Contributions to nephrology
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Dysnatremias (hypo- and hypernatremia) are common in patients admitted to the intensive care unit (ICU) with a prevalence approaching 20-30% in some studies. Recent data reveals that both hypo- and hypernatremia present on admission to or developing in the ICU are independent risk factors for poor prognosis. The origin of hypernatremia in the ICU is often iatrogenic and due to inadequate free water replacement of ongoing water losses. ⋯ The appropriate use of hypertonic (3%) saline in the treatment of hyponatremic encephalopathy has also shown to be very effective and the use of this therapy is reviewed here. Vasopressin receptor antagonists have also been shown to be effective at increasing serum sodium levels in patients with either euvolemic or hypervolemic hyponatremia and represent another therapeutic option. Recent data demonstrates that proper correction of hyponatremia is associated with improved short- and long-term outcomes.
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Endotoxin removal by polymyxin B immobilized cartridge inactivates circulating proapoptotic factors.
Severe sepsis and septic shock continue to be major clinical challenges due to high associated mortality. Lipopolysaccharide (LPS) is a component of the cell membrane of Gram-negative bacteria, and is believed to initiate septic-induced signaling, inflammation and organ damage, including acute renal failure. Polymyxin B (PMX-B) hemoperfusion of septic patients can improve survival and decreasing organ dysfunction by removing circulating LPS. Unfortunately, some clinicians have been slow to adopt this novel therapy due to the lack of understanding of the cellular mechanisms involved in this treatment. Apoptosis, or programmed cell death, is known to contribute to acute renal failure and overall organ dysfunction during sepsis, and can be activated by LPS-initiated signaling pathways. Therefore, the protective renal effects associated with PMX-B hemoperfusion of septic patients may result from alterations in cellular apoptosis. This chapter will review recent data regarding the role of apoptosis prevention in the mechanism leading to the improved outcome and decreased acute renal failure associated with PMX-B hemoperfusion during sepsis. ⋯ The protective effects of extracorporeal therapy with PMX-B on the development of acute renal failure result, in part, through its ability to reduce the systemic proapoptotic activity of septic patients on renal cells.
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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.