Abstract: SA-PO0335
When Statins Strike Twice: Seronegative Necrotizing Myopathy Causing Dialysis-Dependent AKI from Myoglobin Cast 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
- Dabech, Abdulaziz, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Chatterjee, Totini S., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Mauiyyedi, Shamila, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
Introduction
Statin-associated necrotizing autoimmune myopathy (NAM) is a rare complication typically associated with anti-HMGCR antibodies. While mild creatine kinase (CK) elevation is common, progression to severe rhabdomyolysis and dialysis-dependent acute kidney injury (AKI) from myoglobin cast nephropathy is exceedingly uncommon. Seronegative NAM is challenging to diagnose, and reports of severe renal involvement remain limited.
Case Description
A 77-year-old man with hypertension, hyperlipidemia and prior rosuvastatin use presented with 4 months of progressive proximal lower extremity weakness, night sweats, and anorexia. Initial labs showed hyponatremia (Na 122 mmol/L) and serum creatinine (SCr) 1.3 mg/dL. He developed oliguric AKI (SCr peaking at 8.5 mg/dL) requiring 3 hemodialysis sessions. CK peaked >14,400 U/L. SPEP identified an IgM kappa spike (0.5 g/dL) consistent with MGUS; cryoglobulins were negative. Thigh MRI showed diffuse intramuscular edema indicating inflammatory myopathy. Kidney biopsy revealed acute tubular injury with myoglobin-positive granular casts, confirming myoglobin cast nephropathy. Immunofluorescence showed mild mesangial IgA and C3 without kappa/lambda restriction in deposits, casts, or droplets. Muscle biopsy demonstrated necrotizing myopathy with minimal inflammation. Extended myositis serologies (including anti-HMGCR, SRP, Jo-1, Mi-2, MDA5, TIF-1γ) were negative, establishing seronegative NAM. He received pulse-dose steroids, IVIG, and mycophenolate mofetil with a prednisone taper. Despite initial HD-dependence, SCr improved to 1.4 mg/dL with reduced proteinuria within 3 weeks.
Discussion
This case demonstrates biopsy-proven myoglobin cast nephropathy causing HD-dependent AKI in statin-associated seronegative NAM. The absence of myositis-specific antibodies highlights serologic limitations and the critical role of tissue diagnosis. Concurrent IgM kappa MGUS and mesangial IgA deposition represents an unusual constellation. Substantial renal recovery following early immunosuppression suggests severe, HD-requiring AKI in NAM is potentially reversible. These findings expand the clinical spectrum of statin-associated NAM and underscore the need for early recognition of seronegative disease with severe renal complications.