domingo, 6 de noviembre de 2016

Falla renal aguda / Acute kidney failure

Noviembre 6, 2016. No. 2502






Interacciones riñón-corazón en falla renal aguda
Kidney-Heart Interactions in Acute Kidney Injury.
Nephron. 2016;134(3):141-144. Epub 2016 Jun 16.
Abstract
Acute kidney injury (AKI) is a common complication in critically ill patients treated in intensive care units. Renal replacement therapy (RRT)-requiring AKI occurs in approximately 5-10% patients in intensive care unit and their mortality rate is unacceptably high (50-60%), despite sufficient control of uremia using remarkably advanced modern RRT techniques. This suggests that there are unrecognized organ interactions following AKI that could worsen the outcomes. Cardiorenal syndrome has been defined based on clinical observations that acute and chronic heart failure causes kidney injury and AKI and that chronic kidney disease worsens heartdiseases. Possible pathways that connect these 2 organs have been suggested; however, the precise mechanisms are yet to be clarified, particularly in AKI-induced cardiac dysfunction. This review focuses on acute cardiac dysfunction in the setting of AKI. A recent animal study demonstrated the dysregulation of mitochondrial dynamics caused by an increased dynamin-related protein 1 expression and cellular apoptosis of the heart in a renal ischemia reperfusion model. Although the precise mechanisms that induce cardiac mitochondrial injury in AKI remain unclear, cardiac mitochondria injury could be a novel candidate of drug targets against high mortality in severe AKI. © 2016 S. Karger AG, Basel
Papel de la lesión renal en la sepsis
Role of kidney injury in sepsis.
J Intensive Care. 2016 Mar 23;4:17. doi: 10.1186/s40560-016-0146-3. eCollection 2016.
Abstract
Kidney injury, including acute kidney injury (AKI) and chronic kidney disease (CKD), has become very common in critically ill patients treated in ICUs. Many epidemiological studies have revealed significant associations of AKI and CKD with poor outcomes of high mortality and medical costs. Although many basic studies have clarified the possible mechanisms of sepsis and septic AKI, translation of the obtained findings to clinical settings has not been successful to date. No specific drug against human sepsis or AKI is currently available. Remarkable progress of dialysis techniques such as continuous renal replacement therapy (CRRT) has enabled control of "uremia" in hemodynamically unstable patients; however, dialysis-requiring septic AKI patients are still showing unacceptably high mortality of 60-80 %. Therefore, further investigations must be conducted to improve the outcome of sepsis and septic AKI. A possible target will be remote organ injury caused by AKI. Recent basic studies have identified interleukin-6 and high mobility group box 1 (HMGB1) as important mediators for acute lung injury induced by AKI. Another target is the disease pathway that is amplified by pre-existing CKD. Vascular endothelial growth factor and HMGB1 elevations in sepsis were demonstrated to be amplified by CKD in CKD-sepsis animal models. Understanding the role of kidney injury as an amplifier in sepsis and multiple organ failure might support the identification of new drug targets for sepsis and septic AKI.
KEYWORDS: Acute kidney injury; Chronic kidney disease; High mobility group box 1; Lung injury; Sepsis

XIII Congreso Virtual Mexicano de Anestesiología
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Octubre a Diciembre 2016

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L Congreso Mexicano de Anestesiología
Noviembre 2-6, 2016
2º Curso Internacional de Simulación en Vía Aérea - FIDIVA Chile
7 y 8 de Noviembre en el Campus de la Universidad Finis Terrae
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