Abstract: SA-PO0341
Zoledronic Acid-Associated Acute Interstitial Nephritis, Acute Tubular Injury, and Myoglobin Nephropathy
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Bui, Albert, Mayo Clinic in Florida, Jacksonville, Florida, United States
- Edwards, Eric, Mayo Clinic in Florida, Jacksonville, Florida, United States
- Manohar, Sandhya, Mayo Clinic in Florida, Jacksonville, Florida, United States
- Salem, Fadi E., Mayo Clinic in Florida, Jacksonville, Florida, United States
- Baker, Lyle Wesley, Mayo Clinic in Florida, Jacksonville, Florida, United States
Introduction
Zoledronic acid is an intravenous (IV) bisphosphonate associated with acute tubular injury (ATI), collapsing focal segmental glomerulosclerosis, Fanconi syndrome, and thrombotic microangiopathy. Acute interstitial nephritis (AIN) is rarely reported, let alone concurrent myoglobin nephropathy. We present a biopsy-proven case of severe acute kidney injury (AKI) associated with concomitant AIN, acute tubular injury, and myoglobin nephropathy following zoledronic acid exposure.
Case Description
A 74-year-old female with chronic kidney disease stage 3a (baseline serum creatinine [sCr] 1.0-1.2 mg/dL), osteoporosis, and hyperlipidemia on chronic rosuvastatin (20 mg daily) presented with hypoglycemia and was incidentally found to have AKI stage 3. Her sCr was 1.2 mg/dL one day prior to IV zoledronic acid administration. Approximately 10 days later, she presented with severe AKI.
Labs demonstrated sCr 10.45 mg/dL, bicarbonate 16 mEq/L, creatine kinase 365 U/L (reference range 26-192 U/L), pyuria, hematuria, urine protein-creatinine ratio 2.43 g/g and unrevealing serologic evaluation. Despite empiric antibiotics and volume repletion, kidney function worsened, prompting kidney biopsy. Histopathology demonstrated diffuse ATI with eosinophilic casts, hypersensitivity-type AIN with scattered eosinophils, and focal myoglobin-positive tubular casts consistent with myoglobin nephropathy (Figure 1).
Given the temporal association, findings were attributed to zoledronic acid toxicity, potentially worsened by concurrent rosuvastatin use. After glucocorticoid therapy, kidney function returned to baseline over 10 weeks.
Discussion
Bisphosphonate nephrotoxicity most commonly manifests as acute tubular injury; however, biopsy-proven AIN remains rare. This case showed concurrent AIN, acute tubular injury, and myoglobin nephropathy following recent zoledronic acid exposure. Although CK elevation was modest, biopsy demonstrated myoglobin-positive casts supporting pigment-associated tubular injury. Zoledronic acid and statins both inhibit key enzymes in the mevalonate pathway, thereby reducing ubiquinone and inhibiting ATP synthesis. Overall, this can lead to muscle cell apoptosis. This case highlights the importance of considering multiple concurrent mechanisms of kidney injury in patients receiving IV bisphosphonates and reinforces the diagnostic value of kidney biopsy in severe or atypical AKI presentations.