Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (774 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the renal glomeruli (kidney glomerulus) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to hematuria; proteinuria; hypertension; and renal insufficiency.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Glomerulonephritides; Kidney Scarring; Scarring, Kidney; Bright Disease.
Where it fits in the MeSH classification
- Broader topics
- Nephritis
- Narrower topics
- Anti-Glomerular Basement Membrane Disease; Glomerulonephritis, IGA; Glomerulonephritis, Membranoproliferative; Glomerulonephritis, Membranous; Glomerulosclerosis, Focal Segmental; Lupus Nephritis
- See also
- Kidney Failure, Chronic
Related concepts
- Kidney Glomerulus
- Hematuria
- Proteinuria
- Hypertension
- Renal Insufficiency
Research landscape
PubMed indexes 56,655 records tagged with the MeSH heading “Glomerulonephritis” (counts retrieved 2026-11-04). 9,164 of them (16.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 26,530 records.
Reviews account for 7,616 records (13.4%) and meta-analyses for 440. Randomized controlled trials number 675 (1.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 26,530 |
| 2000-2009 | 9,493 |
| 2010-2019 | 11,468 |
| 2020 onward | 9,164 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 7,616 | 13.4% |
| Meta-analyses | 440 | 0.8% |
| Randomized controlled trials | 675 | 1.2% |
Method: PubMed query "Glomerulonephritis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Efficacy and Safety of Atrasentan in Patients with IgA Nephropathy Receiving Sodium-Glucose Cotransporter 2 Inhibitors: Placebo-Controlled, Crossover Trial | 2026 | Randomized controlled trial Design not recorded in structured metadata | 5 | cc by PMID 41904616 · DOI · PMC13567876 |
| Systematic prioritization of potential therapeutic targets for glomerulonephritis using multi-omics Mendelian randomization | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41990104 · DOI · PMC13108903 |
| Amplification cycles through innate lymphoid cells at the onset of lupus nephritis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41909692 · DOI · PMC13018116 |
Efficacy and Safety of Atrasentan in Patients with IgA Nephropathy Receiving Sodium-Glucose Cotransporter 2 Inhibitors: Placebo-Controlled, Crossover Trial [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Key pointsPatients with IgA nephropathy and proteinuria are at risk of kidney failure despite use of guideline-recommended renin-angiotensin system and sodium-glucose cotransporter 2 (SGLT2) inhibition.
- Closing excerpt
- Clinical trial registry name and registration numberNCT05834738 .
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (318 words)
Key pointsPatients with IgA nephropathy and proteinuria are at risk of kidney failure despite use of guideline-recommended renin-angiotensin system and sodium-glucose cotransporter 2 (SGLT2) inhibition. Atrasentan reduces proteinuria in IgA nephropathy, but its efficacy as adjunct to renin-angiotensin system and SGLT2 inhibition has not been rigorously tested. Atrasentan provided a clinically meaningful reduction in proteinuria in adults with IgA nephropathy treated with renin-angiotensin system and SGLT2 inhibitors.BackgroundAtrasentan, a highly selective endothelin-A receptor antagonist, is approved for proteinuria reduction in adults with IgA nephropathy. Renin-angiotensin system inhibitors (RASi) and sodium-glucose cotransporter 2 inhibitors (SGLT2i) are guideline recommended, yet the additional benefit of atrasentan has not been rigorously determined.MethodsWe performed a randomized, double-blind, placebo-controlled crossover study of atrasentan in adults with IgA nephropathy, eGFR ≥30 ml/min per 1.73 m 2 , and urinary protein >0.5 g/d while on maximal, stable RASi and SGLT2i. Participants were randomized 1:1 to either sequence AB or sequence BA (0.75 mg atrasentan [A] once daily during period 1 and matching placebo [B] during period 2, or vice versa), with a 12-week washout period in between. The primary end point was the change in urinary protein-to-creatinine ratio (UPCR) to week 12. The secondary end point was the change in UPCR to week 24. Safety end points included the type, incidence, severity, seriousness, and relatedness of adverse events (AEs).ResultsWe recruited 54 participants with mean age 48 years (SD 12), 43% female, mean (SD) eGFR 63 (22) ml/min per 1.73 m 2 , and median UPCR 1.0 g/g (Q1-Q3, 0.7-1.4). Treatment with atrasentan versus placebo resulted in a difference in geometric mean percentage change in UPCR at week 12 of -25.3% (95% confidence interval, -36.8 to -11.7; P ConclusionsAtrasentan provided a clinically meaningful reduction in proteinuria in adults with IgA nephropathy and proteinuria ≥0.5 g/d treated with RASi and SGLT2i therapy. Atrasentan was well tolerated, and no new safety signals emerged.Clinical trial registry name and registration numberNCT05834738 .
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41904616 · DOI · PMC13567876
Systematic prioritization of potential therapeutic targets for glomerulonephritis using multi-omics Mendelian randomization [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease.
- Closing excerpt
- Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (285 words)
Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease. Traditional treatments such as corticosteroids and immunosuppressants are limited by variable efficacy and severe adverse effects, highlighting the need for novel therapeutic targets and personalized strategies. We performed a systematic multi-omics Mendelian randomization (MR) analysis applying established proteomic and transcriptomic quantitative trait loci (pQTL/eQTL) resources to genome-wide association studies (GWAS) of four GN subtypes: acute, chronic, IgA nephropathy, and membranous nephropathy. Bayesian colocalization was used to strengthen causal inference, while independent replication and meta-analysis were conducted using the FinnGen cohort. Mouse knockout phenotypes, drug reposition, and computational pharmacology algorithm were applied to evaluate translational potential. Proteomic-wide MR revealed MTR as protective in chronic GN and HCK as a risk factor for membranous nephropathy, whereas CD302 and CDKN1B showed protective effects. Transcriptomic-wide MR identified candidate genes across GN subtypes: RECQL, BRSK2, and MGP in acute GN; AFM, CFHR5, and EPHB2 in chronic GN; IL6R, MBL2, and PRSS3 in IgA nephropathy; and TIMP4, HCK, and PEAR1 in membranous nephropathy. Bayesian colocalization analysis provided strong support for shared causal variants (PPH4 > 0.8) for HCK, CD302, TIMP4, PEAR1, PARP1, and FHIT. Replication and meta-analysis in the FinnGen cohort provided additional consistency across datasets, while downstream translational annotations highlighted IL6R, MBL2, C5, and CD55 as potential hub targets within immune and complement-related pathways. This integrative multi-omics study provides novel insights into the genetic architecture and therapeutic landscape of GN, identifying potential therapeutic targets that may inform precision nephrology and drug repurposing. Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41990104 · DOI · PMC13108903
Amplification cycles through innate lymphoid cells at the onset of lupus nephritis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Disease progression in autoimmune conditions such as systemic lupus erythematosus (SLE) is highly heterogeneous, and the cellular and molecular mechanisms driving disease-onset dynamics remain incompletely understood.
- Closing excerpt
- Overall, our findings lay the groundwork towards a mathematical model of immune-tissue cellular crosstalk, enabling quantification of disease severity and prediction of responses to biologic treatments in autoimmune diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (171 words)
Disease progression in autoimmune conditions such as systemic lupus erythematosus (SLE) is highly heterogeneous, and the cellular and molecular mechanisms driving disease-onset dynamics remain incompletely understood. Here, based on single-cell transcriptomics data on lupus-prone NZB/W F1 mice, we derived a mathematical cell-cell interaction model recapitulating early dynamics of innate immune cells in lupus nephritis. We identified a diverse landscape of tissue-associated ILC and vessel-associated NK cell populations. We conceived a scalable mathematical framework for analysis of immune-cell interaction dynamics. A specific model formulation considers ILC as amplifiers of inflammatory processes in the presence of autoantibodies in lupus-prone individuals. Systematic model analyses highlight the impact of positive feedback loops and spontaneous inflammatory events or environmental stimuli, and the timing-dependent effectiveness of depletion therapies. Additionally, our model links the critical role of ILC populations to hallmarks of SLE such as highly heterogeneous disease dynamics. Overall, our findings lay the groundwork towards a mathematical model of immune-tissue cellular crosstalk, enabling quantification of disease severity and prediction of responses to biologic treatments in autoimmune diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41909692 · DOI · PMC13018116
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article A systematic review and meta-analysis of pregnancy outcomes in patients with systemic lupus erythematosus and lupus nephritis [4]
- Research article Risk of End-Stage Renal Disease in Patients With Lupus Nephritis, 1971-2015: A Systematic Review and Bayesian Meta-Analysis [5]
- Research article Phospholipase A2 receptor autoantibodies and clinical outcome in patients with primary membranous nephropathy [6]
- Research article The genetic architecture of membranous nephropathy and its potential to improve non-invasive diagnosis [7]
- Research article Evaluation of the Oxford Classification of IgA nephropathy: a systematic review and meta-analysis [8]
- Research article Plasma exchange for renal vasculitis and idiopathic rapidly progressive glomerulonephritis: a meta-analysis [9]
References
- Heerspink HJL, Noronha IL, Górriz JL, Lim SK, Kotwal SS, Kirsztajn GM, et al.. Efficacy and Safety of Atrasentan in Patients with IgA Nephropathy Receiving Sodium-Glucose Cotransporter 2 Inhibitors: Placebo-Controlled, Crossover Trial. . 2026. PMID 41904616 · DOI · PMC13567876
- Li G, Jianhan F, Gu J, Wang Y, Liu J, Yang D, et al.. Systematic prioritization of potential therapeutic targets for glomerulonephritis using multi-omics Mendelian randomization. . 2026. PMID 41990104 · DOI · PMC13108903
- Kreider RL, Biniaris-Georgallis SI, Grothey B, Triantafyllopoulou A, Steinheuer LM, Thurley K. Amplification cycles through innate lymphoid cells at the onset of lupus nephritis. . 2026. PMID 41909692 · DOI · PMC13018116
- Smyth A, Oliveira GH, Lahr BD, Bailey KR, Norby SM, Garovic VD. A systematic review and meta-analysis of pregnancy outcomes in patients with systemic lupus erythematosus and lupus nephritis. Clin J Am Soc Nephrol. 2010. PMID 20688887 · DOI · PMC3001786
- Tektonidou MG, Dasgupta A, Ward MM. Risk of End-Stage Renal Disease in Patients With Lupus Nephritis, 1971-2015: A Systematic Review and Bayesian Meta-Analysis. Arthritis Rheumatol. 2016. PMID 26815601 · DOI · PMC5071782
- Hoxha E, Thiele I, Zahner G, Panzer U, Harendza S, Stahl RA. Phospholipase A2 receptor autoantibodies and clinical outcome in patients with primary membranous nephropathy. J Am Soc Nephrol. 2014. PMID 24610926 · DOI · PMC4033365
- Xie J, Liu L, Mladkova N, Li Y, Ren H, Wang W, et al.. The genetic architecture of membranous nephropathy and its potential to improve non-invasive diagnosis. Nat Commun. 2020. PMID 32231244 · DOI · PMC7105485
- Lv J, Shi S, Xu D, Zhang H, Troyanov S, Cattran DC, et al.. Evaluation of the Oxford Classification of IgA nephropathy: a systematic review and meta-analysis. Am J Kidney Dis. 2013. PMID 23820066 · DOI
- Walsh M, Catapano F, Szpirt W, Thorlund K, Bruchfeld A, Guillevin L, et al.. Plasma exchange for renal vasculitis and idiopathic rapidly progressive glomerulonephritis: a meta-analysis. Am J Kidney Dis. 2011. PMID 21194817 · DOI · PMC3062650
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.