Contributions to nephrology
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Sepsis-induced acute kidney injury (AKI) is the most common form of AKI observed in critically ill patients. AKI mortality in septic critically ill patients remains high despite our increasing ability to support vital organ systems. This high mortality is partly due to our poor understanding of the pathophysiological mechanisms of sepsis-induced AKI. ⋯ Sepsis-induced renal microvascular alterations (vasoconstriction, capillary leak syndrome with tissue edema, leukocytes and platelet adhesion with endothelial dysfunction and/or microthrombosis) and/or an increase in intra-abdominal pressure could contribute to an increase in RVR. Further studies are needed to explore the time course of renal microvascular alterations during sepsis as well as the initiation and development of AKI. Doppler ultrasonography combined with the calculation of the resistive indices may indicate the extent of the vascular resistance changes and may help predict persistent AKI and determine the optimal systemic hemodynamics required for renal perfusion.
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All aspects of current treatment of acute kidney injury (AKI), including renal replacement therapy (RRT), are basically supportive. Emergent RRT is indicated in the management of AKI with refractory pulmonary edema, hyperkalemia or metabolic acidosis, or when uremic symptoms or signs develop. More aggressive practitioners use prophylactic RRT inpatients with sustained anuria, persistent oliguria with progressive azotemia and a probable glomerular filtration rate < 10 ml/min, or to prevent uncontrolled positive fluid balance in patients with AKI. ⋯ The approach to RRT dosing in AKI is more evidence-based. Outcomes in single-center studies of higher intensity versus standard RRT (intermittent and/or continuous) have been in consistent. However, two large multicenter negative randomized trials have shifted the weight of evidence towards suggesting provision of an effectively delivered standard dose of RRT in AKI, rather than seeking to increase RRT intensity.
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Sepsis is the most common cause of acute kidney injury (AKI). There has been a growing body of evidence demonstrating the association between worsening of kidney function during sepsis and the risk of short- and long-term mortality. AKI in sepsis is associated with poor outcome and independently predicts increased mortality. ⋯ The expanding population of patients with sepsis and AKI, and the associated excess mortality provide a strong basis for further research aimed at addressing more rigorously all potentially modifiable factors to reduce this burden to patients and health care systems. Better insights into bidirectional and synergistic pathways linking sepsis and AKI might open the window for new therapeutic approaches that interrupt this vicious circle. Here, we discuss the rationale for and the current understanding of the bidirectional relationship between AKI and sepsis.
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Review Comparative Study
Acute kidney injury, acute lung injury and septic shock: how does mortality compare?
Acute kidney injury (AKI), acute lung injury (ALI) and sepsis are all commonly encountered in critically ill patients. Although considered as separate conditions, largely for therapeutic purposes, a common inflammatory response is often implicated in their pathophysiologies and they are frequently present simultaneously. Mortality rates in critically ill patients suffering from renal failure, respiratory failure or severe sepsis are quite similar at about 40%, and all increase substantially when these conditions coexist. Most intensive care unit patients will die from multiple rather than individual organ failure, and further research is needed to evaluate the patterns of organ failure in surviving and nonsurviving critically ill patients, as well as the importance and mechanisms of organ-organ crosstalk in such patients.
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In order to prevent a disease, its temporal nature (or at least when it starts) needs to be clearly defined. In acute kidney injury (AKI), this is usually not possible because the current diagnostic criteria are retrospective. Contrast-induced nephropathy (CIN) and cardiac surgery-associated acute kidney injury (CSA-AKI) are both thought of as potentially preventable acute renal lesions because the timing of the insult is known precisely. ⋯ Despite this, progress in prevention has been slow, and to date there are no therapies indicated for preventing either CIN or CSA-AKI. The best we can currently do is to recommend aggressive parenteral hydration, avoid compounds we know are nephrotoxic, and avoid unnecessary hypoxia and hypotension. While there is still clearly a long way to go before either of these acute kidney conditions can be described as preventable, the use of major adverse kidney events - death, dialysis and incident or progressive chronic kidney disease at 90 days - as a composite endpoint in clinical trials of putative prevention agents would represent a significant step forwards.