Dengue haemorrhagic fever-induced acute kidney injury without hypotension, haemolysis or rhabdomyolysis

Lima, Emerson Silva; Gorayeb, Fernanda S.; Zanon, Jeferson Rodrigo; Nogueira, Maurício Lacerda; Ramalho, Horácio José; Burdmann, Emmanuel A.

doi:10.1093/ndt/gfm431

Cited by 45 publications

(35 citation statements)

References 23 publications

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“…28,29,[44][45][46][47] In contrast to the liver, other organs such as kidney are not affected in our mouse model. Cases of dengue-induced acute kidney injury have been reported, as summarized by Lima et al 48 In this study, we were unable to observe BUN increase or renal pathological changes in DV NS1-immunized mice. Also, IgG from DV NS1-immunized mice did not bind to kidney tissue.…”

Section: Discussioncontrasting

confidence: 71%

Liver injury caused by antibodies against dengue virus nonstructural protein 1 in a murine model

Lin

Wan

Chen

et al. 2008

Laboratory Investigation

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Clinical manifestations of severe dengue diseases include thrombocytopenia, vascular leakage, and liver damage. Evidence shows that hepatic injury is involved in the pathogenesis of dengue infection; however, the mechanisms are not fully resolved. Our previous in vitro studies suggested a mechanism of molecular mimicry in which antibodies directed against dengue virus (DV) nonstructural protein 1 (NS1) cross-reacted with endothelial cells and caused inflammatory activation and apoptosis. In this study, the pathogenic effects of anti-DV NS1 antibodies were further examined in a murine model. We found, in liver sections, that anti-DV NS1 antibodies bound to naive mouse vessel endothelium and the binding activity was inhibited by preabsorption of antibodies with DV NS1. Active immunization with DV NS1 resulted in antibody deposition to liver vessel endothelium, and also apoptotic cell death of liver endothelium. Liver tissue damage was observed in DV NS1-immunized mice by histological examination. The serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were increased in mice either actively immunized with DV NS1 protein or passively immunized with antibodies obtained from DV NS1-immunized mice. Furthermore, histological examination revealed mononuclear phagocyte infiltration and cell apoptosis in mice passively immunized with antibodies obtained from mice immunized with DV NS1. Increased AST and ALT levels were observed in mice passively immunized with purified immunoglobulin G (IgG) from dengue patients compared with normal control human IgG-immunized mice. The increased AST and ALT levels were inhibited when dengue patient serum IgG was preabsorbed with DV NS1. In conclusion, active immunization with DV NS1 protein causes immune-mediated liver injury in mice. Passive immunization provides additional evidence that anti-DV NS1 antibodies may play a role in liver damage, which is a pathologic manifestation in dengue virus disease.

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Section: Discussioncontrasting

confidence: 71%

Liver injury caused by antibodies against dengue virus nonstructural protein 1 in a murine model

Lin

Wan

Chen

et al. 2008

Laboratory Investigation

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“…Immunocomplexes (IgG, IgM or both, and C3) were found at glomerulus and arterioles wall in 10 cases biopsied 2 weeks after the onset of symptoms. Lima et al (2007) reported a patient who developed AKI due to DHF without hypotension, haemolysis or rhabdomyolysis. The serum creatinine was 9.9 mg/dl, and urinalysis showed hematuria and proteins ++/3.…”

Section: Discussionmentioning

confidence: 99%

Dengue Hemorrhagic Fever in the State of Ceará, Brazil, 2005

Daher¹,

Lima²,

Brunetta³

et al. 2010

VR&R

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“…Dengue-induced AKI is usually associated with shock, hemolysis, or rhabdomyolysis, 22 but it may occur without any of these triggering factors. 23 There is no specific treatment of dengue fever. Therapy is mostly supportive, avoiding the use of aspirin and nonsteroidal antiinflammatory drugs.…”

Section: Leptospirosismentioning

confidence: 99%