Abstract: SA-PO0964
Kidneys Don't Lie, but Supplements Might?
Session Information
- Pathology: Updates and Insights
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1800 Pathology and Lab Medicine
Authors
- Bommireddi, Akshay, Harbor-UCLA Medical Center, Torrance, California, United States
- Nast, Cynthia C., Cedars-Sinai, Los Angeles, California, United States
- Dukkipati, Ramanath B., Harbor-UCLA Medical Center, Torrance, California, United States
- Shah, Anuja P., Harbor-UCLA Medical Center, Torrance, California, United States
Group or Team Name
- Harbor-UCLA Nephrology.
Introduction
Interstitial nephritis (IN) is an inflammatory process affecting the kidney interstitium with or without tubular inflammation. Frequent causes include medications, infections and autoimmune disorders. Creatine supplements have been associated with elevated serum creatinine, but its nephrotoxicity is controversial. Here we describe a case where creatine supplement ingestion likely induced acute on chronic IN. Cystatin C was used as a confirmatory marker for kidney function.
Case Description
A 27-year-old man presents with a 6 week history of abdominal pain and diarrhea. Three months prior he started a new creatine supplement for muscle strength, taking about 5g/day. He denied any other medication, supplement, or drug use. The admission serum creatinine was 5.81 mg/dL and Cystatin C was 2.03 mg/L. Urinalysis showed > 50 white blood cells, no red blood cells, and 50mg/dL of protein. CT abdomen pelvis showed no evidence of renal stones or hydronephrosis, but illustrated loss of haustra throughout the colon with terminal ileum wall thickening. Colonoscopy findings showed ulcerative colitis (UC). Renal biopsy showed acute on chronic tubulointerstitial nephritis with findings suggestive of exposure to a tubulotoxin (Figure 1). The patient was advised to stop supplement intake and started on methylprednisolone pulse therapy, followed by prednisone taper over six weeks. One month after presentation, the creatinine improved to 2.68 mg/dL with a Cystatin C of 1.76. He has yet to start mesalamine therapy for UC.
Discussion
Possible etiologies for the patient's IN include the creatine supplement and UC. IN occurs less often in UC compared to Crohn's disease, usually after mesalamine therapy, and coupled with the tubular cell dysmorphic lysosomes, are more suggestive of tubulotoxin exposure as the cause in this patient. This case highlights the role of tubular cell findings in toxin induced IN, which helped with diagnosis and treatment for this patient. It also brings awareness of the discordance between Cystatin C and creatinine based estimates of kidney function in patients taking creatine.