Kidney Week

Abstract: SA-PO0618

Phosphate Lost to Cancer: A Case of Tumor-Induced Osteomalacia

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

• Alqudah, Zain Mohamad, SUNY Upstate Medical University, Syracuse, New York, United States

Zain Mohamad Alqudah, MD

• Rehman, Tanzeel, SUNY Upstate Medical University, Syracuse, New York, United States

Tanzeel Rehman, MD, MBBS

• Naseeb, Muhammad, SUNY Upstate Medical University, Syracuse, New York, United States

Muhammad Naseeb, MBBS

• Min, Brian, SUNY Upstate Medical University, Syracuse, New York, United States

Brian Min, MD

• Bukhari, Syed Hassan Raza, SUNY Upstate Medical University, Syracuse, New York, United States

Syed Hassan Raza Bukhari, MD, FASN

Introduction

Renal phosphate homeostasis is regulated by proximal tubular reabsorption, and influenced by hormones such as PTH and fibroblast growth factor 23 (FGF 23). Disorders of hypophosphatemia may result from decreased intake, GI losses, or renal phosphate wasting.

Case Description

46-year-old man with history of type II diabetes and hypertension initially presented with progressive hip pain, leading to left femoral neck stress fracture requiring surgical fixation along with severe hypophosphatemia and hyperphosphaturia. Later he further developed additional atraumatic fractures, along with muscle weakness. No previous history of malabsorption, bariatric surgery, or use of medications known to cause renal phosphate wasting.
Laboratory evaluation revealed, serum Cr 1.0 mg/dL, bicarbonate 25 mEq/L, K 3.8 mEq/L, Ca of 8.5 mg/dL, severely low serum phosphate level of 1.3 mg/dL, iPTH 46.5 pg/mL, 25 Vit-D level 12.5 pg/mL, 1,25 vit-D3 25.4 and ALP 570 U/L. Urinalysis was unremarkable. 24-hour urine phosphorus excretion was high 1202 mg with fractional excretion (FEPO4) 30. Urine amino acid analysis and glycosuria screening were normal, urine pH 5.5, and FGF-23 was elevated 179. Renal tubular disorder panel was negative. Genetic testing for X-linked hypophosphatemia was negative. DEXA scan was normal. Despite persistent hypophosphatemia, FEPO4 remained elevated suggestive of impaired tubular absorption rather than decreased intake or GI loss.
Despite treatment with 25 Vit-D, calcitriol, and supplemental high dose phosphate and persistently low phosphate levels with atraumatic fractures raised concern for occult malignancy.
PET imaging revealed an intensely DOTATATE-avid soft tissue lesion located in proximal right thigh and planned for surgical resection. Case presentaion suggested tumor-induced osteomalacia (TIO).

Discussion

FGF-23 downregulates sodium-phosphate co-transporters in proximal tubule and reduces 1-alpha hydroxylase activity, thereby decreasing active vitamin D levels. The absence of glycosuria, aminoaciduria, and bicarbonate wasting argued against generalized proximal tubulopathy and suggested isolated phosphate wasting disorders including hereditary conditions (e.g., X-linked hypophosphatemia) and acquired causes such as TIO. A thorough work up for unexplained phsophate wasting may be the presenting feature of serious underlying malignant disease and early suspicion can aid in prompt diagnosis and early treatment.