Abstract: PO0302
Oxandrolone-Induced Acute Tubular Necrosis
Session Information
- AKI: Trainee Case Reports
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Zambrano, Cesar, Mount Sinai Medical Center, Miami Beach, Florida, United States
- Celis, Valentina, Mount Sinai Medical Center, Miami Beach, Florida, United States
- Olayiwola, Ayoola O., Mount Sinai Medical Center, Miami Beach, Florida, United States
- Barreiro Sacco, Susana, Mount Sinai Medical Center, Miami Beach, Florida, United States
Introduction
Oxandrolone is an anabolic-androgenic steroid (AAS) indicated as adjunctive therapy to promote weight gain in chronic wasting conditions. It is also used off-label by many sports and bodybuilding enthusiasts to increase muscle mass. Common adverse effects include transient elevations in transaminase levels and reduction in HDL cholesterol level. Mostly, kidney complications occur after long-term administration. Renal disorders range from a mild, reversible rise in serum creatinine and BUN to irreversible CKD and FSG. We hereby present a case of acute tubular necrosis in the setting of Oxandrolone use.
Case Description
A 30-year-old previously healthy male presented to the ED with complaints of nausea and vomiting. He reported intentional caloric restriction and intense exercise over the past month, along with using under-the-counter oral Oxandrolone. Labwork revealed AGMA and ketosis (CO2 17.2mmol/L, AG 24.4 mmol/L, β-hydroxybutyrate 48.97 mg/dL) elevated Creatinine (2.8 mg/dL). Glucose, LFTs and CPK were WNL. UA revealed Ketones, Protein 100 mg/dL, RBC 10-25. US and CT of abdomen and pelvis were unremarkable. He was started on IVF and anti-emetics with resolution of symptoms and starvation ketoacidosis. Renal function, however, progressively worsened. BUN/Cr < 20, FeNa 1.4% and no improvement with IVF was consistent with intrarenal etiology. Further work up revealed low C3, normal C4, negative ANA, ANCA, GBM Ab, dsDNA Ab, ASO, LAC, Cryoglobulin, Hepatitis B and Hepatitis C serology. Kidney biopsy was performed given rapid deterioration of renal function with creatinine peak at 6.06. Histology, Immunofluorescence and Electron Microscopy revealed ATN with unremarkable glomeruli. Kidney function gradually improved after 8 days, and patient was discharged in stable condition with follow up with nephrologist.
Discussion
Use of AAS has risen into a worldwide substance abuse problem. Although renal damage secondary to AAS use is rare, they have been demonstrated to cause glomerular damage as FSGS. Tubular injury, however, has only been seldomly reported in the setting of AAS use. Given the rise of uncontrolled use of AAS and the rarity of this type of injury in an otherwise young and healthy population, it is important to inquire further on a possible direct causal relationship. Increased compound risk with commonly coexistent excess creatine and protein intake should also be considered.