Kidney Week

Abstract: SA-PO0319

Special K, Special Trouble: Ketamine Bladder Syndrome Unmasked by Life-Threatening AKI

Session Information

• AKI: Epidemiology and Risk Factors
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

• Hoch, Virginia, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States

Virginia Hoch, MD, MPH

• Moorthi, Kmlst, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States

Kmlst Moorthi, MD, FASN

Introduction

Ketamine’s rising popularity as a recreational drug has unmasked previously underappreciated toxicities. More than 20% of chronic users develop ketamine bladder syndrome (KBS), a constellation of lower and upper urinary tract pathology including urinary urgency, suprapubic pain, papillary necrosis, and obstructive uropathy. Early symptoms may mimic cystitis, leading to diagnostic delay, irreversible uropathy, and renal dysfunction. We report a case of KBS presenting with severe acute kidney injury (AKI) and life-threatening electrolyte derangements.

Case Description

A 38-year-old woman was brought to the emergency department with agitation and suspected intoxication. She was tachycardic, hypertensive, and encephalopathic. Laboratory work up is shown in Table 1. ECG showed peaked T waves. CT imaging revealed severe bilateral hydroureteronephrosis without calculi. She was medically stabilized and transferred to the ICU. She was initially anuric despite Foley catheterization but urine output then improved. Over the following days, the AKI and hyperkalemia resolved; hyponatremia was corrected gradually with free water restriction. Upon further probing, she disclosed long-standing ketamine use. Pre-discharge imaging showed persistent bilateral hydroureteronephrosis, which continued on outpatient follow-up.

Discussion

Though ketamine has historically been considered a relatively “safe” recreational agent, uropathy is an increasingly recognized complication that may lead to severe renal dysfunction. Proposed mechanisms include direct urothelial toxicity, detrusor and ureteral fibrosis, and reduced bladder compliance leading to functional outlet obstruction without obstructing lesions. Prompt ketamine cessation is the cornerstone of management; however, urodynamic abnormalities may persist despite abstinence, and refractory cases may require surgical reconstruction. This case highlights the importance of maintaining a high index of suspicion for KBS in young patients presenting with otherwise unexplained obstructive uropathy or AKI, particularly when standard etiologies are absent. Early recognition offers the best opportunity to prevent irreversible renal injury.