Abstract: SA-PO0336
Biopsy-Proven Myoglobin Cast Nephropathy with Normal Levels of Serum Creatine Kinase After Initiation of Semaglutide
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
- Marnet, Erica, Yale School of Medicine, New Haven, Connecticut, United States
- Onuchic, Fernando, Yale School of Medicine, New Haven, Connecticut, United States
- Al-kharouf, Issa, Yale School of Medicine, New Haven, Connecticut, United States
- Rao, Arundati, Yale School of Medicine, New Haven, Connecticut, United States
Introduction
Myoglobin induced acute kidney injury (M-AKI) is a well-recognized injury pattern in the context of rhabdomyolysis and accounts for 7 – 10% of AKI cases in the US. Semaglutide has been associated with AKI, specifically prerenal given GI SA and AIN. We present a case of biopsy-proven myoglobin cast nephropathy with minimal elevation of CK, a week following initiation of semaglutide.
Case Description
50-year-old male with 2-year history of orthotopic heart transplant, CKD (baseline Cr 1.5 mg/dL), DM, and alcohol use presented with volume overload and oliguria, despite diuretics. A week prior to presentation, semaglutide was prescribed with the development of diarrhea, anorexia, nausea, and vomiting. Despite reduced oral intake, he continued to exercise and take diuretics, ARB, and MRA. Exam was notable for bilateral LE edema, without focal weakness. His chemistry was notable for Cr of 9.31, gap metabolic acidosis, low rapamycin levels, and urinalysis with 2+ protein, pyuria, microscopic hematuria. UPCR was 1.2g/g, and UACR 500mg/g. CT A/P showed bilateral perinephric stranding. CK was 306 U/L. On admission, semaglutide, ARB, MRAs were held. Given pyuria and concern for AIN, he was started on pulse dose steroids. His kidney biopsy showed severe acute tubular injury with myoglobin casts, 20% of IFTA, patchy tubulointerstitial nephritis. SV40 and IF were negative. Steroids were rapidly tapered; he required 4 HD treatments, followed by renal recovery to baseline GFR. Statins were temporarily discontinued, and repeat CPK remained normal. Semaglutide was not resumed.
Discussion
Our case illustrates that low CK levels do not exclude M-AKI. Cases reported with CK < 5,000 U/L occurred in the context of dehydration, acidosis, and delayed presentation. We suspect semaglutide initiation contributed to AKI; though prior reports describe prerenal azotemia or AIN. High index of suspicion, drug discontinuation, and supportive care are essential for favorable outcomes.
(A) IHC for Myoglobin; (B) H&E showing patchy tubulointerstitial nephritis