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Advances in membrane biology for continuous renal replacement therapy

  • C. Tetta
  • A. Brendolan
  • V. D’Intini
Conference paper

Abstract

Acute renal failure (ARF) is increasingly seen as part of the multiple organ dysfunction syndrome (MODS) in critically ill patients [1,2]. MODS is the most-frequent cause of death in patients admitted to intensive care units [3]. Severe sepsis and septic shock are the primary causes of MODS [4, 5] and develop as a result of the host response to infection of Gram-negative and Gram-positive bacteria [6]. Infectious sepsis and non-infectious systemic inflammatory response syndrome (SIRS) encompass a complex mosaic of interconnected events. Molecules such as bacterial lipopolysaccharides (LPS), microbial lipopeptides, microbial DNA, peptidoglycan and lipoteichoic acid trigger interact with the Toll-like receptors and related molecules (MD-2, MyD88), the principal sensors of the innate immune response [7–9]. Stimulus-receptor coupling activates different signal transduction pathways, leading to exacerbated generation of cytokines, and phospholipase A2-dependent, arachidonic acid-derived platelet-activating factor (PAF), leukotrienes, and thromboxanes. At the plasma level, activation of the complement (C3a, C5a, and their desarginated products) and coagulation pathways interacts with the process, as products generated in the fluid phase may in turn trigger and sustain cell activation. Other agents play a role in the pathophysiology of sepsis, such as surface-expressed and soluble adhesion molecules, kinins, thrombin, myocardial depressant substance(s), endorphin, and heat shock proteins.

Keywords

Acute Renal Failure Systemic Inflammatory Response Syndrome Continuous Renal Replacement Therapy Multiple Organ Dysfunction Syndrome Nephrol Dial Transplant 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Italia 2003

Authors and Affiliations

  • C. Tetta
  • A. Brendolan
  • V. D’Intini

There are no affiliations available

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