Una revisión de las estrategias de protección renal
A review of renal protection strategies Erna Meyer Southern African Journal of Anaesthesia and Analgesia 2015 Abstract Globally, more than 10 million people are affected every year by acute kidney injury (AKI) and approximately 6% of hospital patients sustain some degree of kidney injury during their hospital event. Reducing perioperative kidney injury may significantly improve patient outcomes. As perioperative physicians, we are in a position to have some influence on renal outcomes.This article is a review of the current literature on the relevance of renal protection, definitions, mechanisms and new biomarkers of AKI, as well as improved renal perfusion strategies. It specifically considers the renal effects of general and regional anaesthesia, intra-abdominal pressure and abdominal compartment syndrome. The usefulness of certain drugs is investigated. Mechanisms of injury by nephrotoxins, as well as strategies to minimise these injuries, are discussed. Intravenous fluids are briefly mentioned as they relate to renal function. PDF |
Anestésicos volátiles y falla renal aguda: riesgos, mecanismos y ventana terapéutica potencial
Volatile anesthetics and AKI: risks, mechanisms, and a potential therapeutic window. Fukazawa K, Lee HT. J Am Soc Nephrol. 2014 May;25(5):884-92. doi: 10.1681/ASN.2013111215. Epub 2014 Feb 7. Abstract AKI is a major clinical problem with extremely high mortality and morbidity. Kidney hypoxia or ischemia-reperfusion injury inevitably occurs during surgery involving renal or aortic vascular occlusion and is one of the leading causes of perioperative AKI. Despite the growing incidence and tremendous clinical and financial burden of AKI, there is currently no effective therapy for this condition. The pathophysiology of AKI is orchestrated by renal tubular and endothelial cell necrosis and apoptosis, leukocyte infiltration, and the production and release of proinflammatory cytokines and reactive oxygen species. Effective management strategies require multimodal inhibition of these injury processes. Despite the past theoretical concerns about the nephrotoxic effects of several clinically utilized volatile anesthetics, recent studies suggest that modern halogenated volatile anesthetics induce potent anti-inflammatory, antinecrotic, and antiapoptotic effects that protect against ischemic AKI. Therefore, the renal protective properties of volatile anesthetics may provide clinically useful therapeutic intervention to treat and/or prevent perioperative AKI. In this review, we outline the history of volatile anesthetics and their effect on kidney function, briefly review the studies on volatile anesthetic-induced renal protection, and summarize the basic cellular mechanisms of volatile anesthetic-mediated protection against ischemic AKI. KEYWORDS: acute renal failure; ischemia-reperfusion; ischemic renal failure PDF |
Estrategias de preacondicionamiento por lesión por isquemia y reperfusión renal: implicaciones de la "ventana de tiempo" en el precondicionamiento isquémico remoto.
Preconditioning strategies for kidney ischemia reperfusion injury: implications of the "time-window" in remote ischemic preconditioning. Yoon YE, Lee KS, Choi KH, Kim KH, Yang SC, Han WK. PLoS One. 2015 Apr 16;10(4):e0124130. doi: 10.1371/journal.pone.0124130. eCollection 2015. Abstract Remote ischemic preconditioning (IP) is a potential renoprotective strategy. However, there has been no demonstrated result in large animals and the role of time window in remote IP remains to be defined. Using a single-kidney porcine model, we evaluated organ protective function of remote IP inrenal ischemia reperfusion injury. Fifteen Yorkshire pigs, 20 weeks old and weighing 35-38 kg were used. One week after left nephrectomy, we performed remote IP (clamping right external iliac artery, 2 cycles of 10 minutes) and right renal artery clamping (warm ischemia; 90 minutes). The animals were randomly divided into three groups: control group, warm ischemia without IP; group 1 (remote IP with early window [IP-E]), IP followed by warm ischemia with a 10-minute time window; and group 2 (remote IP with late window [IP-L]), IP followed by warm ischemia after a 24-hour time window. There were no differences in serum creatinine changes between groups. The IP-L group had lower urinary neutrophil gelatinase-associated lipocalin than control and IP-E at 72 hours post-ischemia. At 72 hours post-ischemia, the urinary kidney injury molecule-1 (KIM-1) was lower in the IP-L group than in the control and IP-E groups, and the IP-L group KIM-1 was near pre-ischemic levels, whereas the control and IP-E group KIM-1 levels were rising. Microalbumin also tended to be lower in the IP-L group. Taken together, remote IP showed a significant reduction in renal injury biomarkers from ischemia reperfusion injury. To effectively provide kidney protection, remote IP might require a considerable, rather than short, time window of ischemia. PDF
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