ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: FR-PO693

Use of Anti-FGF-23 Monoclonal Antibody for the Treatment of Severe Hypophosphatemia Secondary to Tumor-Induced Osteomalacia

Session Information

Category: Trainee Case Report

  • 1500 Onco-Nephrology

Authors

  • Lucas, Anika, Duke University, Durham, North Carolina, United States
  • Ortiz Melo, David I., Duke University Medical Center, Durham, North Carolina, United States
  • Wolf, Myles, Duke University, Durham, North Carolina, United States
Introduction

Hypophosphatemia in patients with cancer may be due to poor oral intake or more commonly from drug-induced tubulopathies leading to renal phosphate wasting. Tumor-induced osteomalacia (TIO), also known as oncogenic osteomalacia, is a rare paraneoplastic cause of hypophosphatemia and hyperphosphaturia, as a result of constitutive release of fibroblast growth factor-23 (FGF-23). Here we present a case of profound hypophosphatemia secondary to oncogenic osteomalacia that improved with administration of burosumab, a monoclonal IgG1 antibody against FGF-23.

Case Description

A 68-year-old man with history of metastatic prostate cancer s/p prostatectomy, presented with several months of generalized weakness, worsening fatigue, muscle cramps and paresthesia. A whole-body bone scan showed extensive osseous metastatic disease. Laboratory data revealed serum phosphorus of 0.9mg/dL and inappropriately elevated random urinary phosphate (125 mg/dL; FEPO4 70%), indicative of renal phosphate wasting. His renal function was normal (serum creatinine 0.9 mg/dL) and ionized calcium was 1.07 mmol/L (normal 1.15-1.32mmol/L). Further work up revealed 25(OH)-Vitamin D level of 40 ng/mL and 1,25 (OH)2Vitamin D level of 28 pg/mL. His serum FGF-23 levels were remarkably elevated (812 RU/mL, normal <180 RU/mL). Patient was diagnosed with oncogenic osteomalacia and was initially treated with oral phosphate and active vitamin D supplementation, which was unsuccessful (serum phosphorous persistently <1.0 mg/dL). He was then started on burosumab 90 mg every 2 weeks. After three doses, his phosphorus levels increased to 2 mg/dL and 1,25 (OH)2Vitamin D level increased to 62 pg/mL.

Discussion

Burosumab is a human IgG1 monoclonal antibody directed against FGF-23 that has been approved for X-linked hypophosphatemia. By decreasing levels of FGF-23, burosumab increases both renal reabsorption and gastrointestinal absorption of phosphorus. Although burosumab is not yet approved for the treatment of hypophosphatemia in oncogenic osteomalacia, our case reveals another application for burosumab in this setting, specially in patients with refractory and symptomatic hypophosphatemia.