Hypophosphatemia

Phosphate & FGF23medium

A 74-year-old man with hypertension and gastroesophageal reflux is evaluated for diffuse bone pain and is found to have hypophosphatemia (serum phosphate 1.6 mg/dL). For several years he has taken large daily doses of over-the-counter aluminum hydroxide antacids for reflux. He denies fever, weight loss, myalgias, weakness, or diarrhea, has an excellent appetite, and eats a normal balanced diet. Serum calcium and creatinine are normal, and there is no glucosuria, aminoaciduria, or metabolic acidosis. Which of the following is the most likely cause of his hypophosphatemia?

  1. A.Renal phosphate wasting from Fanconi syndrome
  2. B.FGF23-mediated renal phosphate wasting from tumor-induced osteomalacia
  3. C.FGF23 excess from a PHEX mutation, i.e., X-linked hypophosphatemia
  4. D.Decreased intestinal phosphate absorption from chronic antacid useCorrect

Explanation

Aluminum- (and magnesium-) containing antacids bind dietary phosphate in the gut, and chronic high-dose use causes hypophosphatemia (and can cause osteomalacia and bone pain) through decreased intestinal absorption, not renal wasting. The clues here are years of aluminum hydroxide antacid use with an otherwise normal diet and no evidence of renal phosphate wasting. Fanconi syndrome would show glucosuria, aminoaciduria, and a proximal (type 2) renal tubular acidosis, none of which are present. Tumor-induced osteomalacia and PHEX-related X-linked hypophosphatemia cause FGF23-mediated renal phosphate wasting; XLH also presents in childhood, making it implausible in a 74-year-old with a clear antacid history.

Why each option

A.
Fanconi syndrome causes renal phosphate wasting with glucosuria/aminoaciduria/proximal RTA, absent here.
B.
Tumor-induced osteomalacia causes FGF23-mediated renal phosphate wasting, not decreased gut absorption.
C.
PHEX mutations (X-linked hypophosphatemia) cause renal phosphate wasting and present in childhood, not new-onset at 74.
D.
Correct. Chronic aluminum-containing antacids bind gut phosphate and reduce absorption, producing hypophosphatemia and osteomalacia.

Reference: Felsenfeld AJ, Levine BS. Approach to treatment of hypophosphatemia. Am J Kidney Dis. 2012;60(4):655-661.

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