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. 2019 May;40(2):79–97. doi: 10.33176/AACB-18-00017

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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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The epithelial linings in the kidney tubules are prone to ischaemic and reperfusion injury as well as direct nephrotoxicity. These conditions induce inflammation and alterations in the cell cycle, which may result in cell damage, apoptosis or necrotic cell death. Remnant viable epithelial cells can proliferate and thereby enable tissue repair. When repair mechanisms are insufficient, persistent injury results in acute tubular necrosis with tubular atrophy and interstitial fibrosis.