Sepsis, kidney and multiple organ dysfunction : 3rd by Ronco, Claudio

By Ronco, Claudio

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Additional info for Sepsis, kidney and multiple organ dysfunction : 3rd International Course on Critical Care Nephrology, Vicenza, June 2004 : proceedings

Sample text

Both of which minimize oxidative injury. However, inflammation is also destructive. Local abscess formation causes local necrosis, and generalized inflammation can induce both increased necrosis and apoptosis leading to multiple systems organ failure [30]. However, sepsis also carries a strong anti-inflammatory response, with expression of anergy and increased susceptibility to nosocomial infection. All acute severe processes result in the expression in the systemic circulation of cytokines. However, it is difficult to assess the degree of inflammatory stimulation by measuring serum cytokine levels.

Heat shock proteins are classified by the molecular size. This classification is not arbitrary because their functions tend to also follow class size. They are cellular chaperones that prevent nascent proteins from being degraded by cytosolic enzymes. They also aid in the subsequent quaternary folding of nascent proteins prior to export. As a repair process, they aid in the tertiary and quaternary refolding of intracellular protein structure after heat or ionizing radiationinduced unfolding (denaturation).

Pathophysiology of Ischemic Acute Renal Failure 29 37 38 39 40 41 Thadhani R, Pascual M, Bonventre JV: Acute renal failure. N Engl J Med 1996;334:1448–1460. Tolkoff-Rubin NE, Rubin RH, Bonventre JV: Noninvasive renal diagnostic studies. Clin Lab Med 1988;8:507–526. Vetterlein F, Pethö A, Schmidt G: Distribution of capillary blood flow in rat kidney during postischemic renal failure. Am J Physiol 1986;251:H510–H519. Zhou W, Farrar CA, Abe K, Pratt JR, Marsh JE, Wang Y, Stahl GL, Sacks SH: Predominant role for C5b-9 in renal ischemia/reperfusion injury.

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