1. Basic metabolic panel. Low bicarbonate level may point to acidosis or changes secondary to respiratory alkalosis. Fanconi syndrome may be associated with low bicarbonate, low potassium, and possibly elevated creatinine levels. Low calcium level points to rickets (not XLH) or hungry bone syndrome. High calcium level may point to hyperparathyroidism, but in children most have secondary hyperparathyroidism with normal or low calcium.
2. ABGs. Evaluate acid-base status; look for respiratory alkalosis or metabolic acidosis.
3. CBC with differential. Hypophosphatemia may cause hemolysis and thrombocytopeni a. Increased WBC with left shift may suggest sepsis.
4. Creatinine phosphokinase. Check for rhabdomyolysis if muscle tenderness is present.
5. Uric acid. Low in patients with volume overload or Fanconi syndrome.
6. Vitamin D levels. 25-Hydroxyvitamin D is diagnostic of vitamin D deficiency. No need to routinely check 1,25-dihydroxyvitamin D levels.
7. Urine studies. Spot urine for phosphorus and creatinine allows measurement of phosphate excretion to see if etiology is increased renal loss, as in Fanconi syndrome. Fanconi syndrome is characterized by glucosuria, renal tubular acidosis, aminoaciduria, and excretion of small-molecular-weight proteins such as ^-microglobulin.
C. Radiographic and Other Studies. Consider skeletal survey to look for changes characteristic of rickets, osteomalacia, or hyper-
parathyroidism. Changes may not point to exact etiology; antacid abuse can lead to osteomalacia.
V. Plan. Mild hypophosphatemia is a common finding in hospitalized patients, usually due to transcellular shifts of phosphate into intracellular fluid, and requires no specific therapy. Moderate hypophosphatemia can be treated with oral supplementation, but severe or symptomatic hypophosphatemia may require careful par-enteral correction.
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