Renal phosphate wastage and hypophosphatemia is the most common divalent ion abnormality in transplant patients. The causes include: 1) secondary hyper-parathyroidism which may persist for up to a year after kidney transplantation (PTH causes the kidney to waste phosphate in the urine; 2) glucocorticoids inhibit the tubular reabsorption of phosphate and contribute to phosphate wastage in the urine; 3) calcium containing antacids prescribed to correct hypocalemia bind dietary phosphate in the GI tract, and 4) the adequacy of renal function i.e., a well-functioning kidney excretes more phosphate while a poorly functioning kidney does not.

Clinical manifestations of hypophosphatemia are only seen if serum phosphorus is less than 1 mg/dl. Muscle weakness, rhabdomyolysis, respiratory failure from diaphragmatic muscle weakness and congestive heart failure may occur. Other manifestations include: paresthesias, confusion, seizures, coma, hemolysis, platelet dysfunction, and metabolic acidosis. Treatment of hypophosphatemia must be given with extreme care in renal failure to prevent causing hyperphosphatemia Moderate hypophosphatemia can be treated orally with skim milk (contains about 1000 mg of phosphorus per liter) or Neutra-phos tablets (250 mg of phosphorus q-day to q.i.d. Oral phosphorus can cause diarrhea. Treatment of severe hypophosphatemia (< 1.0 mg/dl) if the patient is asymptomatic may be by oral replacement 3 g/day for a week. If the patient is symptomatic, replacement should be intravenously 2 mg/kg body weight as the sodium salt infused over six hours, then phosphorus should be rechecked and continued until serum phosphorus exceeds 1 mg/dl. Intravenous phosphorus may produce hypocalcemia and metastatic calcifications (especially if the calcium—phosphorus product exceeds 60 mg/dl).

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