• Vincent Audard, Sébastien Homs, Anoosha Habibi, Frederic Galacteros, Pablo Bartolucci, Bertrand Godeau, Bertrand Renaud, Yves Levy, Philippe Grimbert, Philippe Lang, Christian Brun-Buisson, Laurent Brochard, Frederique Schortgen, Bernard Maitre, and Armand Mekontso Dessap.
• Nephrology and Renal Transplantation Department and Institut Francilien de Recherche en Nephrologie et Transplantation (IFRNT), Henri Mondor Hospital, 51 Avenue du Marechal de Lattre de Tassigny Creteil, France. vincent.audard@hmn.aphp.fr
• Nephrol. Dial. Transplant. 2010 Aug 1; 25 (8): 2524-9.

BackgroundThe association between chronic kidney involvement and sickle cell disease (SCD) has been well characterized, but our knowledge on acute kidney injury (AKI) in relation to SCD remains limited.MethodsWe retrospectively assessed 254 episodes of vaso-occlusive complication in 161 SCD patients who were admitted to our hospital: these included 174 episodes of painful crisis (PC), 58 episodes of moderate acute chest syndrome (ACS) and 22 episodes of severe ACS.ResultsThe overall incidence of AKI [defined according to Acute Kidney Injury Network (AKIN) criteria] during vaso-occlusive complications was low (4.3%) but seemed to be related to its severity: 2.3% for PC vs 6.9% for moderate ACS and 13.6% for severe ACS (P = 0.03). This finding led us prospectively to look at specific risk factors for AKI occurrence in SCD patients admitted to our intensive care unit for severe ACS and, in particular, the possible link between AKI and haemodynamic status (transthoracic echocardiography). Among patients with severe ACS, those with AKI displayed significantly greater aminotransferases, bilirubin and lactate dehydrogenase levels than patients without AKI. Echocardiography identified higher systolic pulmonary artery pressure in patients with AKI than in those without, whereas the cardiac index was similar between groups.ConclusionsAKI incidence during vaso-occlusive complications of SCD is relatively low (<5%) and appears to be confined to patients with ACS and pulmonary hypertension. These findings suggest a pathophysiological process involving right ventricular dysfunction and venous congestion.

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