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


The Latest on Twitter

Kidney Week

Abstract: FR-PO683

Hypophosphatemia and Fibroblast Growth Factor 23 Producing Metastatic Breast Cancer

Session Information

Category: Trainee Case Report

  • 1500 Onco-Nephrology


  • Gutgarts, Victoria, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Glezerman, Ilya, Memorial Sloan Kettering Cancer Center, New York, New York, United States

Fibroblast growth factor-23 (FGF23) is a key regulator of phosphate metabolism and downregulates expression of cotransporters in the kidney essential for phosphate reabsorption. FGF23 mutations cause inherited renal phosphate wasting diseases leading to osteomalacia in adults. In the paraneoplastic setting, FGF23 over secretion leads to tumor-induced osteomalacia (TIO) also known as oncogenic osteomalacia.

Case Description

47-year-old woman with metastatic breast cancer was evaluated for persistent hypophosphatemia. First diagnosed with left mammary duct carcinoma in 2013, she underwent partial mastectomy followed by chemotherapy. She had a reoccurrence in 2016 and failed multiple lines of chemotherapy with new metastasis to the liver and several osseous lesions. Patient was initiated on monthly denosumab one year prior to current visit, with last dose one month ago, for metastatic bone involvement. Phosphorous level on consultation was <0.9 (2.5-4.5)mg/dl with no prior laboratory values. Calcium level was 7.4 (8.5-10.5)mg/dl and Alkaline Phosphatase level was 738 (< = 130)U/L. The fractional urinary excretion of phosphate was elevated at 56%. Etiology for hypophosphatemia was initially thought to be secondary hyperparathyroidism given elevated PTH 488 (12-88)pg/ml due to hypocalcemia in the setting of recent denosumab administration. Phosphorous levels remained low despite aggressive oral calcium and phosphate repletion and oral calcitriol. Given persistent hypophosphatemia, FGF23 was checked and levels returned strikingly elevated at 2430 (< = 180)RU/ml suggesting an FGF23 secreting tumor as the most likely cause for severe hypophosphatemia. Oral phosphate supplementation was continued, though unfortunately, given progression of disease, palliative measures were chosen with a focus on comfort care.


TIO is a rare paraneoplastic syndrome, but when present, downstream effects of phosphaturia can lead to profound weakness and skeletal collapse. Though prior reports have identified bone or soft tissue as the primary site, the case above is unique since the syndrome occurred in metastatic disease with a primary breast cancer. Recognition of TIO is essential since patients that have solitary lesions may undergo resection which may be curative. In patients with several lesions or metastatic cancer, medical therapy can be attempted to improve the quality of life.