Abstract
Acute kidney injury (AKI) is a common complication during inpatient hospitalization, and clinical outcomes remain poor despite advancements in renal replacement therapy. AKI in the setting of multiple organ failure (MOF) remains a formidable challenge to clinicians and incurs an unacceptably high mortality rate. Kidney ischemia-reperfusion injury (IRI) incites a proinflammatory cascade and releases cellular and soluble mediators with systemic implications for remote organ injury. Evidence from preclinical models cites mechanisms of organ crosstalk during ischemic AKI including the expression of cellular adhesion molecules, lymphocyte trafficking, release of proinflammatory cytokines and chemokines, and modification of the host innate and adaptive immune response systems. In this paper, the influence of kidney IRI on systemic inflammation and distant organ injury will be examined. Recent experimental data and evolving concepts of organ crosstalk during ischemic AKI will also be discussed in detail.
Highlights
Despite advancements in renal replacement therapy, acute kidney injury (AKI) is a frequent complication with severe implications for the critically ill patient
It has become apparent that clinically much of the high patient mortality can be attributed to the onset of systemic inflammatory response syndrome (SIRS) and progression to multiple organ failure (MOF)
Kidney ischemia-reperfusion injury (IRI) remains a major cause of AKI in both native and transplanted organs and lacks a specific treatment aside from renal replacement therapy
Summary
Despite advancements in renal replacement therapy, acute kidney injury (AKI) is a frequent complication with severe implications for the critically ill patient. Α-melanocyte-stimulating hormone (αMSH), a cytokine with broad antiinflammatory, anticytotoxic, and antiapoptotic properties, has demonstrated success in treating the inflammatory phenotype in rodents In this model, treatment with α-MSH has attenuated both renal and pulmonary injury during ischemic AKI [13, 17]. The largely unsuccessful effort to ameliorate MOF with specific anti-inflammatory therapeutics highlights the complexity of the systemic response to kidney IRI. From these early experimental studies, it is possible that the multiple inflammatory pathways activated in each organ system represent a unique response to ischemic AKI. We will focus on cellular mediators, those involved in the innate and adaptive immune system, which may connect local ischemic AKI with distant organ injury
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