Bibliographic record
Abstract
IgA nephropathy (IgAN) is the world's most common primary glomerulonephritis and a significant cause of end-stage kidney disease (ESKD).In IgAN immune complexes containing immunoglobulin A (IgA) are deposited into the glomerular mesangium, causing glomerular inflammation.A characteristic presentation of IgAN is transient gross hematuria occurring during mucosal infections.As IgA is the most abundantly produced immunoglobulin in humans and especially on mucosal surfaces, mucosal immunity has been considered to be involved in the pathogenesis of IgAN.Research considering the role of the gastrointestinal mucosa in IgAN started in the 1980s and evidence has since been accumulating on the specific factors between kidneys and intestine.IgAN has also been reported to occur more often in patients with celiac disease (CeD) and inflammatory bowel disease (IBD), compared to patients who do not suffer from diseases of intestine, enteropathies.These findings further support the theory of the presence of a gut-kidney axis.However, many factors on this topic remain unclear.According to the present literature, IgAN and enteropathies have shared genetics.The aim of this thesis is to give a detailed review of what is currently known of the shared genetics of CeD and IBD with IgAN based on current research.In this thesis, first, the characteristics of IgAN, CeD and IBD are reviewed generally.The gut-kidney axis in IgAN, as well as methods used in genetic studies are then introduced.The last section of this thesis focuses on the shared risk genetics of CeD and IBD with IgAN.Currently, there is no solid evidence of specific genetic factors connecting IgAN and CeD.However, genome-wide association studies (GWAS) have discovered susceptibility genes for IgAN that are directly or indirectly related to the risk of IBD too.Among them are genes associated with the IgA in the gut, intestinal epithelial barrier integrity, and response to mucosal pathogens.Other genetic studies have also shown that immune-mediated pathways have a key role both in the pathogenesis of IgAN and that of IBD.However further research is needed to elucidate the true possibility of shared pathogenesis between these complex diseases.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".