Contributions to nephrology
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We evaluated the ability of the endotoxin activity (EA) assay to determine the need for early intervention for endotoxemia using polymyxin B-based hemoperfusion (PMX-DHP) on septic patients. ⋯ The EA assay can identify patients eligible for PMX-DHP treatment and aids its therapeutic dosing.
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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.
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Acute kidney injury (AKI) is frequently encountered in the intensive care unit, and from its inception, morbidity and mortality increase in these patients compared to those without AKI. Despite numerous clinical trials and newer pharmacological agents, very little progress has been made to reduce the deaths that occur in this population. ⋯ This critical loss of balance of these mediators appears to be due both to a reduction in clearance and increase in production as demonstrated by experimental studies of bilateral nephrectomy and ischemia-reperfusion, respectively. The evidence and mechanisms for distant organ injury following AKI will be discussed.