Evidence map›Paper›PMID 22327887›Full record

ReviewPediatric nephrology (Berlin, Germany)2012

Susceptibility to acute pyelonephritis or asymptomatic bacteriuria: host-pathogen interaction in urinary tract infections.

Bryndís Ragnarsdóttir, Catharina Svanborg

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Innate immunity · 2020
    Trial
  3. Trial
  4. Trial
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  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Naturopathic Management of Urinary Tract Infections: A Retrospective Chart Review.Journal of alternative and complementary medicine (New York, N.Y.) · 2021
    Article
  16. Article
  17. Innate immunity and urinary tract infection.Pediatric nephrology (Berlin, Germany) · 2020
    Review
  18. Article
  19. P2XPurinergic signalling · 2019
    Article
  20. Review
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

2 authors at 1 institution in 1 country.

Bryndís RagnarsdóttirInstitute of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology (MIG), Lund University, Sölvegatan 23, 22362, Lund, Sweden.
Catharina SvanborgInstitute of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology (MIG), Lund University, Sölvegatan 23, 22362, Lund, Sweden. Catharina.Svanborg@med.lu.se.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our knowledge of the molecular mechanisms of urinary tract infection (UTI) pathogenesis has advanced greatly in recent years. In this review, we provide a general background of UTI pathogenesis, followed by an update on the mechanisms of UTI susceptibility, with a particular focus on genetic variation affecting innate immunity. The innate immune response of the host is critically important in the antibacterial defence mechanisms of the urinary tract, and bacterial clearance normally proceeds without sequelae. However, slight dysfunctions in these mechanisms may result in acute disease and tissue destruction. The symptoms of acute pyelonephritis are caused by the innate immune response, and inflammation in the urinary tract decreases renal tubular function and may give rise to renal scarring, especially in paediatric patients. In contrast, in children with asymptomatic bacteriuria (ABU), bacteria persist without causing symptoms or pathology. Pathogenic agents trigger a response determined by their virulence factors, mediating adherence to the urinary tract mucosa, signalling through Toll-like receptors (TLRs) and activating the defence mechanisms. In ABU strains, such virulence factors are mostly not expressed. However, the influence of the host on UTI severity cannot be overestimated, and rapid progress is being made in clarifying host susceptibility mechanisms. For example, genetic alterations that reduce TLR4 function are associated with ABU, while polymorphisms reducing IRF3 or CXCR1 expression are associated with acute pyelonephritis and an increased risk for renal scarring. It should be plausible to "individualize" diagnosis and therapy by combining information on bacterial virulence and the host response.

Indexed as

Host-Pathogen InteractionsAcute DiseaseAnimalsAnti-Bacterial AgentsAsymptomatic DiseasesBacteriaBacteriuriaDrug Resistance, BacterialGenetic Predisposition to DiseaseGenetic VariationHeredityHumansImmunity, InnatePhenotypePrognosisPyelonephritisAnti-Bacterial Agents

Identifiers

PMID22327887
OpenAlexW2111560295

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.