Contributions to nephrology
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Acute kidney injury (AKI) remains a major clinical challenge, especially in combination with acute lung injury (ALI). Clinical as well as experimental studies have provided evidence for clinically relevant kidney-lung interactions, ultimately leading to a drastic reduction in survival. The crosstalk between AKI and ALI is a consequence of both direct loss of normal organ function and inflammatory dysregulation resulting from each organ failure. ⋯ Lung protective ventilation, including low tidal volume ventilation, is a cornerstone in the management of ALI. This approach has been shown to attenuate both the direct mechanical effects of ventilation and the inflammatory response arising from ALI and mechanical ventilation, ultimately reducing the incidence of extrapulmonary organ failure. The fact that multiorgan failure is not only the sum of organ functions lost, but also includes inflammatory dysregulation together with a lack of treatment options greatly emphasizes the need for future research in this area.
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Acute kidney injury (AKI) has been shown to be associated with progression to chronic kidney disease (CKD). Multiple studies have shown that subsets of AKI survivors are at high risk for progression to advanced stage CKD and death. Risk factors associated with AKI survivors progressing to CKD have been identified and include advanced age, diabetes mellitus, decreased baseline glomerular filtration rate, severity of AKI and a low concentration of serum albumin. ⋯ The maintenance phase of AKI is longer in duration in comparison to the initiation phase, and thus the logistics are more amenable to study. However, the mainstay of treatment for the maintenance phase of AKI (renal replacement therapy) has been tested extensively and increasing the dose of renal replacement therapy has not been shown to improve outcome. Therefore, the recovery phase of AKI may represent the best opportunity to intervene in the negative outcomes of AKI.
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Acute kidney injury (AKI) can no longer be considered a surrogate marker for severity of illness. Recent epidemiologic data demonstrate the association of AKI and mortality. Even small decreases of kidney function are associated with increased mortality. ⋯ Infection and antimicrobial therapy can be the cause of AKI, but infection can also be a consequence of AKI. Finally, inadequate antimicrobial dosing probably plays an important role in the morbidity and mortality of AKI. These findings have led to a paradigm shift: patients die because of AKI rather than with AKI.
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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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The modern definition and classification of acute kidney injury (AKI) has now been applied to thousands of patients around the world and in different settings. Epidemiology is shedding intense light on the credibility of our fundamental notions of how AKI occurs and why. It is clear from multiple studies that sepsis is the leading etiology of AKI, although other settings associated with systemic inflammation (polytrauma, burns, pancreatitis, cardiopulmonary bypass) also represent important means of exposure. ⋯ Dissonance of mediator secretion and cell responses may lead to persistent injury and de novo chronic kidney disease. A number of soluble mediators initiate a variety of pathophysiological processes as kidney injury evolves. In this chapter, we will discuss the pathogenesis of AKI in light of new information concerning injury and repair, and focus on the controversies arising from emerging evidence.