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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Extracorporeal therapies are able to sustain life through different mechanisms. This approach, called multiple organ support therapy, can in fact obtain blood purification by hemodialysis/hemofiltration to replace kidney function, temperature control, electrolyte and acid-base control to mimic homeostatic regulation of the kidney and circulation, fluid balance control to support the right hydration and cardiac performance, cardiac support removing cardiodepressant substances and equilibrating potassium levels, blood detoxification and liver support by coupled plasma filtration and adsorption or direct adsorption on blood (hemoperfusion), immunomodulation and endothelial support in the presence of sepsis by cutting the peaks of pro- and anti-inflammatory mediators, and immunoadsorption or adsorption of specific substances such as endotoxin. ⋯ Today this is made possible by removal of CO(2) either by complete extracorporeal membrane oxygenation or by using decapneization in conjunction with hemofiltration in a system called DECAP/DECAPSMART. In conclusion, circulating blood outside the body and treating it with different filters or cartridges in a multiple organ support therapy may represent an important support for multiple organ dysfunction conditions induced by sepsis, acute respiratory distress syndrome and in recent times by complicated H1N1-related infections.
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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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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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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.