Abstract: SA-PO0587
Acquired Fanconi Syndrome Secondary to Zoledronate
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Moise, Altagracia C., Stamford Health, Stamford, Connecticut, United States
- St Gilus, Rose H., Stamford Health, Stamford, Connecticut, United States
- Rosen, Raphael Judah, Stamford Health, Stamford, Connecticut, United States
Introduction
Zoledronate is a bone antiresorptive used both for osteoporosis and for bone protection in oncology settings. While zoledronate is well recognized to cause acute kidney injury (AKI), Fanconi syndrome is a less recognized renal adverse effect, caused by direct toxic injury to proximal tubular epithelial cells, resulting in generalized proximal tubular dysfunction. We present a case of Fanconi syndrome developing after zoledronate initiation
Case Description
A 61-year-old woman with multiple myeloma on daratumumab and lenalidomide, with excellent disease control (negative SPEP and normal free light chain ratio), presented with one month of vomiting and diarrhea. Zoledronate had been initiated four months earlier. Laboratory evaluation showed acute kidney injury (creatinine 2.7 mg/dL from baseline 1.0 mg/dL), hypokalemia (3.2 mEq/L), and hypophosphatemia (1.6 mg/dL). Fractional excretion of potassium (FeK) was 39% and fractional excretion of phosphorus (FePO4) was 20%, consistent with renal wasting. Urinalysis demonstrated normoglycemic glycosuria. Zoledronate was held. Renal function and electrolyte abnormalities improved and subsequently normalized with intravenous fluids and repletion.
Three months later, zoledronate was resumed. One month after re-exposure, she was readmitted with recurrent acute kidney injury (creatinine 3.4 mg/dL), hypokalemia (2.6 mEq/L), and hypophosphatemia (1.8 mg/dL). FeK and FePO4 were markedly elevated at 74% and 73%, respectively. Additional workup revealed non-anion gap metabolic acidosis (bicarbonate 11 mEq/L), hypouricemia (uric acid 1.1 mg/dL), recurrent normoglycemic glycosuria, consistent with acquired Fanconi syndrome. Electrolyte abnormalities again improved with supportive therapy, and zoledronate was permanently discontinued. Renal function subsequently improved, and electrolyte supplementation is being tapered
Discussion
Fanconi syndrome in multiple myeloma is typically attributed to light chain-mediated proximal tubular injury; however, medication-induced disease should also be considered. This case highlights recurrent, reversible Fanconi syndrome associated with zoledronate exposure in a patient with otherwise well-controlled myeloma, making light chain-mediated disease unlikely. Clinicians should maintain awareness of bisphosphonate-associated Fanconi syndrome in patients presenting with recurrent hypophosphatemia, hypokalemia, metabolic acidosis, and glycosuria