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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.


IMPACT FACTOR increased in 2015: 3.017
Rank 5 out of 30 in category Medical Laboratory Technology in the 2014 Thomson Reuters Journal Citation Report/Science Edition

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1437-4331
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The severity of pseudohyperkalaemia is not dependent upon the stage of chronic kidney disease: a prospective study

Muhammad Imran1 / 2 / Matthew Howse1 / Peter Williams1 / Graham J. Kemp2, 3 / Norman B. Roberts2

1Department of Nephrology, Royal Liverpool and Broadgreen University Hospital Trust, Liverpool, UK

2Department of Clinical Biochemistry and Metabolic Medicine, Royal Liverpool and Broadgreen University Hospital Trust, Liverpool, UK

3Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK

Corresponding author: Andrew S. Davison, Department of Clinical Biochemistry and Metabolic Medicine, Royal Liverpool and Broadgreen University Hospital Trust, Prescot Street, Liverpool, L7 8XP, UK Phone: +44 151 706 3517, Fax: +44 151 706 5439

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 49, Issue 6, Pages 1005–1009, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2011.165, April 2011

Publication History

Received:
2010-10-28
Accepted:
2011-01-14
Published Online:
2011-04-06

Abstract

Background: Pseudohyperkalaemia may result from delay in centrifugation and storage at 4°C. We investigated whether the stage of chronic kidney disease (CKD), its aetiology or medications influence this.

Methods: Seventy-seven patients with CKD were recruited. Lithium heparin plasma samples were analysed for sodium, potassium, urea and creatinine, chloride, bicarbonate, magnesium, calcium and inorganic phosphate at 0 h and after storage of whole blood at 4°C for 6 h and 20 h. K-EDTA and fluoride-EDTA samples were analysed for full blood count and glucose at 0 h. CKD stage was determined by standard criteria.

Results: K+ increased on average by 1.0 and 3.6 mmol/L after 6 and 20 h storage of whole blood at 4°C, independent of cause or stage of CKD. K+ increase at 6 h was correlated with haemoglobin but not with white blood cell count, platelet count or glucose. Patients taking ACE inhibitors and/or angiotensin receptor blockers (ARBs) had slightly higher K+ at 0 h and increased K+ after storage for 6 h. Na+ decreased on average by 3.8 mmol/L at 20 h and was independent of CKD stage, and correlated with K+ increase.

Conclusions: K+ increased significantly with time in samples stored at 4°C in all stages of CKD. This was greater in some patients on ACE inhibitors and ARBs, and increased with haemoglobin, but was not related to the stage of CKD, white blood cell count or platelet count for the samples used in this study.

Keywords: biochemistry pre-analytical errors; pseudohyperkalaemia

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