Potential interventions in sepsis-related acute kidney injury

Abstract

Sepsis is an important cause of morbidity and mortality. Acute kidney injury often complicates sepsis, leading to greater complexity, cost of care, and worsening prognosis. In recent years, a consensus definition of acute kidney injury has been developed, facilitating research into the pathophysiology and epidemiology of this disorder. New and emerging biomarkers to recognize kidney injury before functional abnormalities are manifest may allow early recognition and facilitate prevention or treatment. Furthermore, advances in the clinical management of sepsis may have secondary benefits with respect to renal outcomes. Existing and hybrid extracorporeal therapies are being investigated not only as means to replace lost kidney function but also to modulate the immune response to sepsis. For those who have more advanced forms of kidney injury, strategies to promote renal recovery are being sought to minimize the long-term consequences of impaired kidney function. This review provides an update on the current state of the science and a glimpse toward the future of intervention in sepsis-related acute kidney injury.

Figure 1.

Pathogenic mechanisms of sepsis-related acute kidney injury.

Figure 2.

Peak concentration hypothesis. Peaks of mediators characteristic of systemic inflammatory response syndrome (SIRS) and compensated anti-inflammatory response syndrome (CARS) may be seen in sequence or in parallel. Broad-based control of peaks with continuous renal replacement therapy (CRRT) is hypothesized to lessen the degree of imbalance and restore immunohomeostasis. IL-1, interleukin-1; IL-10, interleukin-10; PAF, platelet-activating factor; TNF, tumor necrosis factor. Adapted from reference (19), with permission from WileyBlackwell Publishing, Ltd.