Contributions to nephrology
-
Acute kidney injury (AKI) has been shown to be associated with progression to chronic kidney disease (CKD). Multiple studies have shown that subsets of AKI survivors are at high risk for progression to advanced stage CKD and death. Risk factors associated with AKI survivors progressing to CKD have been identified and include advanced age, diabetes mellitus, decreased baseline glomerular filtration rate, severity of AKI and a low concentration of serum albumin. ⋯ The maintenance phase of AKI is longer in duration in comparison to the initiation phase, and thus the logistics are more amenable to study. However, the mainstay of treatment for the maintenance phase of AKI (renal replacement therapy) has been tested extensively and increasing the dose of renal replacement therapy has not been shown to improve outcome. Therefore, the recovery phase of AKI may represent the best opportunity to intervene in the negative outcomes of AKI.
-
Acute kidney injury (AKI) remains a major clinical challenge, especially in combination with acute lung injury (ALI). Clinical as well as experimental studies have provided evidence for clinically relevant kidney-lung interactions, ultimately leading to a drastic reduction in survival. The crosstalk between AKI and ALI is a consequence of both direct loss of normal organ function and inflammatory dysregulation resulting from each organ failure. ⋯ Lung protective ventilation, including low tidal volume ventilation, is a cornerstone in the management of ALI. This approach has been shown to attenuate both the direct mechanical effects of ventilation and the inflammatory response arising from ALI and mechanical ventilation, ultimately reducing the incidence of extrapulmonary organ failure. The fact that multiorgan failure is not only the sum of organ functions lost, but also includes inflammatory dysregulation together with a lack of treatment options greatly emphasizes the need for future research in this area.
-
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.
-
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.
-
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.