Contributions to nephrology
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Sepsis is the most common cause of acute kidney injury (AKI). There has been a growing body of evidence demonstrating the association between worsening of kidney function during sepsis and the risk of short- and long-term mortality. AKI in sepsis is associated with poor outcome and independently predicts increased mortality. ⋯ The expanding population of patients with sepsis and AKI, and the associated excess mortality provide a strong basis for further research aimed at addressing more rigorously all potentially modifiable factors to reduce this burden to patients and health care systems. Better insights into bidirectional and synergistic pathways linking sepsis and AKI might open the window for new therapeutic approaches that interrupt this vicious circle. Here, we discuss the rationale for and the current understanding of the bidirectional relationship between AKI and sepsis.
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Acute kidney injury (AKI) is associated with a heavy burden of morbidity and mortality, despite advances in intensive care and the management of high-risk patients. Numerous clinical trials have failed to ameliorate the outcomes of AKI. ⋯ Similarly, a multidisciplinary dialogue is making progress towards standardization of the clinical trial endpoints to prove efficacy and effectiveness in AKI research. Taken together with the increasing availability of timely, sensitive, and specific novel biomarkers of kidney damage, we are poised to use these tools to conduct successful clinical trials of agents for the prevention and treatment of this devastating clinical syndrome.
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Comparative Study Controlled Clinical Trial
Comparison of efficacy between continuous hemodiafiltration with a PMMA high-performance membrane dialyzer and a PAN membrane hemofilter in the treatment of septic shock patients with acute renal failure.
The aim of this study was to investigate whether continuous hemodiafiltration (CHDF) with a high-performance membrane dialyzer made of polymethylmethacrylate (PMMA-CHDF) in the treatment of septic shock patients with acute renal failure (ARF) is clinically relevant. 30 patients were treated with PMMA-CHDF. 13 patients treated with CHDF used a hemofilter made of polyacrylonitrile membrane (PAN-CHDF). Systolic blood pressure significantly increased in the PMMA-CHDF group following 24 h of treatment (p < 0.01), whereas it did not improve in the PAN-CHDF group. Urine volume significantly increased in the PMMA-CHDF group following 24 h of treatment which was more than in the PAN-CHDF group (p < 0.05). 28-day survival was 83.3% in the PMMA-CHDF group and 30.8% in the PAN-CHDF group, respectively (p < 0.01). We can assume that PMMA-CHDF in the treatment of septic shock patients with ARF is clinically relevant.
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Endothelial cells play a key role in initiating and propagating the inflammatory response seen in ischemia, infections and sepsis. Situated in a key position between the epithelial cells and white blood cells (WBC), they interact and respond to signals from both cell types. ⋯ This last event is in large part responsible for a chronic reduction in regional perfusion, subsequent increased vulnerability to recurrent acute kidney injury, and acceleration of chronic kidney disease progression to end-stage renal disease. Glomerular endothelial dysfunction may lead to preglomerular shunting of blood flow allowing kidney blood flow to remain close to normal while resulting in a reduction in glomerular filtration rate.
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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.