Evidence map›Paper›PMID 32635646›Full record

ReviewToxins2020

Immune Dysfunction in Uremia 2020.

Gerald Cohen

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 3 pooled it
11.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

115 citing papers in PubMed, 3 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Risk Factors for Secondary Immunodeficiency in the Aged.The journal of allergy and clinical immunology. In practice · 2026
    Review
  8. Article
  9. Article
  10. CutaneousInternational journal of molecular sciences · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Review
  16. Article
  17. Review
  18. Article
  19. Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026
    Review
  20. Article

55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Gerald CohenDepartment of Nephrology and Dialysis, Medical University of Vienna, Vienna A-1090, Austria.
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease and infections are major causes for the high incidence of morbidity and mortality of patients with chronic kidney disease. Both complications are directly or indirectly associated with disturbed functions or altered apoptotic rates of polymorphonuclear leukocytes, monocytes, lymphocytes, and dendritic cells. Normal responses of immune cells can be reduced, leading to infectious diseases or pre-activated/primed, giving rise to inflammation and subsequently to cardiovascular disease. This review summarizes the impact of kidney dysfunction on the immune system. Renal failure results in disturbed renal metabolic activities with reduced renin, erythropoietin, and vitamin D production, which adversely affects the immune system. Decreased kidney function also leads to reduced glomerular filtration and the retention of uremic toxins. A large number of uremic toxins with detrimental effects on immune cells have been identified. Besides small water-soluble and protein-bound compounds originating from the intestinal microbiome, several molecules in the middle molecular range, e.g., immunoglobulin light chains, retinol-binding protein, the neuropeptides Met-enkephalin and neuropeptide Y, endothelin-1, and the adipokines leptin and resistin, adversely affect immune cells. Posttranslational modifications such as carbamoylation, advanced glycation products, and oxidative modifications contribute to uremic toxicity. Furthermore, high-density lipoprotein from uremic patients has an altered protein profile and thereby loses its anti-inflammatory properties.

Indexed as

AnimalsCardiovascular DiseasesCommunicable DiseasesGlomerular Filtration RateHumansImmune SystemKidneyRenal Insufficiency, ChronicToxins, BiologicalUremiaToxins, Biologicalautophagycardiovascular diseaseerythropoietinimmune cellsinfectionsinflammationoxidative stressrenin-angiotensin- systemuremic toxinsvitamin D

Identifiers

PMID32635646
PMCPMC7404977
OpenAlexW3041177062

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.