| Summary: | Hypophosphatemia from renal phosphate wasting during the immediate postoperative kidney transplant period is common and improves with supplementation. We report a case of hypophosphatemia secondary to small bowel bypass surgery and over the counter antacid use in a patient with stage 4 chronic kidney disease (CKD) many years after simultaneous liver-kidney transplant (SLKT).
A 43-year-old man with a history of alcoholic end-stage liver disease and hepatorenal syndrome status post SLKT 5 years prior presented with recurrent small bowel obstruction which persisted despite conservative treatment. Following exploratory laparotomy, he had a jejunal bypass surgery due to the intra-operative finding of jejunum adherent to a single mass. Due to the friability of the tissue, lysis of the adhesions was felt to be unsafe. Postoperatively, he developed hypophosphatemia and severe malnutrition due to short bowel syndrome. He required total parenteral nutrition which led to improvement in serum phosphorus. However, hypophosphatemia recurred and the lowest level of 1.1 mg/dl occurred during the transition from parenteral nutrition to partial enteral nutrition. On review of medication, he had been taking over the counter antacids for “indigestion”. Serum calcium was low normal and intact parathyroid hormone was within normal range. The patient also had vitamin D deficiency with a total 25-OH vitamin D of 23 ng/ml. The serum phosphorus improved after stopping antacids but remained persistently low normal despite oral supplementation, and he continues to require intermittent intravenous phosphate supplementation.
Although hyperphosphatemia is common in CKD, hypophosphatemia can occur from overzealous dietary restrictions and use of phosphate binders. Aluminum hydroxide is a potent phosphate binder commonly found in over the counter antacids. Ongoing review of medications (both prescription and over the counter) is important to prevent hypophosphatemia. In addition, intestinal bypass, especially jejunal bypass, contributes to hypophosphatemia, and our case underscores the importance of the jejunum in phosphate absorption.
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