Contributions to nephrology
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Intravenous fluids are commonly administered to patients with developing septic acute kidney injury (AKI). Conversely, fluids are just as commonly removed with diuretics or renal replacement therapy (RRT) techniques or ultrafiltration in patients with cardiorenal syndromes (CRS). In both groups, there is controversy regarding fluid management. ⋯ However, in patients with either septic AKI or CRS, hypovolemia and renal hypoperfusion can occur if excessive fluid removal is pursued with diuretics or extracorporeal therapy. Thus, accurate assessment of fluid status and careful definition of targets are needed to improve clinical outcomes. Controlled studies of conservative versus liberal fluid management in patients with AKI or CRS seem justified.
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The care of acute kidney injury (AKI) in critically ill children shares several features with adult AKI with some critical distinctions: in both settings, however, the exact identification of renal dysfunction, in-depth knowledge of disparate risk factors and patient-specific management are the primary targets in order to provide optimal care. This article will specifically review recent work published on pediatric AKI about definition and epidemiology, the possible etiologies in specific conditions, and the newest laboratory investigations necessary to diagnose AKI severity. A short description of pediatric renal replacement therapies and their potential application to extracorporeal membrane oxygenation will also be described.
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Acute kidney injury (AKI) occurring after cardiac surgery is common and extends intensive care unit and hospital length of stay, as well as increases mortality rates. Its causes are multifactorial, and are not limited to ischemia and nephrotoxin administration. ⋯ Certain etiological factors are peculiar to the cardiac surgery setting, such as routine use of cardiopulmonary bypass, and various degrees of hypothermia, which is probably nephroprotective from an ischemia point of view, but which also worsens hemolysis from the pump and thus may actually exacerbate the problem. In this paper we review the place of antifibrinolytic therapy, hemodynamic control on bypass, and the correct level of oxygen delivery in the development of AKI after open heart surgery.
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Acute lung injury (ALI) and acute kidney injury (AKI) are complications often encountered in the setting of critical illness. Both forms of end-organ injury commonly occur in similar settings of systemic inflammatory response syndrome, shock, and evolving multiple organ dysfunction. Distant organ effects of apparently isolated injuries to the lungs, gut, and kidneys have all been discovered in recent years. In this review of the emerging evidence of deleterious bidirectional organ crosstalk between the lungs and kidney, we will focus on the role of ventilator-induced kidney injury in the pathogenesis of AKI in patients with ALI.
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Septic acute kidney injury (AKI) is the most common form of AKI seen in critically ill patients in developed countries. Its pathogenesis has been traditionally attributed to ischemia secondary to decreased cardiac output and hypotension, which trigger sustained renal vasoconstriction and in turn exacerbate and sustain the ischemia. ⋯ Furthermore, the induction of prolonged severe subtotal ischemia by acute occlusion of the renal artery does not seem to trigger subsequent renal vasoconstriction and, finally, experimental studies suggest that immune-mediated injury may be a more likely cause of tubular cell dysfunction than ischemia. These lines of evidence suggest that the pathogenesis of AKI is complex, does not simply involve ischemia, and may differ according to the etiological trigger.