Early plasma increase in creatinine following significant kidney hypoperfusion

Background: The limitation of plasma creatinine in AKI diagnosis is mainly due to its delayed increase from time of insult, and hence resulted in delayed diagnosis. Earlier diagnosis is made possible with the discovery of various new AKI biomarker of injury. However, their performance in heterogenou...

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Main Authors:	Md Ralib, Azrina, Pickering, John W., Thann, Martin, Endre, Zoltan H.
Format:	Conference or Workshop Item
Language:	English
Published:	2012
Subjects:	R Medicine (General)
Online Access:	http://irep.iium.edu.my/37398/ http://irep.iium.edu.my/37398/1/11._Translational_2012_Early_Cr.pdf

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spelling	iium-373982014-08-11T07:51:42Z http://irep.iium.edu.my/37398/ Early plasma increase in creatinine following significant kidney hypoperfusion Md Ralib, Azrina Pickering, John W. Thann, Martin Endre, Zoltan H. R Medicine (General) Background: The limitation of plasma creatinine in AKI diagnosis is mainly due to its delayed increase from time of insult, and hence resulted in delayed diagnosis. Earlier diagnosis is made possible with the discovery of various new AKI biomarker of injury. However, their performance in heterogenous ICU population is influenced by the time of measurement from time of insult. We aimed to investigate this by measuring these biomarkers near to the time of insult, in the emergency department (ED), and during the first week of ICU and hospital stay in 3 patient groups identified as high risk for AKI. Methods: Plasma and urinary cystatin C (CysC) and neutrophil-gelatinase-associated-lipocalin (NGAL), urine gamma-glutamyl transpeptidase (GGT), α- and π- glutamyl S-transferase (GST) were measured in patients following cardiac arrest, sustained or profound hypotension, or probable ruptured abdominal aortic aneurysm. Sampling was done at ED arrival, ICU entry, and at 4, 8, 16 h, and on day 2, 4 and 7. AKI was defined as creatinine increase >0.3mg/dl within 48-h or 50% within 7-days for <48-h (T-AKI) or ≥48-h (Sustained-AKI). Results: Of the 77 patients, 45 developed AKI (27 T-AKI, 18 Sustained-AKI). In 37 (80%) AKI was diagnosed in the ED, with the mean time of insult of 1.2 ± 0.7 hours. Only a maximum percentage of 27 ± 13 % can be explained by total loss of GFR for the duration from insult to measurement. In 17 of these, AKI was no longer present on ICU entry based on creatinine, and there was no associated increase in injury biomarkers. Plasma and urine NGAL, and cystatin C increased progressively from no AKI, T-AKI and S-AKI [p<0.0001]. Urine NGAL and π-GST measured on ICU admission predicted death and dialysis. Conclusions: Early increase of plasma creatinine following significant renal hypoperfusion is common and cannot be solely explained by reduced renal perfusion. Sustained-AKI is associated in a more severe renal tubular injury. In the presence of high creatinine in the ED, urine NGAL or π-GST measurement may assist in further clinical decision making. 2012 Conference or Workshop Item PeerReviewed application/pdf en http://irep.iium.edu.my/37398/1/11._Translational_2012_Early_Cr.pdf Md Ralib, Azrina and Pickering, John W. and Thann, Martin and Endre, Zoltan H. (2012) Early plasma increase in creatinine following significant kidney hypoperfusion. In: Translational Nephrology: From Mechanisms to Therapeutics, Meeting of the Renal Scientists, Australia and New Zealand Society of Nephrology, in conjunction with The Kidney in Health and Disease Research Theme, University of Chicago, 24-25 Aug. 2012, Queenstown, New Zealand.
repository_type	Digital Repository
institution_category	Local University
institution	International Islamic University Malaysia
building	IIUM Repository
collection	Online Access
language	English
topic	R Medicine (General)
spellingShingle	R Medicine (General) Md Ralib, Azrina Pickering, John W. Thann, Martin Endre, Zoltan H. Early plasma increase in creatinine following significant kidney hypoperfusion
description	Background: The limitation of plasma creatinine in AKI diagnosis is mainly due to its delayed increase from time of insult, and hence resulted in delayed diagnosis. Earlier diagnosis is made possible with the discovery of various new AKI biomarker of injury. However, their performance in heterogenous ICU population is influenced by the time of measurement from time of insult. We aimed to investigate this by measuring these biomarkers near to the time of insult, in the emergency department (ED), and during the first week of ICU and hospital stay in 3 patient groups identified as high risk for AKI. Methods: Plasma and urinary cystatin C (CysC) and neutrophil-gelatinase-associated-lipocalin (NGAL), urine gamma-glutamyl transpeptidase (GGT), α- and π- glutamyl S-transferase (GST) were measured in patients following cardiac arrest, sustained or profound hypotension, or probable ruptured abdominal aortic aneurysm. Sampling was done at ED arrival, ICU entry, and at 4, 8, 16 h, and on day 2, 4 and 7. AKI was defined as creatinine increase >0.3mg/dl within 48-h or 50% within 7-days for <48-h (T-AKI) or ≥48-h (Sustained-AKI). Results: Of the 77 patients, 45 developed AKI (27 T-AKI, 18 Sustained-AKI). In 37 (80%) AKI was diagnosed in the ED, with the mean time of insult of 1.2 ± 0.7 hours. Only a maximum percentage of 27 ± 13 % can be explained by total loss of GFR for the duration from insult to measurement. In 17 of these, AKI was no longer present on ICU entry based on creatinine, and there was no associated increase in injury biomarkers. Plasma and urine NGAL, and cystatin C increased progressively from no AKI, T-AKI and S-AKI [p<0.0001]. Urine NGAL and π-GST measured on ICU admission predicted death and dialysis. Conclusions: Early increase of plasma creatinine following significant renal hypoperfusion is common and cannot be solely explained by reduced renal perfusion. Sustained-AKI is associated in a more severe renal tubular injury. In the presence of high creatinine in the ED, urine NGAL or π-GST measurement may assist in further clinical decision making.
format	Conference or Workshop Item
author	Md Ralib, Azrina Pickering, John W. Thann, Martin Endre, Zoltan H.
author_facet	Md Ralib, Azrina Pickering, John W. Thann, Martin Endre, Zoltan H.
author_sort	Md Ralib, Azrina
title	Early plasma increase in creatinine following significant kidney hypoperfusion
title_short	Early plasma increase in creatinine following significant kidney hypoperfusion
title_full	Early plasma increase in creatinine following significant kidney hypoperfusion
title_fullStr	Early plasma increase in creatinine following significant kidney hypoperfusion
title_full_unstemmed	Early plasma increase in creatinine following significant kidney hypoperfusion
title_sort	early plasma increase in creatinine following significant kidney hypoperfusion
publishDate	2012
url	http://irep.iium.edu.my/37398/ http://irep.iium.edu.my/37398/1/11._Translational_2012_Early_Cr.pdf
first_indexed	2023-09-18T20:53:40Z
last_indexed	2023-09-18T20:53:40Z
_version_	1777410161028104192

Early plasma increase in creatinine following significant kidney hypoperfusion

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