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First evidence of subclinical renal tubular injury during sickle-cell crisis
BACKGROUND: The pathophysiologic mechanisms classically involved in sickle-cell nephropathy include endothelial dysfunction and vascular occlusion. Arguments demonstrating that ischemia-reperfusion injury-related kidney damage might coincide with vaso-occlusive crisis (VOC) are lacking. METHODS: In...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006801/ https://www.ncbi.nlm.nih.gov/pubmed/24779676 http://dx.doi.org/10.1186/1750-1172-9-67 |
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author | Audard, Vincent Moutereau, Stéphane Vandemelebrouck, Gaetana Habibi, Anoosha Khellaf, Mehdi Grimbert, Philippe Levy, Yves Loric, Sylvain Renaud, Bertrand Lang, Philippe Godeau, Bertrand Galactéros, Frédéric Bartolucci, Pablo |
author_facet | Audard, Vincent Moutereau, Stéphane Vandemelebrouck, Gaetana Habibi, Anoosha Khellaf, Mehdi Grimbert, Philippe Levy, Yves Loric, Sylvain Renaud, Bertrand Lang, Philippe Godeau, Bertrand Galactéros, Frédéric Bartolucci, Pablo |
author_sort | Audard, Vincent |
collection | PubMed |
description | BACKGROUND: The pathophysiologic mechanisms classically involved in sickle-cell nephropathy include endothelial dysfunction and vascular occlusion. Arguments demonstrating that ischemia-reperfusion injury-related kidney damage might coincide with vaso-occlusive crisis (VOC) are lacking. METHODS: In this prospective study, we sought to determine whether tubular cells and glomerular permeability might be altered during VOC. Urine neutrophil gelatinase-associated lipocalin (NGAL) levels and albumin-excretion rates (AER) of 25 patients were evaluated prospectively during 25 VOC episodes and compared to their steady state (ST) values. RESULTS: During VOC, white blood-cell counts (WBC) and C-reactive protein (CRP) were significantly higher than at ST but creatinine levels were comparable. Urine NGAL levels were significantly increased during VOC vs ST (P = 0.007) and remained significant when normalized to urine creatinine (P = 0.004), while AER did not change significantly. The higher urine NGAL concentration was not associated with subsequent (24-48 hour) acute kidney injury. Univariate analysis identified no significant correlations between urine NGAL levels and laboratory parameters during VOC. CONCLUSIONS: These results demonstrated that subclinical ischemia-reperfusion tubular injury is common during VOC and highlight the importance of hydroelectrolyte monitoring and correction during VOC. |
format | Online Article Text |
id | pubmed-4006801 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40068012014-05-02 First evidence of subclinical renal tubular injury during sickle-cell crisis Audard, Vincent Moutereau, Stéphane Vandemelebrouck, Gaetana Habibi, Anoosha Khellaf, Mehdi Grimbert, Philippe Levy, Yves Loric, Sylvain Renaud, Bertrand Lang, Philippe Godeau, Bertrand Galactéros, Frédéric Bartolucci, Pablo Orphanet J Rare Dis Research BACKGROUND: The pathophysiologic mechanisms classically involved in sickle-cell nephropathy include endothelial dysfunction and vascular occlusion. Arguments demonstrating that ischemia-reperfusion injury-related kidney damage might coincide with vaso-occlusive crisis (VOC) are lacking. METHODS: In this prospective study, we sought to determine whether tubular cells and glomerular permeability might be altered during VOC. Urine neutrophil gelatinase-associated lipocalin (NGAL) levels and albumin-excretion rates (AER) of 25 patients were evaluated prospectively during 25 VOC episodes and compared to their steady state (ST) values. RESULTS: During VOC, white blood-cell counts (WBC) and C-reactive protein (CRP) were significantly higher than at ST but creatinine levels were comparable. Urine NGAL levels were significantly increased during VOC vs ST (P = 0.007) and remained significant when normalized to urine creatinine (P = 0.004), while AER did not change significantly. The higher urine NGAL concentration was not associated with subsequent (24-48 hour) acute kidney injury. Univariate analysis identified no significant correlations between urine NGAL levels and laboratory parameters during VOC. CONCLUSIONS: These results demonstrated that subclinical ischemia-reperfusion tubular injury is common during VOC and highlight the importance of hydroelectrolyte monitoring and correction during VOC. BioMed Central 2014-04-29 /pmc/articles/PMC4006801/ /pubmed/24779676 http://dx.doi.org/10.1186/1750-1172-9-67 Text en Copyright © 2014 Audard et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Audard, Vincent Moutereau, Stéphane Vandemelebrouck, Gaetana Habibi, Anoosha Khellaf, Mehdi Grimbert, Philippe Levy, Yves Loric, Sylvain Renaud, Bertrand Lang, Philippe Godeau, Bertrand Galactéros, Frédéric Bartolucci, Pablo First evidence of subclinical renal tubular injury during sickle-cell crisis |
title | First evidence of subclinical renal tubular injury during sickle-cell crisis |
title_full | First evidence of subclinical renal tubular injury during sickle-cell crisis |
title_fullStr | First evidence of subclinical renal tubular injury during sickle-cell crisis |
title_full_unstemmed | First evidence of subclinical renal tubular injury during sickle-cell crisis |
title_short | First evidence of subclinical renal tubular injury during sickle-cell crisis |
title_sort | first evidence of subclinical renal tubular injury during sickle-cell crisis |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006801/ https://www.ncbi.nlm.nih.gov/pubmed/24779676 http://dx.doi.org/10.1186/1750-1172-9-67 |
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