Evidence map›Paper›PMID 26371597›Full record

ArticleTransplantation2015

Recurrent Primary Focal Segmental Glomerulosclerosis Managed With Intensified Plasma Exchange and Concomitant Monitoring of Soluble Urokinase-Type Plasminogen Activator Receptor-Mediated Podocyte β3-integrin Activation.

Oliver Staeck, Torsten Slowinski, Ina Lieker, Kaiyin Wu, Birgit Rudolph, Danilo Schmidt, Susanne Brakemeier, Hans-Hellmut Neumayer, Changli Wei, Jochen Reiser and 3 more

Abstract read
In one paragraph

Article in Transplantation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Observational
  10. Article
  11. Article
  12. Recurrent andFrontiers in immunology · 2019
    Review
  13. Article
  14. Article
  15. suPAR and chronic kidney disease-a podocyte story.Pflugers Archiv : European journal of physiology · 2017
    Review
  16. Review
  17. Article
  18. Review
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 2 countries.

Oliver Staeck1 Department of Nephrology, Charité Universitätsmedizin Berlin, Berlin, Germany. 2 Department of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany. 3 Department of Medicine, Rush University Medical Center, Chicago, IL.
Torsten Slowinski
Ina Lieker
Kaiyin Wu
Birgit Rudolph
Danilo Schmidt
Susanne Brakemeier
Hans-Hellmut Neumayer
Changli Wei
Jochen Reiser
Klemens Budde
Fabian Halleck
Dmytro Khadzhynov
Charité - Universitätsmedizin Berlin · DERush University Medical Center · US

Funding

Role of Circulating suPAR in FSGSR01DK101350 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI REISER, JOCHEN · 2013 to 2017
$2.6M
NIDDK NIH HHS R01 DK101350
6 · The paper itself

Abstract

backgroundPrimary focal segmental glomerulosclerosis (FSGS) often causes nephrotic proteinuria and frequently results in end-stage renal disease and recurrence after kidney transplantation. Recent studies describe soluble urokinase-type plasminogen activator receptor (suPAR) as a circulating factor implicated in FSGS.

methodsThis single-center study included 12 adult patients with histologically proven primary FSGS (n = 2) or recurrent FSGS after transplantation (n = 10). The effect of plasma exchange (PE) on clinical outcome, suPAR levels, and in vitro podocyte β3-integrin activation was investigated over a median of 11 (6-18) sessions of PE.

resultsThe course of treatment was monitored in a total of 70 sessions of PE, which partly eliminated suPAR, with a mean reduction of 37 ± 12% of serum concentration per session. However, a substantial rebound was observed between sessions, with suPAR levels reaching 99 ± 22% of the pretreatment levels after a median of 4 days. Podocyte β3-integrin activation dropped significantly after PE but rebounded within 4 days concomitant with a rising suPAR level. In 11 of 12 patients, multimodal treatment (including extensive PE) reduced proteinuria significantly (from 5.3 [2.0-7.8] to 1.0 [0.4-1.6] g/d), indicating clinical efficacy of the therapy. One patient suffered allograft loss due to FSGS recurrence. A persisting response was independent of a lasting reduction in the level of total suPAR because there was no sustained significant change in suPAR levels before and after the course of intensified treatment (3814 ± 908 to 3595 ± 521 pg/mL; P = 0.496).

conclusionsWe conclude that multimodal therapy including extensive PE was associated with stabilization of recurrent FSGS and a temporary lowering of plasma suPAR as well as podocyte β3-integrin activation. Whether a sustained lowering of total suPAR results in further improved outcomes requires additional study.

Indexed as

AdultFemaleFollow-Up StudiesGlomerulosclerosis, Focal SegmentalHumansIntegrin beta3MaleMonitoring, PhysiologicPlasma ExchangePodocytesReceptors, Urokinase Plasminogen ActivatorRecurrenceRetrospective StudiesIntegrin beta3Receptors, Urokinase Plasminogen Activator

Identifiers

PMID26371597
PMCPMC4900174
OpenAlexW2400935465

What OpenQuestion holds

Textmetadata
LicenceTDM
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.