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 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.
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.
Vincent
V
Audard
Stéphane
S
Moutereau
Gaetana
G
Vandemelebrouck
Anoosha
A
Habibi
Mehdi
M
Khellaf
Philippe
P
Grimbert
Yves
Y
Levy
Sylvain
S
Loric
Bertrand
B
Renaud
Philippe
P
Lang
Bertrand
B
Godeau
Frédéric
F
Galactéros
Pablo
P
Bartolucci
D058186:Acute Kidney Injury / Q000209:etiology*; D000328:Adult; D000755:Anemia, Sickle Cell / Q000150:complications*; D005260:Female; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000293:injuries*; D008297:Male