ReviewCureus2020
Panoramic Dominance of the Immune System in Cardiorenal Syndrome Type I.
Review in Cureus, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Heart Failure-Focus on Kidney Replacement Therapy: Why, When, and How?International journal of molecular sciences · 2025Review
- Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4.International journal of molecular sciences · 2023Review
- New Insight in Cardiorenal Syndrome: From Biomarkers to Therapy.International journal of molecular sciences · 2023Review
- Acute Cardiorenal Syndrome: Epidemiology, Pathophysiology, Assessment, and Treatment.Reviews in cardiovascular medicine · 2023Review
- Beyond the Cardiorenal Syndrome: Pathophysiological Approaches and Biomarkers for Renal and Cardiac Crosstalk.Diagnostics (Basel, Switzerland) · 2022Review
- Thromboinflammatory Biomarkers of Cardiorenal Syndrome in Patients With End-Stage Renal Disease.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Physiological organ cross-talk is necessary to maintain equilibrium and homeostasis. Heart and kidney are the essences of this equilibrium. Organ failure in either of these organs can perturb the bidirectional communication between them, impinging this unpleasant vascular and cellular milieu on other distant organs. Cardiorenal syndrome (CRS) type I occurs due to acute deterioration of cardiac function, ultimately causing acute kidney injury (AKI). This syndrome is an intricate condition with neurohormonal and inflammatory aspects. Inflammation creates a vicious circle filled with the innate and adaptive immune systems, pro-inflammatory cytokines, chemokines to actuate hemodynamic compromise in CRS type I patients. Pro-inflammatory cytokines not only aggravate fluid retention and venous congestion but also initiate apoptosis and oxidative stress. The immune response's primary motive is to elicit the heart and kidney to produce cytokines, intensifying the inflammatory process. Despite the possible standard of care, patient mortality, treatment cost, readmissions are extreme in CRS type I, and inflammation certainly has critical inferences warranting future research in humans.
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.