Evidence map›Paper›PMID 26788465›Full record

ReviewWorld journal of nephrology2016

Secondary amyloidosis in autoinflammatory diseases and the role of inflammation in renal damage.

Roberto Scarpioni, Marco Ricardi, Vittorio Albertazzi

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Article
  7. The Emerging Specialty of Cardio-Rheumatology.Current atherosclerosis reports · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Kidney Involvement in Autoinflammatory Diseases.Kidney diseases (Basel, Switzerland) · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Continuous veno-venous hemofiltration for severe acute pancreatitis.The Cochrane database of systematic reviews · 2019
    Review
  19. Article
  20. An inflammatory profile linked to increased suicide risk.Journal of affective disorders · 2019
    Article
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 2 countries.

Roberto ScarpioniRoberto Scarpioni, Marco Ricardi, Vittorio Albertazzi, Department of Nephrology and Dialysis, AUSL Hospital "Guglielmo da Saliceto", 29121 Piacenza, Italy.
Marco RicardiRoberto Scarpioni, Marco Ricardi, Vittorio Albertazzi, Department of Nephrology and Dialysis, AUSL Hospital "Guglielmo da Saliceto", 29121 Piacenza, Italy.
Vittorio AlbertazziRoberto Scarpioni, Marco Ricardi, Vittorio Albertazzi, Department of Nephrology and Dialysis, AUSL Hospital "Guglielmo da Saliceto", 29121 Piacenza, Italy.
Creative Research Enterprises (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The release of proinflammatory cytokines during inflammation represents an attempt to respond to injury, but it may produce detrimental effects. The inflammasome is a large, multiprotein complex that drives proinflammatory cytokine production in response to infection and tissue injury; the best-characterized inflammasome is the nod-like receptor protein-3 (NLRP3). Once activated, inflammasome leads to the active form of caspase-1, the enzyme required for the maturation of interleukin-1beta. Additional mechanisms bringing to renal inflammatory, systemic diseases and fibrotic processes were recently reported, via the activation of the inflammasome that consists of NLRP3, apoptosis associated speck-like protein and caspase-1. Several manuscripts seem to identify NLRP3 inflammasome as a possible therapeutic target in the treatment of progressive chronic kidney disease. Serum amyloid A (SAA), as acute-phase protein with also proinflammatory properties, has been shown to induce the secretion of cathepsin B and inflammasome components from human macrophages. SAA is a well recognised potent activator of the NLRP3. Here we will address our description on the involvement of the kidney in autoinflammatory diseases driven mainly by secondary, or reactive, AA amyloidosis with a particular attention on novel therapeutic approach which has to be addressed in suppressing underlying inflammatory disease and reducing the SAA concentration.

Indexed as

AmyloidosisAutoinflammatory diseaseCaspaseChronic kidney diseaseDialysisInflammationInterleukin-1Nod-like receptor protein-3Proteinuria

Identifiers

PMID26788465
PMCPMC4707170
OpenAlexW2262446102

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.