Sepsis-Associated Acute Kidney Injury: Macrohemodynamic and Microhemodynamic Alterations in the Renal Circulation

Prowle, John R.; Bellomo, Rinaldo

doi:10.1016/j.semnephrol.2015.01.007

Cited by 108 publications

(71 citation statements)

References 79 publications

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“…Recent research indicates inflammatory mediators causing tubular cell dysfunction and cell cycle arrest along with the associated microcirculatory dysfunction as the trigger for SA-AKI 5. This process is in keeping with cellular injury processes resulting in multiorgan dysfunction such as that seen in severe sepsis.…”

Section: Pathophysiologymentioning

confidence: 90%

Update on sepsis-associated acute kidney injury: emerging targeted therapies

Doyle¹,

Forni²

2016

BTT

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Sepsis-associated acute kidney injury (SA-AKI) is an independent predictor of increased mortality and morbidity. It is essential that further advances in the treatment of sepsis should prioritize targeted therapies in SA-AKI in order to improve these bleak outcomes. As yet, a unique therapy that effectively reduces the impact of acute kidney injury has not been demonstrated. However, the emergence of novel targeted therapies, perhaps in combination, has the possibility of significantly reducing the long-term sequelae of an episode of SA-AKI. In this review, we will focus on the shared etiology of these conditions and how this is managed with targeted therapy and finally the emerging novel therapies that may play an additional role to current treatment strategies.

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Section: Pathophysiologymentioning

confidence: 90%

Update on sepsis-associated acute kidney injury: emerging targeted therapies

Doyle¹,

Forni²

2016

BTT

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“…These changes broadly mediate injury across numerous organ systems of relevance to sepsis outcomes, including the lung 31 , kidney 32 , and brain 33 . Importantly, there is no discrete, readily-apparent inflection point at which beneficial microvascular responses to infection change to pathologic contributors to sepsis.…”

Section: Evidence Of Microvascular Dysfunction During Sepsismentioning

confidence: 99%

Endothelial and Microcirculatory Function and Dysfunction in Sepsis

Colbert

Schmidt

2016

Clinics in Chest Medicine

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SYNOPSISThe microcirculation is a series of arterioles, capillaries, and venules that performs essential functions of oxygen and nutrient delivery, customized to the unique physiologic needs of the supplied organ. The homeostatic microcirculatory response to infection, which includes barrier hyperpermeability, leukocyte adhesion, and coagulation activation, can become harmful if overactive and/or dysregulated, contributing to the organ failure characteristic of sepsis. In humans, pathologic microcirculatory dysfunction can be directly visualized by intravital microscopy or indirectly measured via detection of circulating biomarkers, such as endothelial glycocalyx fragments. While several treatments have been shown to protect the microcirculation during sepsis, these therapies have not improved patient outcomes when applied indiscriminately. Future outcomes-oriented studies are needed to test the utility of sepsis therapeutics when applied in a manner "personalized" to a patient's microcirculatory dysfunction.

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“…Prerenal AKI is found most commonly in patients undergoing cardiac surgery who have undergone cardiopulmonary bypass procedures [2425]. However, recent investigations have shown that in addition to hemodynamic alterations, inflammation and direct nephrotoxic effects on tubular cells play crucial roles in inducing AKI in patients after cardiac surgery [26]. Additionally, factors not related to the surgical procedure itself, such as the presence of valvular disease, inotropic use, or postoperative intra-aortic balloon pump support, can reduce renal blood flow, subsequently aggravating the damage caused by cardiopulmonary bypass.…”

Section: Pathophysiologymentioning

confidence: 99%

Postoperative acute kidney injury

Park

2017

Korean J Anesthesiol

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Acute kidney injury (AKI) after cardiac surgery is a common and serious complication. Several definitions of AKI have been proposed recently, and include both increases in serum creatinine levels and decreases in urine output as diagnostic criteria. The pathophysiology of postoperative AKI is complex and involves both ischemic injury and systemic inflammation. Identifying risk factors, such as old age, underlying diabetes, heart failure, and obesity, may aid in the application of preventative methods for postoperative AKI. Additionally, recognizing different risks after different types of surgical procedures would be valuable. Novel biomarkers that could detect AKI more precisely at an earlier time point are being investigated. Several new biomarkers have been assessed in large multi-center studies and are believed to accommodate conventional clinical findings in diagnosing postoperative AKI. In high-risk patients, preventative measures, such as the maintenance of adequate hemodynamics and sufficient fluid resuscitation, could lower the incidence of postoperative AKI. Avoiding nephrotoxic agents and optimizing preoperative hemoglobin levels to avoid excessive transfusions would also be beneficial. In situations in which medical management fails to maintain sufficient urine output and acid–base and electrolyte homeostasis, early initiation of renal replacement therapy should be considered.

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Sepsis-Associated Acute Kidney Injury: Macrohemodynamic and Microhemodynamic Alterations in the Renal Circulation

Cited by 108 publications

References 79 publications

Update on sepsis-associated acute kidney injury: emerging targeted therapies

Update on sepsis-associated acute kidney injury: emerging targeted therapies

Endothelial and Microcirculatory Function and Dysfunction in Sepsis

Postoperative acute kidney injury

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