ReviewJournal of biomedicine & biotechnology2012
Pathological scenario with the mannose-binding lectin in patients with IgA nephropathy.
Review in Journal of biomedicine & biotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Research progress on the lectin pathway of complement in IgA nephropathy.Frontiers in immunology · 2026Review
- Omics are Getting Us Closer to Understanding IgA Nephropathy.Archivum immunologiae et therapiae experimentalis · 2023Review
- Complement activation is associated with crescent formation in IgA nephropathy.Virchows Archiv : an international journal of pathology · 2020Article
- Serum C3/C4 ratio is a novel predictor of renal prognosis in patients with IgA nephropathy: a retrospective study.Immunologic research · 2018Article
- Mannose-Binding Lectin Levels Could Predict Prognosis in IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Article
- Increased C4 and decreased C3 levels are associated with a poor prognosis in patients with immunoglobulin A nephropathy: a retrospective study.BMC nephrology · 2017Article
- C4d deposits in IgA nephropathy: where does complement activation come from?Pediatric nephrology (Berlin, Germany) · 2017Article
- Immunoglobulin A nephropathy: a pathophysiology view.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Review
- C3a, C5a renal expression and their receptors are correlated to severity of IgA nephropathy.Journal of clinical immunology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A deeper understanding of the mechanism of complement activation may help to elucidate the pathogenesis of IgA nephropathy (IgAN). Traditionally, the activation of an alternative pathway (AP) has been recognized as an enhancer mechanism of glomerular damage. This paper documents contemporary information concerning the possible pathological mechanisms of the lectin pathway (LP) in the circulation and in the glomerulus. The circulating initiator of LP activation is not fully understood. However, ligands for mannose-binding lectin (MBL) which are among the starter molecules of the LP are aberrant glycosylated molecules-containing immune complex. Recent reports have focused on N-glycans on secretory IgA as a candidate ligand. Mesangial deposits of MBL are seen in 25% of patients with IgAN. Mesangial deposits of MBL and C4 and/or C4 breakdown products are implicated as markers for disease progression of IgAN. On the other hand, patients with MBL deficiency tend to show better clinical presentation and lower levels of urinary protein and serum creatinine than MBL-sufficient patients. It is now recognized that involvement of AP and LP constitutes an additional mechanism for explaining the progression of IgAN.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.