Evidence map›Paper›PMID 36369988›Full record

ReviewImmunological reviews2023

Kidney diseases.

Erica Daina, Monica Cortinovis, Giuseppe Remuzzi

Open access · hybridAbstract readReview
In one paragraph

Review in Immunological reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. C3G and Ig-MPGN-treatment standard.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  8. The human factor H protein family - an update.Frontiers in immunology · 2024
    Review
  9. Review
  10. Review
  11. Kidney diseases.Immunological reviews · 2023
    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

3 authors at 1 institution in 1 country.

Erica DainaIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.ORCID 0000-0002-2419-5493
Monica CortinovisIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.ORCID 0000-0001-9834-7069
Giuseppe RemuzziIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.ORCID 0000-0002-6194-3446
Mario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation and accelerated activation of the alternative pathway (AP) of complement is known to cause or accentuate several pathologic conditions in which kidney injury leads to the appearance of hematuria and proteinuria and ultimately to the development of chronic renal failure. Multiple genetic and acquired defects involving plasma- and membrane-associated proteins are probably necessary to impair the protection of host tissues and to confer a significant predisposition to AP-mediated kidney diseases. This review aims to explore how our current understanding will make it possible to identify the mechanisms that underlie AP-mediated kidney diseases and to discuss the available clinical evidence that supports complement-directed therapies. Although the value of limiting uncontrolled complement activation has long been recognized, incorporating complement-targeted treatments into clinical use has proved challenging. Availability of anti-complement therapy has dramatically transformed the outcome of atypical hemolytic uremic syndrome, one of the most severe kidney diseases. Innovative drugs that directly counteract AP dysregulation have also opened new perspectives for the management of other kidney diseases in which complement activation is involved. However, gained experience indicates that the choice of drug should be tailored to each patient's characteristics, including clinical, histologic, genetic, and biochemical parameters. Successfully treating patients requires further research in the field and close collaboration between clinicians and researchers who have special expertise in the complement system.

Indexed as

Atypical Hemolytic Uremic SyndromeKidney DiseasesComplement ActivationComplement System ProteinsHumansKidneyComplement System Proteinsalternative pathway of complementcomplement inactivating agentscomplement systemglomerular diseasesrare kidney diseases

Identifiers

PMID36369988
PMCPMC10099622
OpenAlexW4308834311

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.