Kidney and Urinary Tract Involvement in Kawasaki Disease

Watanabe, Toru

doi:10.1155/2013/831834

Cited by 47 publications

(35 citation statements)

References 65 publications

(88 reference statements)

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“…We failed to observe a significant elevation in TM and AT before IVIG in this study; this agrees with previous findings that urinary TM levels are significantly elevated in the acute phase and decline to within the normal range in the recovery phase [30]. Hypoalbuminemia is often associated with KD and is thought to result from extravasation due to enhanced vascular permeability [31] and/or to increased renal excretion [32,33]. As both soluble TM and AT have a mass close to that of albumin, their levels will likely decrease in KD patients with hypoalbuminemia.…”

Section: Discussionsupporting

confidence: 91%

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Sakurai¹,

Takatsuka²,

Onaka³

et al. 2014

Int Arch Allergy Immunol

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Background: Kawasaki disease (KD) is an acute systemic vasculitis of unknown etiology. Although endothelial cell damage associated with vasculitis might lead to the hypercoagulability that is involved in coronary artery disease, the changes in coagulation after intravenous immunoglobulin therapy (IVIG) have not been well investigated in KD. The aims of this study were to address the changes in coagulation before and after IVIG in KD, and to further elucidate the coagulation-inflammation axis, with special attention to endothelial damage. Methods: We retrospectively collected the laboratory data before and after IVIG in 26 pediatric KD patients treated at the Nara Prefecture Western Medical Center between May 2010 and April 2012. Prothrombin time (PT), activated partial thromboplastin time (APTT) and levels of fibrin/fibrinogen degradation products (FDP) and D-dimer were assessed as coagulation markers. Fibrinogen, ferritin, serum amyloid A, procalcitonin and urine F2 microglobulin were assessed as inflammation markers. Thrombomodulin, antithrombin, factor VIII activity (FVIII:C), and von Willebrand factor antigen (VWF:Ag) were used to assess endothelial damage. Results: Prolonged PT and APTT before IVIG were significantly shortened after IVIG, and elevated levels of FDP and D-dimer were significantly decreased. Elevated levels of inflammation markers had decreased significantly after IVIG, but levels of FVIII:C and VWF:Ag remained high, even after IVIG. Conclusions: Ameliorated inflammation by IVIG might improve the hypercoagulable state. Nevertheless, our results suggest that endothelial damage might be prolonged in IVIG-treated patients. Control of endothelial damage in KD is critical. i 2014 S. Karger AG, Basel

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Section: Discussionsupporting

confidence: 91%

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Sakurai¹,

Takatsuka²,

Onaka³

et al. 2014

Int Arch Allergy Immunol

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“…As KD is a disease of medium-vessel vasculitis, renal or intrarenal arterial inflammation might be the major cause of AKI. Earlier review summarized and indicated that vasculitis of arteries in the kidney, immune-complexmediated renal injuries, and T-cell immune-regulatory abnormalities might be underlying mechanisms, although the precise mechanism of kidney involvement and renal injury in KD patients remains unclear (9).…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury in patients with Kawasaki disease

et al. 2016

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“…Although patients with KD often present with sterile pyuria and trace proteinuria, other kidney complications in KD are uncommon[4]; however, several laboratory and imaging studies have shown that a number of patients with KD develop subclinical kidney injury[5,6]. …”

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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Kidney and Urinary Tract Involvement in Kawasaki Disease

Cited by 47 publications

References 65 publications

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Persistent Endothelial Damage after Intravenous Immunoglobulin Therapy in Kawasaki Disease

Acute kidney injury in patients with Kawasaki disease

Clinical features of acute kidney injury in patients with Kawasaki disease

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