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Abstract: PO1910

A Case of Oncogenic Osteomalacia with Urinary Phosphate Wasting Masked by AKI

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology


  • Wickman, Terrance, Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States
  • Kanduri, Swetha Rani, Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States
  • Kovvuru, Karthik, Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States
  • Velez, Juan Carlos Q., Ochsner Medical Center - New Orleans, New Orleans, Louisiana, United States

Hypophosphatemia in patients with oncogenic osteomalacia (OO) is due to excess production of fibroblast growth factor 23 (FGF-23) causing urinary phosphate wasting. However, in patients with coexisting acute kidney injury (AKI), hypophosphatemia may normalize as the AKI worsens potentially masking renal phosphate wasting. In-appropriately low or normal phosphorous levels in patients with AKI should prompt further work up to identify potential renal phosphate wasting.

Case Description

36-year-old morbidly obese woman presented with right-sided abdominal pain and fatigue for 2 weeks. Initial laboratory evaluation revealed AKI (Cr 2.1 mg/dL, baseline 1.2) that failed IV fluid therapy prompting nephrology consultation. Other labs included urine protein creatinine ratio 0.2 g/g, alkaline phosphate (895 U/L), mild hyperbilirubinemia (1.8 mg/dL), mild hypercalcemia (corrected Ca 11 mg/dL), hypophosphatemia (1.8 mg/dL), low vitamin D (28 ng/mL), normal PTH (19 pg/mL), normal PTHrP (2.2 pmol/L) and low normal calcitriol (28 pg/ml). Kidney ultrasound was normal. Liver ultrasound revealed an ill-defined mass not seen in CT scan. FGF-23 levels were sent due to suspicion of OO and returned very high at 12,715 RU/ml. Patient was readmitted to the hospital for accelerated work up to identify the source of FGF-23. Repeat labs on admission showed Cr of 2.2 mg/dL, normal phosphorous 3.2 mg/dL and bilirubin 12 mg/dL. Random liver biopsy showed tumor cells positive for CD56 and Ki-67, with a proliferation rate of 80% indicating high grade metastatic neuro endocrine tumor. Localization of primary tumor was unsuccessful. Oncology was consulted and chemotherapy was entertained, but the patient rapidly deteriorated and opted for comfort measures.


Reduced phosphate excretion in patients with AKI leads to hyperphosphatemia, stimulating FGF-23 production to facilitate phosphaturia. However, when AKI is associated with inappropriately low or normal phosphate levels, renal phosphate wasting from other causes should be suspected. Fractional excretion of phosphate might also be falsely low as the decreased eGFR can potentially hinder phosphate excretion. Early detection and accelerated work up could potentially lead to early diagnosis and appropriate treatment.