NDT Advance Access originally published online on March 6, 2006
Nephrology Dialysis Transplantation 2006 21(7):1996-1998; doi:10.1093/ndt/gfl085
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Case Report
Combined therapy with dialysis and glucocorticoids in critically ill renal failure patients
Nephrology Department, University of São Paulo School of Medicine, São Paulo, São Paulo, Brazil
Correspondence and offprint requests to: Antonio Carlos Seguro, Laboratório de Pesquisa Básica LIM-12, Faculdade de Medicina da USP sala 3310, Av. Dr Arnaldo 455, São Paulo, SP 01246-903, Brazil. Email: trulu@usp.br
Keywords: critical illness; glucocorticoids; mineralocorticoids; Na+K+-exchanging ATPase; renal dialysis; sodium channels/epithelial sodium channel
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| Introduction |
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Sepsis syndrome is a significant cause of mortality in the dialysis population, accounting for more than 75% of all deaths from infection [1]. During many acute illnesses, including sepsis, an increase in serum levels of cortisol is an important physiological response that is protective against injury. This response is secondary to increased production of corticotropin-releasing hormone and corticotropin, as well as to a reduction in negative feedback from cortisol [2]. However, in addition to the well-known effect that pre-existing conditions have on the hypothalamic-pituitary-adrenal axis, it has recently been reported that cortisol deficiency occurs during the course of acute illness [3]. This blunting of the physiological response results from elevated cytokine levels, which induce systemic or tissue-specific corticosteroid resistance [4].
Cortisol deficiency in intensive care patients can be difficult to discern clinically, as clinical indicators of the diagnosis are frequently non-specific [
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Case 2
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