Hyperphosphatemia in patients with chronic kidney disease

Abstract

Kidney plays a crucial role in phosphate homeostasis. Chronic kidney disease (CKD) activates compensating mechanisms, such as elevated FGF-23 and PTH production, which are directed to maintain serum phoshorus concetration within normal range. These mechanisms are suffcient in early CKD, but further progression of CKD leads to hyperphosphatemia. Elevated phosphorus concentration is involved in pathophysiology of CKD complications, and is a marker of increased risk of death. Many phosphate-binding drugs (PBAs) are available, and PBAs are commonly used in CKD patients. Treatment with PBAs is successful in lowering serum phosphorus concantration, but evidence that this therapy improves outcomes is still lacking. KDIGO 2017 Guidelines modify previous recommendations regarding mineral and bone disorders in patients with CKD. Decisions about phosphate-lowering treatment should be based on progressively or persistently elevated serum phosphate, and should consider calcium and PTH concentration. Treatment of hyperphosphatemia involves PBAs with restriciton of calcium-based phosphate binders, but also diet modification and adequate dialysis.