Treatment of Fibroblast Growth Factor-23-Mediated Renal Phosphate Wasting With Burosumab in a Patient With Chronic Kidney Disease 3b: A Case Report

We describe the case of a 72-year-old man with chronic kidney disease (CKD) 3b due to hypertensive nephrosclerosis, noted to have persistent hypophosphatemia and mildly elevated fibroblast growth factor-23 (FGF-23). His serum phosphorus level was chronically low, averaging 1.6 mg/dL, despite taking six to eight 250 mg packets of an oral elemental phosphate supplement daily. His parathyroid hormone (PTH) level was 204 pg/mL (normal range: 10-65 pg/mL), and his serum alkaline phosphatase (ALP) level was within the normal range at 55 U/L. His fractional excretion of phosphate was found to be 59%, confirming excessive urinary losses as the primary reason for the low serum phosphorus levels. Numerous PET/CT scans failed to localize an FGF-23-producing tumor. As part of his treatment plan, he was started on burosumab 50 mg injected subcutaneously every four weeks. Within six weeks, his serum phosphorus normalized, and oral supplementation was discontinued. His PTH level normalized, and his kidney function stabilized after an acute kidney injury. No further adverse events occurred, and he tolerated the burosumab without issue. This current case illustrates successful correction of renal phosphate wasting with burosumab in a patient with CKD and non-localizable FGF-23. This suggests that targeted anti-FGF-23 therapy can be considered for intolerable or ineffective conventional therapy even in moderate CKD.