of evolving understanding of phosphate disorders in CKD and their cardiovascular implications. The moderator highlighted a shift from viewing PTH as central in CKD–mineral bone disorder to recognizing FGF23 as a key phosphaturic hormone that rises with phosphate excess, lowers active vitamin D, promotes hypocalcemia, and worsens secondary hyperparathyroidism. Large observational studies in dialysis, CKD, and even people with normal kidney function consistently link higher (even “normal-range”) serum phosphate to all-cause and cardiovascular mortality. Proposed mechanisms include increased left ventricular mass, vascular/medial calcification, arterial stiffness, and endothelial dysfunction. However, randomized trials of phosphate binders have often failed to show clear improvements in surrogate or clinical outcomes, raising the need to prove causality.<br /><br />Dr. Hilgalland discussed treatment targets and limitations of current strategies. Despite widespread binder use, most dialysis patients do not reach strict phosphate goals. KDIGO guidelines now recommend lowering elevated phosphate “toward normal” with low-quality evidence. Trials comparing strict versus standard targets show mixed results; the HILO trial was inconclusive due to poor separation and under-enrollment. Emerging work questions whether fasting serum phosphate is the best risk marker, emphasizing whole-body phosphorus balance and early upstream changes (FGF23, PTH). Dietary restriction can unintentionally reduce protein intake and increase mortality risk, whereas reducing phosphate additives may lower phosphate without harming nutrition.<br /><br />Dr. Dillon reviewed cardiovascular effects and binder choice, emphasizing KDIGO’s suggestion (2B) to limit calcium-based binders. Evidence suggests sevelamer may reduce all-cause mortality versus calcium (low-certainty), while lanthanum shows no clear advantage, possibly influenced by calcium dose and background diet. He concluded binder selection should also consider pill burden, tolerability, cost, and individualized patient factors. Q&A emphasized the importance of vitamin D therapy, residual kidney function, individualized protocols, and potential (but not definitive) roles for vitamin K2 in calcification.

Asset Subtitle

Moderator(s): Michel Chonchol

Presentation(s):

Introduction - Michel Chonchol
Current Phosphorus Targets in CKD: Evidence and Available Strategies - Kathleen Hill Gallant
Cardiovascular Effects of Hyperphosphatemia: Does Treatment Modality Matter? - John Dillon

Support is provided by an educational grant from Ardelyx, Inc.

Meta Tag

Date 11/6/2025

Pathway 1 CKD Non-Dialysis

Session ID 519588

Keywords

chronic kidney disease (CKD)

CKD–mineral and bone disorder (CKD-MBD)

phosphate disorders

fibroblast growth factor 23 (FGF23)

secondary hyperparathyroidism (PTH)

serum phosphate and cardiovascular mortality

vascular/medial calcification and arterial stiffness

phosphate binders (sevelamer, calcium-based, lanthanum)

dietary phosphate restriction and phosphate additives