Abstract: SA-PO0620
Acute Liver Injury-Associated Renal Phosphate Wasting Perpetuating a Vicious Cycle of Hypophosphatemia and Rhabdomyolysis
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Rjob, Ashraf S., The Ohio State University Wexner Medical Center Division of Nephrology, Columbus, Ohio, United States
- Mehta, Puja, The Ohio State University Wexner Medical Center Division of Nephrology, Columbus, Ohio, United States
- Altantawi, Omar, White River Health System Inc, Batesville, Arkansas, United States
Introduction
Hypophosphatemia in acute liver failure is attributed to phosphate uptake by regenerating hepatocytes and considered prognostically favorable. Recent evidence shows ALF-associated hypophosphatemia involves renal phosphate wasting without kidney damage or phosphatonin elevation, and acute hepatitis may produce hepatic FGF23. The clinical impact of this liver-driven phosphaturia is underexplored.
Case Description
A 22-year-old active man with congenital solitary kidney presented after near-syncope following a 4-mile run and acute alcohol intake (~5 beers). Phosphorus was 1.0 mg/dL, CK 277 U/L. CK peaked at 28,300 U/L (day 6) with AST/ALT 10,980/8,780 U/L, INR 5.8, transient AKI, and type 2 myocardial injury. Despite aggressive phosphate repletion, hypophosphatemia persisted during active liver injury. FEPhos remained elevated despite low serum phosphorus, confirming inappropriate phosphaturia. Intact FGF23 was low (14 pg/mL); 1,25(OH)2D was low (16.8 pg/mL), consistent with FGF23-mediated 1α-hydroxylase suppression. Hypophosphatemia and CK improved only with liver recovery. Genetic testing for hereditary hypophosphatemia was nondiagnostic
Discussion
This case demonstrates a vicious cycle: alcohol-induced hypophosphatemia triggered exertional rhabdomyolysis, causing liver injury that perpetuated renal phosphate wasting refractory to repletion, further fueling rhabdomyolysis. The cycle broke only with hepatic recovery. The low intact FGF23 does not exclude a transient hepatic surge given its short half-life (~46 min), and low 1,25(OH)2D supports downstream FGF23 activity. A non-FGF23 pathway (e.g., NAMPT/NAD axis) may also contribute. This challenges the view that ALF-associated hypophosphatemia is solely benign.Acute liver injury can drive phosphaturia that perpetuates rhabdomyolysis, resolving only with hepatic recovery