Evidence map›Paper›PMID 27994478›Full record

ReviewInternational journal of nephrology and renovascular disease2016

Dialysis-related amyloidosis: challenges and solutions.

R Scarpioni, M Ricardi, V Albertazzi, S De Amicis, F Rastelli, L Zerbini

Open access · goldAbstract readReview
In one paragraph

Review in International journal of nephrology and renovascular disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Guideline
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Amyloids and the Heart: An Update.Journal of clinical medicine · 2024
    Review
  17. Observational
  18. Article
  19. Article
  20. Review

6 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

6 authors at 1 institution in 1 country.

R ScarpioniDepartment of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital "Guglielmo da Saliceto", Piacenza, Italy.
M RicardiDepartment of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital "Guglielmo da Saliceto", Piacenza, Italy.
V AlbertazziDepartment of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital "Guglielmo da Saliceto", Piacenza, Italy.
S De AmicisDepartment of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital "Guglielmo da Saliceto", Piacenza, Italy.
F RastelliDepartment of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital "Guglielmo da Saliceto", Piacenza, Italy.
L ZerbiniDepartment of Nephrology and Dialysis, Azienda Unità Sanitaria Local (AUSL) Hospital "Guglielmo da Saliceto", Piacenza, Italy.
Guglielmo da Saliceto Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloidosis refers to the extracellular tissue deposition of fibrils composed of low-molecular-weight subunits of a variety of proteins. These deposits may result in a wide range of clinical manifestations depending upon their type, location, and the amount of deposition. Dialysis-related amyloidosis is a serious complication of long-term dialysis therapy and is characterized by the deposition of amyloid fibrils, principally composed of β2 microglobulins (β2M), in the osteoarticular structures and viscera. Most of the β2M is eliminated through glomerular filtration and subsequent reabsorption and catabolism by the proximal tubules. As a consequence, the serum levels of β2M are inversely related to the glomerular filtration rate; therefore, in end-stage renal disease patients, β2M levels increase up to 60-fold. Serum levels of β2M are also elevated in several pathological conditions such as chronic inflammation, liver disease, and above all, in renal dysfunction. Retention of amyloidogenic protein has been attributed to several factors including type of dialysis membrane, prolonged uremic state and/or decreased diuresis, advanced glycation end products, elevated levels of cytokines and dialysate. Dialysis treatment per se has been considered to be an inflammatory stimulus, inducing cytokine production (such as interleukin-1, tumor necrosis factor-α, interleukin-6) and complement activation. The released cytokines are thought to stimulate the synthesis and release of β2M by the macrophages and/or augment the expression of human leukocyte antigens (class I), increasing β2M expression. Residual renal function is probably the best determinant of β2M levels. Therefore, it has to be maintained as long as possible. In this article, we will focus our attention on the etiology of dialysis-related amyloidosis, its prevention, therapy, and future solutions.

Indexed as

chronic inflammationhigh-flux dialysis membranelong-term dialysismineral bone diseaseβ2 microglobulin

Identifiers

PMID27994478
PMCPMC5153266
OpenAlexW2559748354

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.