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: 4 complete abstracts (647 words), 10 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
The outer zone of the kidney, beneath the capsule, consisting of kidney glomerulus; kidney tubules, distal; and kidney tubules, proximal.
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: Cortex, Kidney.
Where it fits in the MeSH classification
- Broader topics
- Kidney
- Narrower topics
- Kidney Glomerulus
Related concepts
- Kidney
- Kidney Glomerulus
- Kidney Tubules
- Distal
- Proximal
Research landscape
PubMed indexes 53,096 records tagged with the MeSH heading “Kidney Cortex” (counts retrieved 2026-10-31). 4,690 of them (8.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 30,003 records.
Reviews account for 4,847 records (9.1%) and meta-analyses for 23. Randomized controlled trials number 138 (0.3%) 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 | 30,003 |
| 2000-2009 | 9,180 |
| 2010-2019 | 9,223 |
| 2020 onward | 4,690 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,847 | 9.1% |
| Meta-analyses | 23 | 0.0% |
| Randomized controlled trials | 138 | 0.3% |
Method: PubMed query "Kidney Cortex"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications | 2025 | Review article Design not recorded in structured metadata | 26 | cc by PMID 40860185 · DOI · PMC12374811 |
| Spatiotemporal interaction of immune and renal cells controls glomerular crescent formation in autoimmune kidney disease | 2025 | Research article Design not recorded in structured metadata | 16 | cc by PMID 41028563 · DOI · PMC12571875 |
| The Life of a Kidney Podocyte | 2025 | Review article Design not recorded in structured metadata | 15 | cc by PMID 40698593 · DOI · PMC12284917 |
| SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3 | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41316884 · DOI · PMC12904062 |
Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Diabetic kidney disease (DKD) is a serious diabetic complication, the morbidity and mortality of which has rapidly increased worldwide.
- Closing excerpt
- In this review, we summarize and outline the mechanisms of MC injury and the interactions of MCs with other cells and discuss the progress of MC-targeted therapeutics to provide a comprehensive perspective on the prevention and treatment of DKD.
- 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 (131 words)
Diabetic kidney disease (DKD) is a serious diabetic complication, the morbidity and mortality of which has rapidly increased worldwide. As known, the pathogenesis of DKD is complex and includes mesangial cell (MC) proliferation and hypertrophy, mesangial expansion, glomerular basement membrane thickening, podocyte detachment, and tubulointerstitial damage. Thus, the role of MCs cannot be underestimated, as their exclusive positioning and diverse physiological functions are crucial for preserving the glomerular filtration membrane's composition and functionality. Considerable animal studies and clinical trials have elaborated that MCs are pivotal to the occurrence and progression of DKD. In this review, we summarize and outline the mechanisms of MC injury and the interactions of MCs with other cells and discuss the progress of MC-targeted therapeutics to provide a comprehensive perspective on the prevention and treatment of DKD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40860185 · DOI · PMC12374811
Spatiotemporal interaction of immune and renal cells controls glomerular crescent formation in autoimmune kidney disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Rapidly progressive glomerulonephritis (RPGN) is the most aggressive group of autoimmune kidney diseases and is characterized by glomerular crescent formation with proliferation of parietal epithelial cells (PECs).
- Closing excerpt
- These results highlight a spatiotemporally conserved progression program into glomerular crescents and sclerosis and indicate new treatment options for autoimmune kidney disease.
- 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 (163 words)
Rapidly progressive glomerulonephritis (RPGN) is the most aggressive group of autoimmune kidney diseases and is characterized by glomerular crescent formation with proliferation of parietal epithelial cells (PECs). However, the underlying mechanisms of glomerular crescent formation are incompletely understood. Here we provide a high-resolution spatial kidney cell atlas of 57 samples from patients with RPGN (ANCA-associated GN, lupus nephritis and anti-glomerular basement membrane-GN) to characterize the cell signaling pathways in glomerular crescent development. Early platelet-derived growth factor (PDGF) signaling from epithelial and mesangial cells caused PEC activation and proliferation in glomerular crescents, whereas later transforming growth factor (TGF)-β signaling from macrophages, T cells and epithelial and mesangial cells triggered expression of extracellular matrix components in PECs associated with glomerulosclerosis and disease progression. These findings were similar across the different GNs and were functionally validated in experimental GN by PDGF and TGFβ blockade. These results highlight a spatiotemporally conserved progression program into glomerular crescents and sclerosis and indicate new treatment options for autoimmune kidney disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41028563 · DOI · PMC12571875
The Life of a Kidney Podocyte [3]
Abstract reading summary — source excerpts
- Opening excerpt
- AimPodocytes, highly specialized epithelial cells located in the glomerulus of the kidney, are essential to the filtration barrier that ensures separation of blood and urine.
- Closing excerpt
- By highlighting the intricate balance required for podocyte survival, we reinforce their significance as both a cornerstone of renal filtration and a focal point in kidney disease research.
- 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 (204 words)
AimPodocytes, highly specialized epithelial cells located in the glomerulus of the kidney, are essential to the filtration barrier that ensures separation of blood and urine. These cells exhibit a unique architecture, characterized by an intricate network of foot processes interconnected by slit diaphragms, which serve as a critical selective filter for plasma ultrafiltration. This review focusses on synthesizing current knowledge on podocyte physiology, emphasizing the roles of key proteins, signaling pathways, and environmental factors that influence their function.MethodsPublications featuring current advances in molecular biology and imaging techniques were used to summarize new insights into the regulatory pathways governing podocyte homeostasis, as well as the mechanisms of injury and repair.ResultsThe biology of podocytes encompasses diverse processes, including cytoskeletal dynamics, cellular signaling, and interactions with neighboring cells and the extracellular matrix. Disruption of podocyte structure or function is fundamental to a variety of glomerular diseases, which can lead to proteinuria and progressive kidney failure.ConclusionUnderstanding the intricate mechanisms involved in maintaining podocyte homeostasis offers potential therapeutic strategies to protect and restore podocyte integrity, addressing a critical need in nephrology. By highlighting the intricate balance required for podocyte survival, we reinforce their significance as both a cornerstone of renal filtration and a focal point in kidney disease research.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40698593 · DOI · PMC12284917
SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3 [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Podocyte dysfunction represents both an early pathological hallmark and a key driver of proteinuria in diabetic kidney disease (DKD); nevertheless, the potential epigenetic regulatory mechanisms remain poorly defined.
- Closing excerpt
- Collectively, these findings establish SETDB2 as a critical regulator of podocyte integrity and a promising therapeutic target for DKD.
- 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 (149 words)
Podocyte dysfunction represents both an early pathological hallmark and a key driver of proteinuria in diabetic kidney disease (DKD); nevertheless, the potential epigenetic regulatory mechanisms remain poorly defined. Here, the histone methyltransferase SETDB2 is identified as a pivotal epigenetic suppressor of podocyte dysfunction and DKD progression. Glomerular SETDB2 expression exhibits a significant reduce in both DKD patients and mouse models, showing an inverse correlation with disease severity. Podocyte-specific SETDB2 deficiency exacerbates podocytes dysfunction and accelerates DKD progression, whereas its overexpression exerts renal protective effects. Mechanistically, SETDB2 directly enhances H3K9 trimethylation at the Smad3 promoter, thereby repressing SMAD3 expression and activation, ultimately preserving podocyte function. Notably, it identifies TCF21, a transcription factor downregulated in DKD, as a direct upstream regulator of Setdb2 expression via binding to promoter and activating its transcription. Collectively, these findings establish SETDB2 as a critical regulator of podocyte integrity and a promising therapeutic target for DKD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41316884 · DOI · PMC12904062
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 Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group [5]
- Research article Revision of the International Society of Nephrology/Renal Pathology Society classification for lupus nephritis: clarification of definitions, and modified National Institutes of Health activity and chronicity indices [6]
- Research article Glomerular Hyperfiltration in Diabetes: Mechanisms, Clinical Significance, and Treatment [7]
- Research article Obesity-related glomerulopathy: clinical and pathologic characteristics and pathogenesis [8]
- Research article Podocytopathies [9]
- Research article Effects of SGLT2 Inhibitors on Kidney and Cardiovascular Function [10]
References
- Feng L, Feng YY, Ren Q, Fu P, Ma L. Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications. . 2025. PMID 40860185 · DOI · PMC12374811
- Sultana Z, Khatri R, Yousefi B, Shaikh N, Jauch-Speer SL, Schaub DP, et al.. Spatiotemporal interaction of immune and renal cells controls glomerular crescent formation in autoimmune kidney disease. . 2025. PMID 41028563 · DOI · PMC12571875
- Loreth D, Sachs W, Meyer-Schwesinger C. The Life of a Kidney Podocyte. . 2025. PMID 40698593 · DOI · PMC12284917
- Li L, Jiang S, Jin Q, Qu P, Guo Y, Lan X, et al.. SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3. . 2026. PMID 41316884 · DOI · PMC12904062
- Trimarchi H, Barratt J, Cattran DC, Cook HT, Coppo R, Haas M, et al.. Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney Int. 2017. PMID 28341274 · DOI
- Bajema IM, Wilhelmus S, Alpers CE, Bruijn JA, Colvin RB, Cook HT, et al.. Revision of the International Society of Nephrology/Renal Pathology Society classification for lupus nephritis: clarification of definitions, and modified National Institutes of Health activity and chronicity indices. Kidney Int. 2018. PMID 29459092 · DOI
- Tonneijck L, Muskiet MH, Smits MM, van Bommel EJ, Heerspink HJ, van Raalte DH, et al.. Glomerular Hyperfiltration in Diabetes: Mechanisms, Clinical Significance, and Treatment. J Am Soc Nephrol. 2017. PMID 28143897 · DOI · PMC5373460
- D'Agati VD, Chagnac A, de Vries AP, Levi M, Porrini E, Herman-Edelstein M, et al.. Obesity-related glomerulopathy: clinical and pathologic characteristics and pathogenesis. Nat Rev Nephrol. 2016. PMID 27263398 · DOI
- Kopp JB, Anders HJ, Susztak K, Podestà MA, Remuzzi G, Hildebrandt F, et al.. Podocytopathies. Nat Rev Dis Primers. 2020. PMID 32792490 · DOI · PMC8162925
- Vallon V, Verma S. Effects of SGLT2 Inhibitors on Kidney and Cardiovascular Function. Annu Rev Physiol. 2021. PMID 33197224 · DOI · PMC8017904
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 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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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.