Published online Aug 30, 2018. doi: 10.5409/wjcp.v7.i3.83
Peer-review started: June 20, 2018
First decision: June 19, 2018
Revised: August 1, 2018
Accepted: August 6, 2018
Article in press: August 7, 2018
Published online: August 30, 2018
Processing time: 72 Days and 4.1 Hours
Although acute kidney injury (AKI) is a common complication in hospitalized children, AKI has rarely been reported in patients with Kawasaki disease (KD). Herein, we review the clinical trajectories of AKI in patients with KD. A total of 39 patients with KD who developed AKI have been reported in 28 publications as case reports. The causes of AKI include prerenal AKI associated with acute heart failure (AHF), intrinsic AKI caused by tubulointerstitial nephritis (TIN), acute nephritic syndrome (ANS), hemolytic uremic syndrome (HUS), immune complex-mediated nephropathy, rhabdomyolysis, and KD shock syndrome (KDSS). Six of the 39 patients (15.4%) underwent renal replacement therapy. While AHF and multiple organ dysfunction syndrome developed in 41% and 68% of KD patients with AKI, respectively, all patients recovered without any renal sequelae. Although the precise pathogenic mechanism underlying the development of AKI in patients with KD is unknown, several possible mechanisms have been proposed, including T-cell-mediated immunologic abnormalities for TIN, renal and glomerular endothelial injury resulting from vasculitis for HUS, immune complex-mediated kidney injury for immune complex-mediated nephropathy and ASN, and capillary leak and an increased release of cytokines with myocardial dysfunction for KDSS.
Core tip: Acute kidney injury (AKI) has rarely been reported in patients with Kawasaki disease (KD). We review the clinical characteristics of AKI in patients with KD and show that AKI is caused by a number of pathologic changes induced by KD. Patients with KD and AKI had good outcomes, despite the developed of multiple organ dysfunction syndrome. The possible mechanisms underlying the development of AKI in KD include T-cell-mediated immunologic abnormalities, renal and glomerular endothelial injury resulted from vasculitis, immune complex-mediated kidney injury, and capillary leak and the increased release of cytokines with myocardial dysfunction.