Seminars in nephrology
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Sepsis and acute kidney injury (AKI) frequently are combined in critical care patients. They both are associated independently with increased mortality and morbidity. ⋯ In this article, we review the available clinical, laboratory, and imaging tools available for the recognition of septic AKI. Early identification of high-risk patients and targeted preventive and therapeutic measures are key to reducing the mortality and morbidity of the complex syndrome of septic AKI.
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Seminars in nephrology · Jan 2015
ReviewRenal endothelial injury and microvascular dysfunction in acute kidney injury.
The kidney is comprised of heterogeneous cell populations that function together to perform a number of tightly controlled, complex and interdependent processes. Renal endothelial cells contribute to vascular tone, regulation of blood flow to local tissue beds, modulation of coagulation and inflammation, and vascular permeability. ⋯ In recent years, the concept of the vascular endothelium as an organ that is both the source of and target for inflammatory injury has become widely appreciated. Here we revisit the renal endothelium in the light of ever evolving molecular advances.
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Acute kidney injury (AKI) is an epidemic problem. Sepsis has long been recognized as a foremost precipitant of AKI. Sepsis-associated AKI (SA-AKI) portends a high burden of morbidity and mortality in both children and adults with critical illness. ⋯ Rather, current strategies to alleviate poor outcomes focus on clinical risk identification, early detection of injury, modifying clinician behavior to avoid harm, early appropriate antimicrobial therapy, and surveillance among survivors for the longer-term sequelae of kidney damage. Recent evidence has confirmed that patients no longer die with AKI, but from AKI. To improve the care and outcomes for sufferers of SA-AKI, clinicians need a robust appreciation for its epidemiology and current best-evidence strategies for prevention and treatment.
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The renal microcirculation plays a major role in the delivery of blood and oxygen to the kidney. In sepsis, alterations in renal microvascular perfusion, in conjunction with increased oxygen requirements, may contribute to renal failure even when renal macrovascular perfusion is preserved. In this review, we discuss the pathophysiology of the renal microcirculation during sepsis and how it contributes to acute kidney injury. ⋯ Coagulative disorders and glycocalyx disruption also may contribute to the microcirculatory dysfunction. New technologies in experimental models and human beings are being developed to explore renal microcirculation in vivo. These technologies will allow a better understanding of the pathophysiopathology of the renal microcirculation and will help guide specific therapeutic strategies in sepsis-induced acute kidney injury.
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Seminars in nephrology · Jan 2015
ReviewEmerging therapeutic targets of sepsis-associated acute kidney injury.
Sepsis-associated acute kidney injury (SA-AKI) is linked to high morbidity and mortality. To date, singular approaches to target specific pathways known to contribute to the pathogenesis of SA-AKI have failed. ⋯ In this review, we discuss the clinical and experimental basis of emerging therapeutic approaches that focus on targeting early proinflammatory and late anti-inflammatory processes, as well as therapeutics that may enhance cellular survival and recovery. Finally, we include ongoing clinical trials in sepsis.