Abstract: SA-PO1202
Severe Hypophosphatemia-Induced Paralytic Ileus: First Reported Case in a Long-Term Kidney Transplant Recipient with Persistent Tertiary Hyperparathyroidism
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Obata, Shota, Stanford University School of Medicine, Stanford, California, United States
- Joshi, Arpita, Santa Clara Valley Medical Center, San Jose, California, United States
Introduction
Paralytic ileus from severe hypophosphatemia has been documented in surgical and critically ill patients. However, to our knowledge, it has never been reported in kidney transplant recipients, despite their high risk for chronic, PTH-mediated renal phosphate wasting driven by persistent tertiary hyperparathyroidism (HPT). Here, we describe this complication in a long-term recipient.
Case Description
A 43-year-old man presented with sudden-onset severe abdominal pain, nausea, and emesis. Past history was notable for deceased-donor kidney transplantation 6 years ago (after 9 years of hemodialysis for FSGS) and persistent tertiary hyperparathyroidism (peak pre-transplant PTH 1,251 pg/mL). Cinacalcet had been discontinued post-transplant; he was not on phosphate supplementation despite chronic phosphate <2.0 mg/dL. Allograft function was at baseline (creatinine 1.5 mg/dL). Labs showed phosphate 0.8 mg/dL, intact PTH 238 pg/mL, and calcium 9.7 mg/dL. CT demonstrated focal proximal jejunal dilation to 3.6 cm with downstream decompression; although partial obstruction could not be radiographically excluded, rapid resolution after intravenous phosphate replacement (corrected to 1.9 mg/dL) confirmed metabolic ileus. Oral phosphate supplementation was initiated at discharge. A near-identical episode 10 months prior (phosphate 1.3 mg/dL) had resolved following oral intake, reinforcing the diagnosis.
Discussion
Mild post-transplant hypophosphatemia occurs in over 80% of kidney transplant recipients and is often regarded as benign, having been associated with favorable graft function in cohort studies. Post-transplant hypophosphatemia is driven by renal phosphate wasting, primarily induced by FGF23 secretion in the early post-transplant period, and by PTH in later stages. In recipients with persistent tertiary HPT, chronically elevated PTH suppresses proximal-tubule sodium-phosphate cotransporters, sustaining this wasting for years after transplantation. Profound hypophosphatemia depletes intracellular ATP and impairs smooth and skeletal muscle function, manifesting as myopathy, rhabdomyolysis, respiratory weakness, or—as highlighted here—paralytic ileus. Although optimal phosphate targets remain undefined, routine monitoring and proactive repletion in long-term recipients with tertiary HPT are essential to prevent such severe complications.