In adults, hyperphosphatemia is defined as a level >1.8 mmol/L (>5.5 mg/dL). The most common causes are acute and chronic renal failure, but it may also be seen in hypoparathyroidism, vitamin D intoxication, acromegaly, acidosis, rhabdomyolysis, and hemolysis. Hyperphosphatemia in chronic kidney disease lowers blood calcium levels by several mechanisms, including extraosseous deposition of calcium and phosphate, impairment of the bone-resorbing action of PTH, and reduction in 1,25(OH)₂D production due to elevated FGF23 and diminished renal tissue. The clinical consequences of severe hyperphosphatemia are hypocalcemia and calcium phosphate deposition in tissues. Depending on the location of tissue calcifications, serious chronic or acute complications may ensue (e.g., nephrocalcinosis, cardiac arrhythmias). Therapy consists of treating the underlying disorder and limiting dietary phosphorus intake and absorption. Oral aluminum phosphate binders or sevelamer may be used, and hemodialysis should be considered in severe cases.