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Orphanet J Rare Dis. 2014 Apr 29;9:67. doi: 10.1186/1750-1172-9-67.

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

Author information

1
Service de Néphrologie et Transplantation, Institut Francilien de Recherche en Néphrologie et Transplantation (IFRNT), Hôpital Henri-Mondor, Assistance Publique-Hôpitaux de Paris (AP-HP), Université Paris-Est Créteil (UPEC), 51, ave du Marechal-de-Lattre-de-Tassigny, Créteil Cedex, 94010, France. vincent.audard@hmn.aphp.fr.

Abstract

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.

PMID:
24779676
PMCID:
PMC4006801
DOI:
10.1186/1750-1172-9-67
[Indexed for MEDLINE]
Free PMC Article

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