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Abstract: PO1193

Resistant Hypophosphatemia with Vitamin D Deficiency

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Mahmoud, Yasmin N., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Hamid, Akbar H., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Mohamed, Ammar N., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Mallappallil, Mary C., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Oh, Man S., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
  • Salifu, Moro O., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
Introduction

The renal regulation of phosphate homeostasis is mediated mainly by reabsorption of P by NaPi-IIc in the proximal tubule, whereas intestinal absorption is mediated by NaPi-IIb. Normally, about 2/3 of dietary intake (1500 mg/day) is absorbed, but when given by mouth as Na or K phosphate, absorption is nearly 100% in a normal person. We report here a patient with severe hypophosphatemia due to phosphate malabsorption caused by prior gastric bypass surgery along with vitamin D deficiency.

Case Description

A 34 year old African American female with past medical history of benign carcinoid syndrome, pernicious anemia, Hashimoto thyroiditis, and gastric sleeve surgery for morbid obesity 3.5 years ago, was admitted for acute dizziness and lightheadedness at rest without vertigo. Initial labs were: BUN 4 mg/dL; creatinine 0.6 mg/dL; Ca 9.2 mg/dL; Mg 2.17 mg/dL; P 1.3 mg/dL; 25-OH vitamin D 10.88 ng/mL; 1,25(OH)2 vitamin D 15.3 pg/mL; PTH 77.7 pg/mL; urine P 77 mg/dL; urine creatinine 342.51 mg/dL. She has been getting vitamin B12 injections for her pernicious anemia. She was treated with oral Na and K phosphate solution containing 560 mg of P, 320 mg of Na, and 500 mg of K in each dose for every 4 hours, and once daily dose of IV K phosphate containing 465 mg of phosphate for 14 days. She was also treated with 800 units of vitamin D2 daily. Serum phosphate remained persistently low around 1.8 mg/dL despite the above treatment.

Discussion

Hypophosphatemia in our patient was caused by impaired intestinal absorption of phosphate, and inappropriately increased urinary excretion due to secondary hyperparathyroidism due to vitamin D deficiency. The total daily amount of phosphate the patient received while in the hospital was 3825 mg per day. A 24 hour urine excretion of P estimated from urine creatinine concentration (342 mg/dL), assuming normal GFR (180 L/day), is very low (245 mg/day). Although P administered as Na or K salt is well absorbed in a normal person, she was unable to absorb P likely due to the gastric sleeve surgery causing rapid emptying of the gastric content, simulating the dumping syndrome, resulting in diarrhea by unabsorbed Na and K phosphate. Further impairment in intestinal P absorption may have been caused by vitamin D deficiency due to the inadequate dosing (800 units daily) and the inappropriate vitamin D type (Vitamin D2 instead of D3).