Abstract: PUB018
Zoledronic Acid-Associated Proximal Tubular Dysfunction and AKI: A Case Report
Session Information
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Alle, Naga Ruthvika, Penn Medicine, Philadelphia, Pennsylvania, United States
- Malchione, Nicholas M., Penn Medicine, Philadelphia, Pennsylvania, United States
- Hilburg, Rachel, Penn Medicine, Philadelphia, Pennsylvania, United States
Introduction
Zoledronic acid is a commonly used bisphosphonate for treatment of hypercalcemia of malignancy. Nephrotoxicity is reported with its use, the mechanism of which is believed secondary to tubular injury via endocytic uptake by tubular cells. Here we report a case of acute kidney injury (AKI) with proximal tubular injury/likely acquired Fanconi syndrome following administration of intravenous zoledronic acid.
Case Description
An 83-year-old woman with non-small cell lung cancer with recently diagnosed bone metastases presented to the hospital with generalized weakness and altered mental status. She was found to have severe, symptomatic hypercalcemia with a serum calcium of 14.5 mg/dL; 15.9mg/dL when corrected for hypoalbuminemia, with an ionized calcium of 2.07 mmol/L. On presentation, her serum creatinine (SCr) was at her baseline of 0.9 mg/dL, with no history of underlying kidney disease. For her hypercalcemia, she promptly received isotonic IV fluids and zoledronic acid 4mg IV. On hospital day 2, she received calcitonin, furosemide IV bolus, and continued fluids. On hospital day 4, her calcium normalized and maintenance fluids were discontinued. She developed an AKI on hospital day 7 with SCr 1.3 mg/dL, which further increased to a peak of 2.2 mg/dL. This was associated with new onset glucosuria with euglycemia, hypophosphatemia, hypokalemia, metabolic acidosis, and an elevated urine protein:creatinine ratio of 5.6 mg/mg. Urine microscopy showed numerous granular casts. This constellation of findings raised concern for proximal tubular dysfunction/Fanconi syndrome. The patient continued to require daily phosphorus and potassium repletion, and SCr remained 2.2mg/dL. Later the patient was deemed not to be a candidate for further cancer directed therapies and was ultimately transitioned to hospice.
Discussion
This case adds to the fund of knowledge of the association of zoledronic acid with tubular injury, specifically proximal tubular injury/acquired Fanconi syndrome. This patient presented with remarkably stable kidney function despite the severity of her hypercalcemia but went on to develop tubular injury following zoledronic acid administration. It is a reminder to clinicians to try to minimize risk factors for tubular injury in the peri-administration period even in patients presenting with normal kidney function.