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Article Dans Une Revue Orphanet Journal of Rare Diseases Année : 2014

First evidence of subclinical renal tubular injury during sickle-cell crisis.

Vincent Audard
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Gaetana Vandemelebrouck
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Mehdi Khellaf
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Philippe Grimbert
Yves Levy
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Sylvain Loric
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Bertrand Renaud
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Philippe Lang
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Bertrand Godeau
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Frédéric Galactéros
Pablo Bartolucci
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Résumé

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.

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Génétique
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Dates et versions

inserm-00986268 , version 1 (02-05-2014)

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Vincent Audard, Stéphane Moutereau, Gaetana Vandemelebrouck, Anoosha Habibi, Mehdi Khellaf, et al.. First evidence of subclinical renal tubular injury during sickle-cell crisis.. Orphanet Journal of Rare Diseases, 2014, 9 (1), pp.67. ⟨10.1186/1750-1172-9-67⟩. ⟨inserm-00986268⟩

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