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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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Clinical paradigm of AKI with pre-renal, renal or post-renal causes. AKI with a pre-renal cause, due to altered effective circulating volume, such as bleeding, dehydration and/or heart failure leading to reduced renal perfusion, is most prevalent in the hospitalised setting. AKI with renal origin may be a result from damage to glomerular, tubular, interstitial or vascular nephron compartments. Reduced urinary output in AKI may be caused by post-renal events such as obstruction of the urinary tract by an enlarged prostate, bilateral kidney stones or encasement by malignancy.