Abstract: SA-PO0104
Rosuvastatin-Induced Acute Tubular Injury Not Associated with Rhabdomyolysis
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Moseley, Allen Kai, Ochsner Health, New Orleans, Louisiana, United States
- Power, Kieran D, Ochsner Health, New Orleans, Louisiana, United States
- Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States
Introduction
Rosuvastatin can lead to acute kidney injury (AKI) due to rhabdomyolysis. Other forms of AKI associated with rosuvastatin are extremely rare. We report a case of a patient who developed AKI due to severe acute tubular injury (ATI) without evidence of rhabdomyolysis associated with exposure to rosuvastatin that promptly resolved following drug discontinuation.
Case Description
A 65-year-old man with hypertension, hyperlipidemia and chronic kidney disease stage 3B presented to clinic for a routine follow-up visit. He had a baseline serum creatinine (sCr) 1.8 mg/dL and urine protein-to-creatinine ratio (UPCR) 0.4 g/g. Two months prior, sCr had increased to 4.2 mg/dL and his primary care provider had stopped valsartan. Labs were repeated and showed a sCr 2.5 mg/dL, so valsartan was resumed at a lower dose. But sCr rose again to 3.8 mg/dL. In addition to valsartan, he was taking benzonatate, rosuvastatin, amlodipine, fish oil, vitamin C and albuterol. He denied NSAIDs or over-the-counter supplements. CPK was normal. UPCR was 0.9 g/g. Urinary sediment microscopy (uSEDI) revealed massive amount of “muddy” brown granular casts (MBGC). Valsartan was stopped again, but sCr remained 3.9 mg/dL. Renal Doppler was performed out of concern for valsartan-triggered ischemic ATI from renal artery stenosis (RAS), but it was normal. One week later, uSEDI revealed persistence of abundant MBGC. A kidney biopsy was performed, which showed ATI, unremarkable glomeruli, and stripped fibrosis. The latter finding renewed the suspicion for an ischemic vascular disorder, but a renal CO2 angiogram was performed and verified absence of RAS. A third uSEDI showed the same results. Based on rare reports found on PubMed, rosuvastatin was stopped. Two weeks later, sCr improved to 1.9 mg/dL, uSEDI turned completely bland and UPCR dropped to 0.1 g/g.
Discussion
Typically statin-induced AKI is linked to rhabdomyolysis. However, our case highlights the rare occurrence of rosuvastatin-induced ATI independently of muscle breakdown. uSEDI can be useful to diagnose and manage this entity. The pathogenesis for the mechanism of injury is not fully understood but there is some evidence for decreased receptor-mediated endocytosis in proximal renal tubules by statins. Practitioners must be cognizant of this potential complication of rosuvastatin use.