Sterile pyuria in patients with Kawasaki disease originates from both the urethra and the kidney

Watanabe, Toru; Abe, Yuki; Sato, Seiichi; Uehara, Yumiko; Ikeno, Kanju; Abe, Tokinari

doi:10.1007/s00467-007-0449-7

Cited by 38 publications

(37 citation statements)

References 24 publications

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“…KD patients show abnormal urinary findings such as proteinuria, hematuria and sterile pyuria, and severe cases may have interstitial nephritis, acute renal failure, etc., rarely. Sterile pyuria is caused less by urethritis than by renal parenchymal injury and inflammation in KD, and it is also closely associated with cytokines14). KD causes also abnormalities in lipid metabolism due to the effects of cytokines such as TNF-α, IL-1 and IL-6.…”

Section: Discussionmentioning

confidence: 99%

Predictors of nonresponse to intravenous immunoglobulin therapy in Kawasaki disease

et al. 2013

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PurposeIt has been reported that 10% to 20% of children with Kawasaki disease (KD) will not respond to intravenous immunoglobulin (IVIG) treatment. In this study, we aimed to identify useful predictors of therapeutic failure in children with KD.MethodsWe examined 309 children diagnosed with KD at the Kyungpook National University Hospital and the Inje University Busan Paik Hospital between January 2005 and June 2011. We retrospectively reviewed their medical records and analyzed multiple parameters in responders and nonresponders to IVIG.ResultsAmong the 309 children, 30 (9.7%) did not respond to IVIG. They had significantly higher proportion of neutrophils, and higher levels of aspartate aminotransferase, alanine aminotransferase (ALT), total bilirubin, and N-terminal fragment of B-type natriuretic peptide than did responders. IVIG-nonresponders had a significantly longer duration of hospitalization, and more frequently experienced coronary artery lesion, and sterile pyuria. No differences in the duration of fever at initial treatment or, clinical features were noted.ConclusionTwo independent predictors (ALT≥84 IU/L, total bilirubin≥0.9 mg/dL) for nonresponse were confirmed through multivariate logistic regression analysis. Thus elevated ALT and total bilirubin levels might be useful in predicting nonresponse to IVIG therapy in children with KD.

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Section: Discussionmentioning

confidence: 99%

Predictors of nonresponse to intravenous immunoglobulin therapy in Kawasaki disease

et al. 2013

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“…Recent studies have suggested that an immunologic reaction is induced in genetically-susceptible hosts upon exposure to the KD trigger[2]. Because KD is a systemic vasculitis, KD can involve multiple organs and tissues, including the kidneys[3]. …”

Section: Introductionmentioning

confidence: 99%

Clinical features of acute kidney injury in patients with Kawasaki disease

Watanabe¹

2018

WJCP

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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.

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“…Renal involvement has been reported in KD, during the course of which sterile pyuria and temporary proteinuria have been the most commonly reported signs [8][9][10]. Temporary proteinuria, probably of both glomerular and tubular origins, has not been reported to be associated with hypoalbuminemia.…”

Section: Discussionmentioning

confidence: 99%

Relapse of nephrotic syndrome triggered by Kawasaki disease

et al. 2017

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Minor infections, allergies, insect bites, and bee stings are commonly reported causes of nephrotic syndrome (NS). Herein, we report, to the best of our knowledge, the first case of NS relapse due to Kawasaki disease (KD). An 8-year-old boy presented with high fever of 4-day duration. He had developed steroid-dependent NS at the age of 4 years and remained in remission after steroid and mizonbin therapy. Renal biopsy, performed at the age of four, showed minimal change (MC) disease. Upon examination, the patient fulfilled 5 of 6 criteria for KD under the Japanese diagnostic guidelines, with positive proteinuria. He was diagnosed with NS relapse caused by KD. Proteinuria resolved after treatment with intravenous immunoglobulin and cyclosporine A. We present the case of an 8-year-old boy, whose NS relapsed due to KD. To the best of our knowledge, this is the first case report. It is necessary to recognize that KD can trigger relapse of MCNS.

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Sterile pyuria in patients with Kawasaki disease originates from both the urethra and the kidney

Cited by 38 publications

References 24 publications

Predictors of nonresponse to intravenous immunoglobulin therapy in Kawasaki disease

Predictors of nonresponse to intravenous immunoglobulin therapy in Kawasaki disease

Clinical features of acute kidney injury in patients with Kawasaki disease

Relapse of nephrotic syndrome triggered by Kawasaki disease

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