Evidence map›Paper›PMID 22430056›Full record

ReviewNature reviews. Nephrology2012

Pathogenesis of IgA nephropathy.

Kar Neng Lai

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 6 pooled it
11.7field-weighted citation impact, top 1% 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

123 citing papers in PubMed, 6 syntheses or guidelines pooled it, 224 citations in OpenAlex.

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63 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

1 author at 1 institution in 1 country.

Kar Neng LaiNephrology Center, 10th floor, Li Shu Pui Block, Hong Kong Sanatorium and Hospital, 2 Village Road, Happy Valley, Hong Kong. knlai@hkucc.hku.hk
Hong Kong Sanatorium and Hospital · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since its first description in 1968, IgA nephropathy has remained the most common form of idiopathic glomerulonephritis leading to chronic kidney disease in developed countries. The exact pathogenesis of IgA nephropathy is still not well defined. Current data implicate an important genetic factor, especially in promoting the overproduction of an aberrant form of IgA1. The immunochemical aberrancy of IgA nephropathy is characterized by the undergalactosylation of O-glycans in the hinge region of IgA1. However, such aberrant glycosylation alone does not cause renal injury. The next stage of disease development requires the formation of glycan-specific IgG and IgA antibodies that recognize the undergalactosylated IgA1 molecule. These antibodies often have reactivity against antigens from extrinsic microorganisms and might arise from recurrent mucosal infection. B cells that respond to mucosal infections, particularly tonsillitis, might produce the nephritogenic IgA1 molecule. With increased immune-complex formation and decreased clearance owing to reduced uptake by the liver, IgA1 binds to the glomerular mesangium via an as yet unidentified receptor. Glomerular IgA1 deposits trigger the local production of cytokines and growth factors, leading to the activation of mesangial cells and the complement system. Emerging data suggest that mesangial-derived mediators following glomerular deposition of IgA1 lead to podocyte and tubulointerstitial injury via mesangio-podocytic-tubular crosstalk. This Review summarizes the latest findings in the pathogenesis of IgA nephropathy.

Indexed as

Antigen-Antibody ComplexB-LymphocytesGenetic LinkageGenome-Wide Association StudyGlomerulonephritis, IGAGlycosylationHumansImmunoglobulin AKidney GlomerulusMesangial CellsRenin-Angiotensin SystemT-LymphocytesAntigen-Antibody ComplexImmunoglobulin A

Identifiers

PMID22430056
OpenAlexW2057402675

What OpenQuestion holds

Textmetadata
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.