Contributions to nephrology
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Acute kidney injury (AKI) is a serious condition that affects many intensive care unit (ICU) patients. The most common causes of AKI in the ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite our increasing ability to support vital organs. ⋯ It would seem logical, therefore, to focus on the glomerulus in trying to understand why such loss of GFR occurs. Recent experimental observations suggest that, at least in the initial phases of septic AKI, profound changes occur which involve glomerular hemodynamics and lead to loss of GFR. These observations imply that changes in the vasoconstrictor tone of both the afferent and efferent arterioles are an important component of the pathogenesis of septic AKI.
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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.
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The modern definition and classification of acute kidney injury (AKI) has now been applied to thousands of patients around the world and in different settings. Epidemiology is shedding intense light on the credibility of our fundamental notions of how AKI occurs and why. It is clear from multiple studies that sepsis is the leading etiology of AKI, although other settings associated with systemic inflammation (polytrauma, burns, pancreatitis, cardiopulmonary bypass) also represent important means of exposure. ⋯ Dissonance of mediator secretion and cell responses may lead to persistent injury and de novo chronic kidney disease. A number of soluble mediators initiate a variety of pathophysiological processes as kidney injury evolves. In this chapter, we will discuss the pathogenesis of AKI in light of new information concerning injury and repair, and focus on the controversies arising from emerging evidence.
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In critically ill patients, acute kidney injury (AKI) is a common complication. In some cases, oliguria may be the only sign verifying this condition. The consensus definitions of RIFLE and AKIN are based on changes in creatinine and urine output and define classes of severity within AKI. ⋯ As a result, they may not be done timely and may be subject to inaccuracies due to human factors. The URINFO(®) system is an innovative digital urine meter that provides continuous minute-to-minute monitoring of urine output, thereby enhancing kidney monitoring and the acquisition of more reliable urine output information in realtime. Consequently, monitoring of urine output with URINFO may enable rapid therapeutic interventions and can be incorporated into patient data systems, thereby improving therapy management.
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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.