Hypophosphatemia

Hyperphosphatemia is a serum phosphate level above 4.5 mg/dL (1.45 mmol/L), most often from reduced renal excretion in advanced chronic kidney disease or from acute cellular lysis in tumor lysis syndrome or rhabdomyolysis. Management sequences correction of the underlying cause and kidney function with dietary phosphate restriction, phosphate binders, and dialysis, while chronic elevation drives CKD-mineral and bone disorder, secondary hyperparathyroidism, and vascular calcification.

Refeeding syndrome is a potentially fatal shift of phosphate, potassium, and magnesium into cells when nutrition is reintroduced too quickly to a malnourished patient, driven by an insulin surge that also causes fluid retention and thiamine depletion. Prevention rests on identifying at-risk patients before feeding, starting calories low, giving thiamine first, and repleting electrolytes proactively rather than reactively.

Diabetic ketoacidosis is a life-threatening hyperglycemic crisis of near-absolute insulin deficiency, most common in type 1 diabetes, producing an anion-gap ketoacidosis from unrestrained lipolysis and osmotic diuresis from severe hyperglycemia. It is diagnosed by hyperglycemia, ketonemia, and an anion-gap metabolic acidosis, and treated with intravenous isotonic saline, an intravenous regular insulin bolus and infusion, and aggressive potassium repletion guided by frequent electrolyte monitoring.

Primary hyperparathyroidism is autonomous PTH oversecretion, most often from a solitary parathyroid adenoma, producing hypercalcemia with an elevated or inappropriately normal PTH and low or low-normal phosphorus. Most patients are asymptomatic and identified on routine labs; parathyroidectomy is curative and is first-line for symptomatic disease or when specific biochemical, skeletal, or renal criteria are met, while observation with annual monitoring suffices for mild, asymptomatic disease.

X-linked hypophosphatemia is an inherited disorder of excess FGF23 activity that causes renal phosphate wasting at the proximal tubule, producing rachitic bone disease in children and osteomalacia in adults despite normal serum calcium and vitamin D. First-line treatment is oral phosphate salts with calcitriol, or burosumab, an anti-FGF23 monoclonal antibody, given alone and never combined with oral phosphate or active vitamin D.

Tumor-induced osteomalacia (oncogenic osteomalacia) is an acquired renal phosphate-wasting disorder caused by a phosphaturic mesenchymal tumor that secretes fibroblast growth factor 23, producing bone pain, muscle weakness, and pseudofractures from impaired mineralization. First-line management is oral phosphate and calcitriol supplementation to restore mineralization while the causative tumor is identified.

Osteomalacia is inadequate mineralization of newly formed bone, most often from severe, prolonged vitamin D deficiency due to poor intake, limited sun exposure, or malabsorption after celiac disease or gastric bypass. It causes diffuse bone pain and tenderness, proximal weakness, and pseudofractures, with elevated alkaline phosphatase, low or low-normal calcium and phosphorus, 25-hydroxyvitamin D usually below 10 ng/mL, and secondary hyperparathyroidism; treatment is vitamin D 50,000 IU weekly for 8 weeks, then daily maintenance, with calcium and correction of the underlying cause.

Hypokalemia is a serum potassium level below 3.5 mEq/L, most often caused by gastrointestinal or renal potassium losses, and it produces weakness, ileus, and arrhythmia risk through altered membrane excitability. Diagnosis rests on the urine potassium-creatinine ratio to separate renal from extrarenal causes, and treatment is intravenous or oral potassium chloride, with concurrent magnesium repletion, dosed to severity and symptoms.

Hypomagnesemia is a serum magnesium level below 1.7 mg/dL, most often caused by gastrointestinal losses, proton pump inhibitors, or renal magnesium wasting from diuretics and other drugs. It causes concurrent hypokalemia and hypocalcemia and can potentiate cardiac arrhythmias, and treatment is intravenous magnesium sulfate for significant symptoms or slow-release oral repletion for milder deficiency.

Rhabdomyolysis is necrosis of skeletal muscle with release of myoglobin, creatine kinase, and intracellular electrolytes into the circulation, diagnosed by a serum creatine kinase at least five times the upper limit of normal (typically over 1500 U/L) with a urine dipstick positive for blood but no red cells on microscopy; treatment is aggressive isotonic intravenous fluid to a urine output of 200 to 300 mL/h and correction of hyperkalemia, with acute kidney injury from pigment nephropathy the dominant complication.