Surgical sepsis and organ crosstalk: the role of the kidney

Abstract

Acute kidney injury (AKI) is a common complication of hospitalized patients, and clinical outcomes remain poor despite advances in renal replacement therapy. The accepted pathophysiology of AKI in the setting of sepsis has evolved from one of simple decreased renal blood flow to one that involves a more complex interaction of intra-glomerular microcirculatory vasodilation combined with the local release of inflammatory mediators and apoptosis. Evidence from preclinical AKI models suggests that crosstalk occurs between kidneys and other organ systems via soluble and cellular inflammatory mediators and that this involves both the innate and adaptive immune systems. These interactions are reflected by genomic changes and abnormal rates of cellular apoptosis in distant organs including the lungs, heart, gut, liver, and central nervous system. The purpose of this article is to review the influence of AKI, particularly sepsis-associated AKI, on inter-organ crosstalk in the context of systemic inflammation and multiple organ failure (MOF).

Figure 1. Surgical Sepsis and Multiple Organ Failure- The Role of the Kidney

Surgical sepsis causes AKI, which in turn contributes to early SIRS and MOF, then late Compensatory Anti-inflammatory Response Syndrome (CARS) and MOF through an altered innate and adaptive immune response.

Figure 2. Vicious cycle of AKI and ALI

AKI induces pathophysiologic effects on the lung via cellular and soluble mediators. ALI, in turn, facilitates and exacerbates kidney dysfunction via metabolic and biochemical derangements.

Figure 3. Acute Kidney Injury and its effects on major organ-systems in the body

AKI manifests distant organ injury in the heart, brain, lungs, liver and gut in a variety of mechanisms, including increased expression of soluble pro-inflammatory mediators, innate and adaptive immunity, cellular apoptosis, physiologic derangements and genomic changes.