The tendency toward phosphate retention develops early in renal disease due to the reduction in the filtered phosphate load. Overt hyperphosphatemia develops when the glomerular filtration rate (GFR) falls below 25 to 40 mL/min per 1.73 [1-3]. (See "Lipid abnormalities in patients with chronic kidney disease not requiring dialysis".)
Hyperphosphatemia alone or in combination with a high serum calcium has been associated with increased mortality in dialysis patients [4,5]. (See "Patient survival and maintenance dialysis", section on 'Disorders of mineral metabolism'.) This association has also been observed in some [6-8], though not all [9,10], studies of patients with less advanced kidney disease. Hyperphosphatemia may also cause significant morbidity [11,12]. (See "Vascular calcification in chronic kidney disease" and "Calciphylaxis (calcific uremic arteriolopathy)".)
Common treatment options for hyperphosphatemia include dietary phosphate restriction and oral phosphate binders and, for dialysis patients, increased dialysis. This topic reviews recommendations regarding target phosphate concentration and treatment options for hyperphosphatemia for chronic kidney disease (CKD) patients.
Recommended goals for serum parathyroid hormone (PTH) concentration for patients with CKD are discussed elsewhere. (See "Management of secondary hyperparathyroidism and mineral metabolism abnormalities in adult predialysis patients with chronic kidney disease", section on 'Goal target levels' and "Management of secondary hyperparathyroidism and mineral metabolism abnormalities in dialysis patients", section on 'Goals of therapy'.)
Mechanisms underlying the physiologic response to phosphate retention are discussed elsewhere. (See "Overview of chronic kidney disease-mineral bone disease (CKD-MBD)".)