Contributions to nephrology
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All aspects of current treatment of acute kidney injury (AKI), including renal replacement therapy (RRT), are basically supportive. Emergent RRT is indicated in the management of AKI with refractory pulmonary edema, hyperkalemia or metabolic acidosis, or when uremic symptoms or signs develop. More aggressive practitioners use prophylactic RRT inpatients with sustained anuria, persistent oliguria with progressive azotemia and a probable glomerular filtration rate < 10 ml/min, or to prevent uncontrolled positive fluid balance in patients with AKI. ⋯ The approach to RRT dosing in AKI is more evidence-based. Outcomes in single-center studies of higher intensity versus standard RRT (intermittent and/or continuous) have been in consistent. However, two large multicenter negative randomized trials have shifted the weight of evidence towards suggesting provision of an effectively delivered standard dose of RRT in AKI, rather than seeking to increase RRT intensity.
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Review Comparative Study
Acute kidney injury, acute lung injury and septic shock: how does mortality compare?
Acute kidney injury (AKI), acute lung injury (ALI) and sepsis are all commonly encountered in critically ill patients. Although considered as separate conditions, largely for therapeutic purposes, a common inflammatory response is often implicated in their pathophysiologies and they are frequently present simultaneously. Mortality rates in critically ill patients suffering from renal failure, respiratory failure or severe sepsis are quite similar at about 40%, and all increase substantially when these conditions coexist. Most intensive care unit patients will die from multiple rather than individual organ failure, and further research is needed to evaluate the patterns of organ failure in surviving and nonsurviving critically ill patients, as well as the importance and mechanisms of organ-organ crosstalk in such patients.
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The pathogenesis of sepsis-induced acute kidney injury (AKI) is not fully understood, and may involve altered systemic hemodynamics and renal circulation, renal hypoxia and perhaps direct tubular toxicity. Oxidative stress, induced by systemic and intrarenal generation of reactive oxygen species (ROS) can directly exert renal parenchymal damage and may intensify renal microvascular and functional dysregulation, with a feedforward loop of hypoxia and ROS generation. Herein we review compelling evidence that sepsis is associated with systemic and intrarenal intense oxidative and nitrosative stress with a depletion of antioxidant capacity. ⋯ Though oxidative and nitrosative stress are likely to participate in the pathogenesis of sepsis-induced AKI, it is impossible to clearly identify their isolated independent role and renal-specific effect since there are complex interactions involved linking various affected organs, ROS generation with altered systemic hemodynamics, compromised microcirculation, hypoxia and distorted cellular function. Facing this complex disease entity, alleviation of oxidative stress single-handedly is unlikely to be effective in the prevention of sepsis-associated renal dysfunction. However, the addition of antioxidants to a comprehensive treatment strategy seems a reasonable approach.
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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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In the US and Europe, approximately 90% of heart failure (HF) hospitalizations are due to symptoms and signs of sodium and fluid excess. Congestion is associated with HF progression. According to data from large national registries, approximately 40% of hospitalized HF patients are discharged with unresolved congestion, which may contribute to unacceptably high rehospitalization rates. ⋯ Clinical studies of ultrafiltration have shown that removal of isotonic fluid relieves symptoms of congestion, improves cardiac filling pressures and exercise capacity, and restores diuretic responsiveness in patients with diuretic resistance, concomitantly with favorable effects on pulmonary function, ventilatory efficiency, and neurohormonal activation. Ultrafiltration has been shown to reduce rehospitalizations in a randomized controlled trial of patients with decompensated HF. Future larger controlled clinical trials should evaluate the effect of ultrafiltration on survival.