Evidence map›Paper›PMID 20832153›Full record

ArticleAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2010

Dense deposit disease associated with monoclonal gammopathy of undetermined significance.

Sanjeev Sethi, William R Sukov, Yuzhou Zhang, Fernando C Fervenza, Donna J Lager, Dylan V Miller, Lynn D Cornell, Srivilliputtur G Santhana Krishnan, Richard J H Smith

Abstract readCase Reports
In one paragraph

Article in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Review
  4. Article
  5. Review
  6. The role of complement in kidney disease.Nature reviews. Nephrology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. A Narrative Review on C3 Glomerulopathy: A Rare Renal Disease.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

9 authors at 3 institutions in 1 country.

Sanjeev SethiDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA. sethi.sanjeev@mayo.edu
William R Sukov
Yuzhou Zhang
Fernando C Fervenza
Donna J Lager
Dylan V Miller
Lynn D Cornell
Srivilliputtur G Santhana Krishnan
Richard J H Smith
Mayo Clinic in Arizona · USMayo Clinic · USOrthopaedic Associates of Michigan · US

Funding

A Collaborative Study of Membranoproliferative Glomerulonephritis Type IIR01DK074409 · NIDDK · UNIVERSITY OF IOWA · PI SMITH, RICHARD J.H. · 2007 to 2011
$1.3M
NIDDK NIH HHS DK074409NIDDK NIH HHS R01 DK074409
6 · The paper itself

Abstract

Dense deposit disease (DDD) is a rare glomerular disease that typically affects children, young adults, and much less commonly, older patients. The pathophysiologic process underlying DDD is uncontrolled activation of the alternative pathway (AP) of complement cascade, most frequently secondary to an autoantibody to C3 convertase called C3 nephritic factor, although mutations in factor H and autoantibodies to this protein can impair its function and also cause DDD. Since 1995, we have diagnosed DDD in 14 patients aged 49 years or older; 10 of these patients (71.4%) carry a concomitant diagnosis of monoclonal gammopathy of undetermined significance (MGUS). In 1 of these 10 patients, the index case described here, we evaluated the AP and showed low serum AP protein levels consistent with complement activity, heterozygosity for the H402 allele of factor H, and low levels of factor H autoantibodies, which can affect the ability of factor H to regulate AP activity. In aggregate, these findings suggest that in some adults with MGUS, DDD may develop as a result of autoantibodies to factor H (or other complement proteins) that on a permissive genetic background (the H402 allele of factor H) lead to dysregulation of the AP with subsequent glomerular damage. Thus, DDD in some older patients may be a distinct clinicopathologic entity that represents an uncommon complication of MGUS.

Indexed as

AutoantibodiesBiopsyComplement Factor HDiagnosis, DifferentialFemaleGlomerulonephritis, MembranoproliferativeHumansKidney GlomerulusMicroscopy, FluorescenceMiddle AgedParaproteinemiasAutoantibodiesComplement Factor H

Identifiers

PMID20832153
PMCPMC3970198
OpenAlexW1969991924

What OpenQuestion holds

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LicenceTDM
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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.