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. 2016 May;37(2):85–98.

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The contents of articles or advertisements in The Clinical Biochemist – Reviews are not to be construed as official statements, evaluations or endorsements by the AACB, its official bodies or its agents. Statements of opinion in AACB publications are those of the contributors. Print Post Approved - PP255003/01665. Copyright © 2005 The Australasian Association of Clinical Biochemists Inc. No literary matter in The Clinical Biochemist – Reviews is to be reproduced, stored in a retrieval system or transmitted in any form by electronic or mechanical means, photocopying or recording, without permission. Requests to do so should be addressed to the Editor. ISSN 0159 – 8090

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Figure 2. — Proposed mechanism of distal organ injury. AKI leads to distant organ injury through a combination of pro-inflammatory and oxidative stress-mediated mechanisms. Serum and distal organ cytokine levels (IL1, IL6, IL10 and TNFa) increase in conjunction with Leukocyte trafficking (neutrophil, lymphocyte and macrophage) and increased oxidative stress (superoxide dismutase, malondialdehyde, and glutathione depletion. In addition, sodium and water channel dysregulation in the lungs aggravate pulmonary edema. - adapted from ref (105).