Evidence map›Paper›PMID 26187133›Full record

ArticleJournal of nephrology2016

C3 glomerulonephritis and autoimmune disease: more than a fortuitous association?

Mariam P Alexander, Fernando C Fervenza, An S De Vriese, Richard J H Smith, Samih H Nasr, Lynn D Cornell, Loren P Herrera Hernandez, Yuzhou Zhang, Sanjeev Sethi

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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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 2 countries.

Mariam P AlexanderDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA.
Fernando C FervenzaDivision of Nephrology and Hypertension, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA.
An S De VrieseDivision of Nephrology, AZ Sint-Jan Brugge, Brugge, Belgium.
Richard J H SmithOtolaryngology and Renal Research Laboratories, Division of Nephrology, Departments of Internal Medicine and Pediatrics, Carver College of Medicine, Iowa, IA, USA.
Samih H NasrDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA.
Lynn D CornellDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA.
Loren P Herrera HernandezDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA.
Yuzhou ZhangOtolaryngology and Renal Research Laboratories, Division of Nephrology, Departments of Internal Medicine and Pediatrics, Carver College of Medicine, Iowa, IA, USA.
Sanjeev SethiDivision of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA. sethi.sanjeev@mayo.edu.
Mayo Clinic · USAZ Sint-Jan · BEWinnMed · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C3 glomerulonephritis (C3GN) results from genetic or acquired dysregulation of the alternative complement pathway. A subset of patients may have clinical and biochemical characteristics compatible with an autoimmune disorder. We studied a cohort of 85 patients with confirmed C3GN (2007-2014), of which ten patients (3 male, 7 female; mean age 38.5 years) had an associated autoimmune disorder. All patients had abnormal ANA titers, 6 also had positive ds-DNA titers. At the time of presentation with C3GN, all 7 female patients had autoimmune-related presentations. Of the 3 male patients, only 1 patient had autoimmune-related presentations. Kidney biopsy showed predominantly mesangial proliferative or membranoproliferative glomerulonephritis. In 5 patients, the alternative pathway was evaluated. All had allele variants/polymorphisms associated with C3GN. One patient was also positive for C3Nefs. Treatment varied form conservative management to the use of prednisone alone or with cytotoxic therapy. Mean serum creatinine decreased from 2.0 to 1.4 mg/dL while proteinuria decreased from 2300 to 994 mg/24 h in 8 patients with follow-up. The study highlights the association between C3GN and autoimmune disorders, particularly in female patients. The study suggests that an autoimmune milieu may act as a trigger for the development of C3GN in genetically susceptible patients. Short-term prognosis of C3GN associated with autoimmune disorders appears excellent.

Indexed as

AutoimmunityComplement ActivationAdultAutoimmune DiseasesBiomarkersComplement C3Complement C3 Nephritic FactorDrug Therapy, CombinationFemaleGenetic MarkersGenetic Predisposition to DiseaseGlomerulonephritis, MembranoproliferativeGlucocorticoidsHumansKidney GlomerulusMaleBiomarkersC3 protein, humanComplement C3Complement C3 Nephritic FactorGenetic MarkersGlucocorticoidsPrednisoneANAAutoimmune diseaseC3 glomerulonephritisC3 glomerulopathyds-DNA

Identifiers

PMID26187133
OpenAlexW2210165534

What OpenQuestion holds

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Registered trials

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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.