Acute Kidney Injury: Definition, Pathophysiology and Clinical Phenotypes

Abstract

Acute kidney injury (AKI) is a clinical syndrome that complicates the course and worsens the outcome in a significant number of hospitalised patients. Recent advances in clinical and basic research will help with a more accurate definition of this syndrome and in the elucidation of its pathogenesis. With this knowledge we will be able to conduct more accurate epidemiologic studies in an effort to gain a better understanding of the impact of this syndrome. AKI is a syndrome that rarely has a sole and distinct pathophysiology. Recent evidence, in both basic science and clinical research, is beginning to change our view for AKI from a single organ failure syndrome to a syndrome where the kidney plays an active role in the progress of multi-organ dysfunction. Accurate and prompt recognition of AKI and better understanding of the pathophysiologic mechanisms underlying the various clinical phenotypes are of great importance to research for effective therapeutic interventions. In this review we provide the most recent updates in the definition, epidemiology and pathophysiology of AKI.

Figure 1.

Aetiologies of acute kidney injury

Figure 2.

Proposed mechanism of distal organ injury. AKI leads to distant organ injury through a combination of pro-inflammatory and oxidative stress-mediated mechanisms. Serum and distal organ cytokine levels (IL1, IL6, IL10 and TNFa) increase in conjunction with Leukocyte trafficking (neutrophil, lymphocyte and macrophage) and increased oxidative stress (superoxide dismutase, malondialdehyde, and glutathione depletion. In addition, sodium and water channel dysregulation in the lungs aggravate pulmonary edema. - adapted from ref (105).

Figure 3.

Kidney-lung interactions. AKI induces pathologic effects on the lung via cellular and soluble mediators. ALI in turn facilitates and exacerbates Kidney injury via metabolic and biochemical derangements. - adapted from ref (108).