ArticleKidney international2021
Impaired angiotensin II type 1 receptor signaling contributes to sepsis-induced acute kidney injury.
Article in Kidney international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06539234 (Angiotensin II Stress Test. Renin Kinetics During Treatment of Vasoplegic Shock With Angiotensin II in Relation to Hemodynamic Response to Treatment With Angiotensin II.), which is not on this map. Cited by 43 papers.
What it found
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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.
Angiotensin II Stress Test. Renin Kinetics During Treatment of Vasoplegic Shock With Angiotensin II in Relation to Hemodynamic Response to Treatment With Angiotensin II.
Who cites it
43 citing papers in PubMed, 64 citations in OpenAlex.
- An index of the initial blood pressure response to angiotensin II treatment and its association with clinical outcomes in vasodilatory shock.Critical care (London, England) · 2025Trial
- Stronger association of intact angiotensinogen with mortality than lactate or renin in critical illness: post-hoc analysis from the VICTAS trial.Critical care (London, England) · 2024Trial
- Olmesartan-Loaded PLGA Nanoparticles Attenuate Methotrexate-Induced Kidney Injury: Association with the AT1R/ERK1/2 Signaling Axis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Current and future strategies aiming at reducing catecholamine exposure in septic shock.Critical care (London, England) · 2026Review
- A novel two-hit murine model of viral-primed sepsis-associated acute kidney injury.American journal of physiology. Renal physiology · 2026Article
- Anti-Inflammatory and Protective Role of tiRNA-Glu-TTC-003 in Pediatric Sepsis Via TREM2/TLR4 Signaling Modulation.Inflammation · 2026Article
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- Causality of genetically predicted solid cancers on risk of sepsis: insights from Mendelian randomization.Discover oncology · 2025Article
- Management of renin-angiotensin system inhibitors prior to major surgery: insights from the STOP-or-NOT trial.British journal of anaesthesia · 2025Article
- Higher circulating ACE2 and DPP3 but reduced ACE and angiotensinogen in hyperreninemic sepsis patients.Clinical science (London, England : 1979) · 2025Article
- Circulating angiotensin-converting enzyme 2 concentration is associated with acute kidney injury and mortality in sepsis.PloS one · 2025Article
- The renin-angiotensin-aldosterone-system in sepsis and its clinical modulation with exogenous angiotensin II.Critical care (London, England) · 2024Review
- Angiotensin II-Real-Life Use and Literature Review.Medicina (Kaunas, Lithuania) · 2024Review
- Impaired angiotensin II signaling in septic shock.Annals of intensive care · 2024Review
- Inhibition of circulating dipeptidyl-peptidase 3 by procizumab in experimental septic shock reduces catecholamine exposure and myocardial injury.Intensive care medicine experimental · 2024Article
- Hemodynamic Support in Sepsis.Anesthesiology · 2024Review
- Review
- Renin in critically ill patients.Annals of intensive care · 2024Review
- Circulating Dipeptidyl Peptidase 3 Modulates Systemic and Renal Hemodynamics Through Cleavage of Angiotensin Peptides.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Sepsis-Associated Acute Kidney Injury: Where Are We Now?Medicina (Kaunas, Lithuania) · 2024Review
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 5 institutions in 2 countries.
Funding
Abstract
In sepsis-induced acute kidney injury, kidney blood flow may increase despite decreased glomerular filtration. Normally, angiotensin-II reduces kidney blood flow to maintain filtration. We hypothesized that sepsis reduces angiotensin type-1 receptor (AT1R) expression to account for this observation and tested this hypothesis in a patient case-control study and studies in mice. Seventy-three mice underwent cecal ligation and puncture (a sepsis model) or sham operation. Additionally, 94 septic mice received losartan (selective AT1R antagonist), angiotensin II without or with losartan, or vehicle. Cumulative urine output, kidney blood flow, blood urea nitrogen, and creatinine were measured. AT1R expression was assessed using ELISA, qPCR, and immunofluorescence. A blinded pathologist evaluated tissue for ischemic injury. AT1R expression was compared in autopsy tissue from seven patients with sepsis to that of the non-involved portion of kidney from ten individuals with kidney cancer and three non-infected but critically ill patients. By six hours post ligation/puncture, kidney blood flow doubled, blood urea nitrogen rose, and urine output fell. Concurrently, AT1R expression significantly fell 2-fold in arterioles and the macula densa. Creatinine significantly rose by 24 hours and sham operation did not alter measurements. Losartan significantly exacerbated ligation/puncture-induced changes in kidney blood flow, blood urea nitrogen, creatinine, and urine output. There was no histologic evidence of cortical ischemia. Significantly, angiotensin II prevented changes in kidney blood flow, creatinine, and urine output compared to vehicle. Co-administering losartan with angiotensin-II reversed this protection. Relative to both controls, patients with sepsis had low AT1R expression in arterioles and macula densa. Thus, murine cecal ligation/puncture and clinical sepsis decrease renal AT1R expression. Angiotensin II prevents functional changes while AT1R-blockade exacerbates them independent of ischemia in mice.
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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.