Abstract: SA-PO0093
Perfusion Under Pressure: Reversing Anuric AKI with Targeted Intra-Abdominal Pressure (IAP) Reduction
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 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
- Nemalidinne, Krishna Vani, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Vanteru, Abinay Siva kumar Reddy, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Chevireddy, Akshara, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Ravula, Sreelakshmi, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Karakala, Nithin, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Holthoff, Joseph H., University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
Introduction
Intra-abdominal hypertension (IAH) is a commonly underrecognized cause of acute kidney injury (AKI). Elevated intra-abdominal pressure (IAP) impairs venous return, reduces renal perfusion, and lowers cardiac output, ultimately leading to decreased eGFR and AKI. We present our approach to managing AKI in a morbidly obese patient with IAH.
Case Description
A 44-year male with decompensated cirrhosis was admitted with severe volume overload. On examination, patient had anasarca, 3+ pedal edema. He reported a 20-pound weight gain within few weeks and was oozing fluid from the skin. CT abdomen also reported moderate pelvic ascites, splenomegaly, mesenteric edema, and vascular congestion. The patient developed anuric AKI, with an initial creatinine of 2.4. CRRT was initiated with aggressive UF to manage volume overload. Simultaneously, IAP was monitored daily using the Accuryn Monitoring System, which uses bladder pressure as a surrogate marker for IAP. The initial IAP was elevated at 22, contributing to poor renal perfusion and persistent anuria. To optimize renal perfusion, we targeted abdominal perfusion pressure (APP) >65 mmHg, which was achieved by a higher MAP goal, guided by the formula: MAP > 65 mmHg + IAP, using vasopressor support as needed. With gradual yet aggressive UF, the patient's weight (down by 70 pounds in just 10 days) and IAP decreased significantly. As IAP values decreased, urine output significantly improved, and the patient transitioned from anuria to oliguria and ultimately to normal urine output, reaching a baseline creatinine of 0.7.
Discussion
Aggressive UF via CRRT not only corrected the fluid imbalance but also resulted in a marked reduction in IAP, directly improving kidney function. This strategy underscores the dynamic interplay between volume status, abdominal pressure, and renal perfusion. This case supports the integration of IAP monitoring into AKI management protocols in critically ill patients.