ArticlePloS one2018
The angiotensin II/AT1 receptor pathway mediates malaria-induced acute kidney injury.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Losartan treatment attenuates the cardiorenal alterations in a rat model of hemorrhagic insular stroke.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026Article
- Antiproteinuric effect of dapagliflozin attenuates tubule-interstitial injury development in subclinical acute kidney injury animal model.Frontiers in pharmacology · 2026Article
- Angiotensin receptor blocker ameliorates the development of tubulointerstitial injury and fibrosis associated with tubular proteinuria observed in subclinical diabetic kidney disease.Frontiers in pharmacology · 2026Article
- Animal Models of Malaria-Associated Acute Kidney Injury.Seminars in nephrology · 2025Review
- CD8Frontiers in cellular and infection microbiology · 2025Article
- Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.Bioscience reports · 2024Review
- Involvement of Inflammatory Cytokines, Renal NaPi-IIa Cotransporter, and TRAIL Induced-Apoptosis in Experimental Malaria-Associated Acute Kidney Injury.Pathogens (Basel, Switzerland) · 2024Article
- PRL2 regulates neutrophil extracellular trap formation which contributes to severe malaria and acute lung injury.Nature communications · 2024Article
- Review
- Novel Experimental Mouse Model to Study Malaria-Associated Acute Kidney Injury.Pathogens (Basel, Switzerland) · 2023Article
- Rapamycin treatment induces tubular proteinuria: role of megalin-mediated protein reabsorption.Frontiers in pharmacology · 2023Article
- The monoterpene 1,8-cineole prevents cerebral edema in a murine model of severe malaria.PloS one · 2022Article
- Experimental malaria-associated acute kidney injury is independent of parasite sequestration and resolves upon antimalarial treatment.Frontiers in cellular and infection microbiology · 2022Article
- Malaria link of hypertension: a hidden syndicate of angiotensin II, bradykinin and sphingosine 1-phosphate.Human cell · 2021Review
- Immunopathology of Acute Kidney Injury in Severe Malaria.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malaria-induced acute kidney injury (MAKI) is a life-threatening complication of severe malaria. Here, we investigated the potential role of the angiotensin II (Ang II)/AT1 receptor pathway in the development of MAKI. We used C57BL/6 mice infected by Plasmodium berghei ANKA (PbA-infected mice), a well-known murine model of severe malaria. The animals were treated with 20 mg/kg/day losartan, an antagonist of AT1 receptor, or captopril, an angiotensin-converting enzyme inhibitor. We observed an increase in the levels of plasma creatinine and blood urea nitrogen associated with a significant decrease in creatinine clearance, a marker of glomerular flow rate, and glomerular hypercellularity, indicating glomerular injury. PbA-infected mice also presented proteinuria and a high level of urinary γ-glutamyltransferase activity associated with an increase in collagen deposition and interstitial space, showing tubule-interstitial injury. PbA-infected mice were also found to have increased fractional excretion of sodium (FENa+) coupled with decreased cortical (Na++K+)ATPase activity. These injuries were associated with an increase in pro-inflammatory cytokines, such as tumor necrosis factor alpha, interleukin-6, interleukin-17, and interferon gamma, in the renal cortex of PbA-infected mice. All modifications of these structural, biochemical, and functional parameters observed in PbA-infected mice were avoided with simultaneous treatment with losartan or captopril. Our data allow us to postulate that the Ang II/AT1 receptor pathway mediates an increase in renal pro-inflammatory cytokines, which in turn leads to the glomerular and tubular injuries observed in MAKI.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.