Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in the Absence and Presence of Chronic Kidney Disease.

Elevated Pi induces myotube atrophy and FGF23 expression in vitro. Mouse models with hyperphosphatemia not only develop skeletal muscle atrophy, but also produce FGF23 in skeletal muscle tissue in the presence and absence of CKD, and a low Pi diet protects the skeletal muscle in CKD mice. Pharmacological approaches targeting Pi uptake or excretion, or inhibition of Pi's direct actions on tissues might alleviate various CKD-associated pathologies. Future studies need to determine whether skeletal muscle-derived FGF23 contributes to tissue injury or is protective against Pi-induced damage.