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Abstract: PO0177

Reflex Anuria: A Forgotten Urologic Etiology of AKI

Session Information

  • AKI Mechanisms - 1
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms

Authors

  • Mahmoud, Hassan, Boston Medical Center, Boston, Massachusetts, United States
  • Bhatia, Jasvinder S., Boston Medical Center, Boston, Massachusetts, United States
Introduction

Reflex anuria (RA) is a rare entity that can lead to severe acute kidney injury (AKI). It was defined by Hull and colleagues in 1980 as “cessation of urine output from both kidneys in response to irritation or trauma to one kidney or its ureter or severe painful stimuli to other pelvic organs”. RA represents a gray area between nephrology and urology that should be considered in the differential diagnosis of AKI. We present a case of AKI and anuria where the prompt recognition and management of RA resulted in full recovery of kidney function and avoidance of renal replacement therapy and unnecessary testing.

Case Description

A 40-year-old male with Crohn's disease status post prior right and left hemicolectomy was admitted with worsening abdominal pain and hematochezia consistent with Crohn's flare. He underwent open abdominoperineal resection. Pre-operatively, urology performed cystoscopy and prophylactic bilateral ureteral stent placement. Stents were removed without complication at the end of the case. On post-op day 1, he developed oliguria that progressed to complete anuria. This was associated with rapid rise in serum creatinine up to 5.5 from baseline of 0.6 (Figure 1). The differential diagnosis was broad, including acute tubular necrosis, vascular thrombosis and obstruction, but because of the temporal relationship with recent procedures, RA was suspected as the etiology of AKI. Patient underwent urgent bilateral ureteral stent placement which was followed by brisk urine output (~11 L/24 hours) and normalization of serum creatinine.

Discussion

RA is a rare diagnosis that requires high index of clinical suspicion. It is a functional rather than parenchymal disease that can cause dramatic cessation of urine output and AKI. Neurovascular reflex leading to arteriolar vasoconstriction and ureteric spasm is a proposed mechanism. This case illustrates that acute anuria and AKI after surgical procedures should prompt nephrology consultants to consider this uncommon diagnosis.

Figure 1. Acute rise in serum creatinine on post-op day 1 followed by rapid resolution of AKI after bilateral ureteral stent placement.