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: PO1194

Severe Hypophosphatemia Induced by Oncogenic Osteomalacia

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Jalal, Abdullah, Overlook Medical Center, Summit, New Jersey, United States
  • Brown, Ryan Patrick, Overlook Medical Center, Summit, New Jersey, United States
Introduction

Oncogenic Osteomalacia (OncOM) is an uncommon paraneoplastic syndrome characterized by FGF-23 overexpression from benign mesenchymal tumors causing severe hypophosphatemia. Very few cases of OncOM with concomitant paraneoplastic syndromes have been described. Herein we present a rare case of carboplatin-associated hyponatremia in the setting of SiADH-induced chronic hyponatremia unmasking an even rarer secondary paraneoplastic syndrome; oncogenic osteomalacia.

Case Description

A 52 year old male with past medical history of chronic hyponatremia on salt tablets secondary to recently diagnosed metastatic small cell lung cancer was admitted for initiation of chemotherapy with carboplatin/etopside. Two days after competing cycle 1 the patient developed acute hyponatremia; serum Na decreased from 141 to 129 mEq/L. Serum electrolytes were (mEq/L): K 3.9, Cl 94, HCO3 28, BUN 20, Cr 0.47. Cortisol (17.8 ug/dl) and TSH (2.28 uIU/ml) were within normal limits. Urine studies noted (mEq/L): Na 75, Cl 69, K 43.5, elevated osmolality 860 mOsm/kg. Etiology of acute hyponatremia was attributed to platinum chemotherapy in the setting of SCC-associated SiADH and patient was treated with tolvaptan after several days of non-response to fluid restriction and urea. Patient’s hyponatremia subsequently corrected but was incidentally noted to have severe hypophosphatemia (<1 mEq/L) refractory to aggressive IV and PO phosphate repletion. ALP was elevated 279 U/L, corrected Ca 10 mEq/L, low 25(OH)-vitamin D 23.8 ng/mL, normal PTH 45.6 pg/mL and PTHrP <0.4 pmol/L. Urinary fractional excretion of phosphorus was increased at 24%. An FGF-23 level obtained 12 days after completing cycle 1 of carboplatin-etopside was considerably elevated at 219 pg/mL. Thus, the patient was diagnosed with oncogenic osteomalacia.

Discussion

This case highlights a unique and diagnostically challenging patient presentation of severe hypophosphatemia in the setting of dual paraneoplastic syndromes. OncOM should be considered in the differential for severe refractory hypophosphatemia. This occurs via FGF-23 mediated downregulation of PCT Na-Pi transporters and 1a-hydroxylase causing renal phosphate wasting and reduced 1,25-hydroxyvitamin D levels. Over time chronic hypophosphatemia impairs bone mineralization causing osteomalacia. Measurement of the fractional excretion of phosphorus is critical and FGF-23 levels should be obtained to confirm diagnosis.