Low-Flow Acute Kidney Injury: The Pathophysiology of Prerenal Azotemia, Abdominal Compartment Syndrome, and Obstructive Uropathy.

Bruce A Molitoris

Journal: Clinical journal of the American Society of Nephrology : CJASN 2022;17(7):1039-1049

PMID: 35584927

Abstract

AKI is a syndrome, not a disease. It results from many different primary and/or secondary etiologies and is often multifactorial, especially in the hospitalized patient. This review discusses the pathophysiology of three etiologies that cause AKI, those being kidney hypoperfusion, abdominal compartment syndrome, and urinary tract obstruction. The pathophysiology of these three causes of AKI differs but is overlapping. They all lead to a low urine flow rate and low urine sodium initially. In all three cases, with early recognition and correction of the underlying process, the resulting functional AKI can be rapidly reversed. However, with continued duration and/or increased severity, cell injury occurs within the kidney, resulting in structural AKI and a longer and more severe disease state with increased morbidity and mortality. This is why early recognition and reversal are critical.

Copyright © 2022 by the American Society of Nephrology.

Address: Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, and Department of Anatomy, Cell Biology and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
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