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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/3071
Title: Correlation of biomarkers for parasite burden and immune activation with acute kidney injury in severe falciparum malaria
Authors: Katherine Plewes
Royakkers, Annick A
Josh Hanson
Md Mahtab Uddin Hasan
Shamsul Alam
Aniruddha Ghose
Maude, Richard J
Stassen, Pauline M
Prakaykaew Charunwatthana
Lee, Sue J
Turner, Gareth DH
Dondorp, Arjen M
Schultz, Marcus J
Mahidol University. Faculty of Tropical Medicine. Mahidol-Oxford Tropical Medicine Research Unit
Keywords: Open Access article;Acute kidney Injury;Pathophysiology;Falciparum malaria;Soluble urokinase-type plasminogen activator receptor;Histidine rich protein-2
Issue Date: 2014
Citation: Malaria Journal. Vol.13, (2014), 91
Abstract: Background: 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-fortrend 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.
URI: http://repository.li.mahidol.ac.th/dspace/handle/123456789/3071
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