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dc.contributor.authorKatherine Plewesen_US
dc.contributor.authorAnnick A. Royakkersen_US
dc.contributor.authorJosh Hansonen_US
dc.contributor.authorMd Mahtab Uddin Hasanen_US
dc.contributor.authorShamsul Alamen_US
dc.contributor.authorAniruddha Ghoseen_US
dc.contributor.authorRichard J. Maudeen_US
dc.contributor.authorPauline M. Stassenen_US
dc.contributor.authorPrakaykaew Charunwatthanaen_US
dc.contributor.authorSue J. Leeen_US
dc.contributor.authorGareth Dh Turneren_US
dc.contributor.authorArjen M. Dondorpen_US
dc.contributor.authorMarcus J. Schultzen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherZaans Medical Hospitalsen_US
dc.contributor.otherAcademic Medical Centre, University of Amsterdamen_US
dc.contributor.otherMenzies School of Health Researchen_US
dc.contributor.otherChittagong Medical College Hospitalen_US
dc.contributor.otherNuffield Department of Clinical Medicineen_US
dc.date.accessioned2018-11-09T02:22:07Z-
dc.date.available2018-11-09T02:22:07Z-
dc.date.issued2014-03-12en_US
dc.identifier.citationMalaria Journal. Vol.13, No.1 (2014)en_US
dc.identifier.issn14752875en_US
dc.identifier.other2-s2.0-84899060619en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84899060619&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/33984-
dc.description.abstractBackground: Acute kidney injury (AKI) complicating severe Plasmodium falciparum malaria occurs in up to 40% of adult patients. The case fatality rate reaches 75% in the absence of renal replacement therapy (RRT). The precise pathophysiology of AKI in falciparum malaria remains unclear. Histopathology shows acute tubular necrosis with localization of host monocytes and parasitized red blood cells in the microvasculature. This study explored the relationship of plasma soluble urokinase-type plasminogen activator receptor (suPAR), as a proxy-measure of mononuclear cell activation, and plasma P. falciparum histidine rich protein 2 (PfHRP2), as a measure of sequestered parasite burden, with AKI in severe malaria. Methods. Admission plasma suPAR and PfHRP2 concentrations were assessed in Bangladeshi adults with severe falciparum malaria (n = 137). Patients were stratified according to AKI severity based on admission creatinine clearance. Results: A total of 106 (77%) patients had AKI; 32 (23%), 42 (31%) and 32 (23%) were classified into 'mild, 'moderate' and 'severe' AKI groups, respectively. Plasma suPAR and PfHRP2 concentrations increased with AKI severity (test-for-trend P <0.0001) and correlated with other markers of renal dysfunction. Admission plasma suPAR and PfHRP2 concentrations were higher in patients who later required RRT (P <0.0001 and P = 0.0004, respectively). In a multivariate analysis, both increasing suPAR and PfHRP2 were independently associated with increasing urine neutrophil gelatinase-associated lipocalin concentration, a marker of acute tubular necrosis (β = 16.54 (95% CI 6.36-26.71) and β = 0.07 (0.02-0.11), respectively). Conclusions: Both sequestered parasite burden and immune activation contribute to the pathogenesis of AKI in severe falciparum malaria. © 2014 Plewes et al.; licensee BioMed Central Ltd.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84899060619&origin=inwarden_US
dc.subjectImmunology and Microbiologyen_US
dc.subjectMedicineen_US
dc.titleCorrelation of biomarkers for parasite burden and immune activation with acute kidney injury in severe falciparum malariaen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1186/1475-2875-13-91en_US
Appears in Collections:Scopus 2011-2015

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