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Cell-free hemoglobin mediated oxidative stress is associated with acute kidney injury and renal replacement therapy in severe falciparum malaria: an observational study Plewes, Katherine; Kingston, Hugh W; Ghose, Aniruddha; Maude, Richard J; Herdman, M. T; Leopold, Stije J; Ishioka, Haruhiko; Hasan, Md. M U; Haider, Md. S; Alam, Shamsul; Piera, Kim A; Charunwatthana, Prakaykaew; Silamut, Kamolrat; Yeo, Tsin W; Faiz, Md. A; Lee, Sue J; Mukaka, Mavuto; Turner, Gareth D; Anstey, Nicholas M; Jackson Roberts, L.; White, Nicholas J; Day, Nicholas P; Hossain, Md. A; Dondorp, Arjen M
Abstract
Background
Intravascular hemolysis is an intrinsic feature of severe malaria pathophysiology but the pathogenic role of cell-free hemoglobin-mediated oxidative stress in severe malaria associated acute kidney injury (AKI) is unknown.
Methods
As part of a prospective observational study, enrolment plasma cell-free hemoglobin (CFH), lipid peroxidation markers (F₂-isoprostanes (F₂-IsoPs) and isofurans (IsoFs)), red cell deformability, and serum creatinine were quantified in Bangladeshi patients with severe falciparum malaria (n = 107), uncomplicated malaria (n = 80) and sepsis (n = 28). The relationships between these indices and kidney function and clinical outcomes were examined.
Results
AKI was diagnosed at enrolment in 58% (62/107) of consecutive patients with severe malaria, defined by an increase in creatinine ≥1.5 times expected baseline. Severe malaria patients with AKI had significantly higher plasma cell-free hemoglobin (geometric mean CFH: 8.8 μM; 95% CI, 6.2–12.3 μM), F₂-isoprostane (56.7 pg/ml; 95% CI, 45.3–71.0 pg/ml) and isofuran (109.2 pg/ml; 95% CI, 85.1–140.1 pg/ml) concentrations on enrolment compared to those without AKI (CFH: 5.1 μM; 95% CI, 4.0–6.6 μM; P = 0.018; F2-IsoPs: 27.8 pg/ml; 95% CI, 23.7–32.7 pg/ml; P
Item Metadata
| Title |
Cell-free hemoglobin mediated oxidative stress is associated with acute kidney injury and renal replacement therapy in severe falciparum malaria: an observational study
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| Creator |
Plewes, Katherine; Kingston, Hugh W; Ghose, Aniruddha; Maude, Richard J; Herdman, M. T; Leopold, Stije J; Ishioka, Haruhiko; Hasan, Md. M U; Haider, Md. S; Alam, Shamsul; Piera, Kim A; Charunwatthana, Prakaykaew; Silamut, Kamolrat; Yeo, Tsin W; Faiz, Md. A; Lee, Sue J; Mukaka, Mavuto; Turner, Gareth D; Anstey, Nicholas M; Jackson Roberts, L.; White, Nicholas J; Day, Nicholas P; Hossain, Md. A; Dondorp, Arjen M
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| Contributor | |
| Publisher |
BioMed Central
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| Date Issued |
2017-04-27
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| Description |
Background
Intravascular hemolysis is an intrinsic feature of severe malaria pathophysiology but the pathogenic role of cell-free hemoglobin-mediated oxidative stress in severe malaria associated acute kidney injury (AKI) is unknown.
Methods
As part of a prospective observational study, enrolment plasma cell-free hemoglobin (CFH), lipid peroxidation markers (F₂-isoprostanes (F₂-IsoPs) and isofurans (IsoFs)), red cell deformability, and serum creatinine were quantified in Bangladeshi patients with severe falciparum malaria (n = 107), uncomplicated malaria (n = 80) and sepsis (n = 28). The relationships between these indices and kidney function and clinical outcomes were examined.
Results
AKI was diagnosed at enrolment in 58% (62/107) of consecutive patients with severe malaria, defined by an increase in creatinine ≥1.5 times expected baseline. Severe malaria patients with AKI had significantly higher plasma cell-free hemoglobin (geometric mean CFH: 8.8 μM; 95% CI, 6.2–12.3 μM), F₂-isoprostane (56.7 pg/ml; 95% CI, 45.3–71.0 pg/ml) and isofuran (109.2 pg/ml; 95% CI, 85.1–140.1 pg/ml) concentrations on enrolment compared to those without AKI (CFH: 5.1 μM; 95% CI, 4.0–6.6 μM; P = 0.018; F2-IsoPs: 27.8 pg/ml; 95% CI, 23.7–32.7 pg/ml; P
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| Subject | |
| Genre | |
| Type | |
| Language |
eng
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| Date Available |
2018-05-16
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| Provider |
Vancouver : University of British Columbia Library
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| Rights |
Attribution 4.0 International (CC BY 4.0)
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| DOI |
10.14288/1.0366869
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| URI | |
| Affiliation | |
| Citation |
BMC Infectious Diseases. 2017 Apr 27;17(1):313
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| Publisher DOI |
10.1186/s12879-017-2373-1
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| Peer Review Status |
Reviewed
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| Scholarly Level |
Faculty
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| Copyright Holder |
The Author(s).
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| Rights URI | |
| Aggregated Source Repository |
DSpace
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Rights
Attribution 4.0 International (CC BY 4.0)