Evidence map›Paper›PMID 30141176›Full record

ArticlePediatric nephrology (Berlin, Germany)2019

The role of properdin in complement-mediated renal diseases: a new player in complement-inhibiting therapy?

Marloes A H M Michels, Elena B Volokhina, Nicole C A J van de Kar, Lambertus P W J van den Heuvel

Open access · hybridAbstract read
In one paragraph

Article in Pediatric nephrology (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

4 authors at 1 institution in 3 countries.

Marloes A H M MichelsRadboud Institute for Molecular Life Sciences, Department of Pediatric Nephrology, Amalia Children's Hospital, Radboud University Medical Center, Geert Grooteplein Zuid 10, PO Box 9101, 6525 GA, Nijmegen, The Netherlands.ORCID 0000-0002-0750-4493
Elena B VolokhinaRadboud Institute for Molecular Life Sciences, Department of Pediatric Nephrology, Amalia Children's Hospital, Radboud University Medical Center, Geert Grooteplein Zuid 10, PO Box 9101, 6525 GA, Nijmegen, The Netherlands.
Nicole C A J van de KarRadboud Institute for Molecular Life Sciences, Department of Pediatric Nephrology, Amalia Children's Hospital, Radboud University Medical Center, Geert Grooteplein Zuid 10, PO Box 9101, 6525 GA, Nijmegen, The Netherlands.
Lambertus P W J van den HeuvelRadboud Institute for Molecular Life Sciences, Department of Pediatric Nephrology, Amalia Children's Hospital, Radboud University Medical Center, Geert Grooteplein Zuid 10, PO Box 9101, 6525 GA, Nijmegen, The Netherlands. bert.vandenheuvel@radboudumc.nl.
Radboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Properdin is known as the only positive regulator of the complement system. Properdin promotes the activity of this defense system by stabilizing its key enzymatic complexes: the complement alternative pathway (AP) convertases. Besides, some studies have indicated a role for properdin as an initiator of complement activity. Though the AP is a powerful activation route of the complement system, it is also involved in a wide variety of autoimmune and inflammatory diseases, many of which affect the kidneys. The role of properdin in regulating complement in health and disease has not received as much appraisal as the many negative AP regulators, such as factor H. Historically, properdin deficiency has been strongly associated with an increased risk for meningococcal disease. Yet only recently had studies begun to link properdin to other complement-related diseases, including renal diseases. In the light of the upcoming complement-inhibiting therapies, it is interesting whether properdin can be a therapeutic target to attenuate AP-mediated injury. A full understanding of the basic concepts of properdin biology is therefore needed. Here, we first provide an overview of the function of properdin in health and disease. Then, we explore its potential as a therapeutic target for the AP-associated renal diseases C3 glomerulopathy, atypical hemolytic uremic syndrome, and proteinuria-induced tubulointerstitial injury. Considering current knowledge, properdin-inhibiting therapy seems promising in certain cases. However, knowing the complexity of properdin's role in renal pathologies in vivo, further research is required to clarify the exact potential of properdin-targeted therapy in complement-mediated renal diseases.

Indexed as

Complement Pathway, AlternativeAtypical Hemolytic Uremic SyndromeComplement C3Complement C3 Convertase, Alternative PathwayGlomerulonephritis, MembranoproliferativeHumansImmunologic FactorsNephritis, InterstitialProperdinProtein StabilityProteinuriaComplement C3Complement C3 Convertase, Alternative PathwayImmunologic FactorsProperdinAtypical hemolytic uremic syndromeC3 glomerulopathyComplement-inhibiting therapyComplement systemProperdinProteinuria-induced tubulointerstitial injury

Identifiers

PMID30141176
PMCPMC6579773
OpenAlexW2888224013

What OpenQuestion 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 OpenQuestion graph.