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Correlation of biomarkers for parasite burden and immune activation with acute kidney injury in severe falciparum malaria

Plewes, Katherine, Royakkers, Annick, Hanson, Josh, Hasan, Md, Alam, Shamsul, Ghose, Aniruddha, Maude, Richard, Stassen, Pauline, Charunwatthana, Prakaykaew, Lee, Sue, Turner, Gareth, Dondorp, Arjen M. and Schultz, Marcus (2014). Correlation of biomarkers for parasite burden and immune activation with acute kidney injury in severe falciparum malaria. Malaria Journal,13(1 - Article No. 91).

Document type: Journal Article
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IRMA ID cmartelxPUB173
Title Correlation of biomarkers for parasite burden and immune activation with acute kidney injury in severe falciparum malaria
Author Plewes, Katherine
Royakkers, Annick
Hanson, Josh
Hasan, Md
Alam, Shamsul
Ghose, Aniruddha
Maude, Richard
Stassen, Pauline
Charunwatthana, Prakaykaew
Lee, Sue
Turner, Gareth
Dondorp, Arjen M.
Schultz, Marcus
Journal Name Malaria Journal
Publication Date 2014
Volume Number 13
Issue Number 1 - Article No. 91
ISSN 1475-2875   (check CDU catalogue  open catalogue search in new window)
Scopus ID 2-s2.0-84899060619
Total Pages 10
Place of Publication United Kingdom
Publisher BioMed Central Ltd.
HERDC Category C1 - Journal Article (DIISR)
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.
Keywords Acute kidney injury
Pathophysiology
Falciparum malaria
Soluble urokinase-type plasminogen activator receptor
Histidine rich protein-2
DOI http://dx.doi.org/10.1186/1475-2875-13-91   (check subscription with CDU E-Gateway service for CDU Staff and Students  check subscription with CDU E-Gateway in new window)


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