Abstract: TH-PO0086
Crystal-Clear Clues: Atypical Cause of AKI in a Patient with Septic Shock
Session Information
- AKI: Pathogenesis and Disease Mechanisms
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Bowling, Carly M, Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Nguyen, Julia, Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Joshi, Megha Raj, Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Watson, Maura A., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
Introduction
Acute rise in serum uric acid (SUA) can cause acute kidney injury (AKI), commonly in high cell turnover states such as tumor lysis syndrome (TLS) or rhabdomyolysis via crystal dependent mechanisms. Mild SUA elevations also contribute to AKI via local inflammation, increased oxidative stress, and renin-angiotensin-aldosterone system activation. Studies suggest hyperuricemia is an independent risk factor for AKI in hospitalized patients, but little evidence exists to support use of urate lowering therapy (ULT) outside of TLS. We present a patient with multifactorial AKI, large urine uric acid crystal burden and hyperuricemia who improved after ULT.
Case Description
A 62-year-old female with a history of vascular disease and recent above the knee amputation (AKA) was admitted to surgical intensive care for postoperative wound infection and septic shock. Operative assessment revealed extensive tissue necrosis of her AKA stump. Her creatinine (Cr) rose from 1.1 mg/dL to 2.75 mg/dL. Post-operative creatinine kinase (CK) was 1,004 U/L. Urine microscopy had muddy brown casts and too numerous to count uric acid crystals which prompted check of SUA (9.1 mg/dL) and urine pH (5.0). G6PD and lead levels were normal. Allopurinol and bicarbonate drip for urine alkalinization were started with rapid Cr improvement, SUA normalization and reduced crystals on serial urine microscopy.
Discussion
Critically ill patients with multifactorial AKI may face worsening renal injury from hyperuricemia with possible crystal nephropathy. Our patient’s hyperuricemia may have been due to tissue hypoxia and necrosis causing a pseudo-TLS. Her CK level and SUA were collected post amputation and tissue washout, making higher pre-procedure levels possible. Evidence has suggested that hypovolemia with acute SUA rise and acidic urine, leads to renal uric acid precipitation associated with AKI. ULT leads to SUA normalization and improved renal function, as was shown in this case. Multimodal AKI treatment approaches, to include ULT, may be indicated in patients with hyperuricemia and clinical conditions consistent with possible crystal nephropathy.
The views expressed in this abstract are those of the author(s) and do not necessarily reflect the official policy of the Department of Defense or the United States Government.