Abstract: SA-PO0358
A Young Man with Uremia, Severe Hyperkalemia, Bilateral Hydronephrosis, and Vanished Bladder
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
- Ohonba, Nosagie, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Sedlacek, Martin, Icahn School of Medicine at Mount Sinai, New York, New York, United States
Introduction
Most patients with uremia, severe hyperkalemia and an empty bladder despite IV saline require emergency hemodialysis. Here we present a rare case of postrenal insufficiency who got away without.
Case Description
A 32 y/o man presented to the ED with two weeks of nausea, vomiting, abdominal pain, syncopal events with falls and head strike. Imaging showed no head trauma or fracture. Blood tests revealed advanced renal insufficiency and severe hyperkalemia with potassium 8.5mEq/l, creatinine 5.82mg/dl, BUN 111mg/dl, bicarbonate 14mEq/l, chloride 88mEq/l, WBC 21k, Hb 9.1g/dl Platelets 790k. A renal ultrasound showed bilateral hydronephrosis and the bladder could not be visualized. A CT showed hydronephrosis, collapsed bladder and hyperemia of the ureteral and bladder walls. A Foley was placed and removed shortly after draining a small amount of urine because of severe pain. Urine toxicology screen was negative. Nephrology was called for emergent dialysis. The patient was not aware of kidney disease and had no family history of renal disease. He had no prior medical care or prior blood tests available. He was cachectic, chronically ill appearing with no other physical signs of uremia. He voided 200ml urine into a urinal during the exam. Repeat potassium after medical treatmet and IV fluids was 5.2mEq/l and the patient improved further and did not require dialysis. The patient revealed heavy ketamine use and a diagnosis of ketamine bladder was made.
Discussion
Ketamine produces toxic metabolites that are excreted by the kidney and cause severe inflammation in the urinary tract. As a result the bladder can shrink and produce renal insufficiency by urinary obstruction. Affected patients lack bladder capacity, have to urinate constantly and tolerate Foley catheters poorly. Ketamine bladder is thought to be irreversible. However, our patient’s serum creatinine decreased from 5.82mg/dl to 2.4mg/dl in eleven days of abstinence from ketamine during hospitalization. The patient was lost to follow up after discharge.