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 (725 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
The duct which coveys urine from the pelvis of the kidney through the ureters, bladder, and urethra.
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: Tracts, Urinary; Tract, Urinary; Urinary Tracts.
Where it fits in the MeSH classification
- Broader topics
- Urogenital System
- Narrower topics
- Kidney; Ureter; Urethra; Urinary Bladder
- See also
- Urography
Related concepts
Research landscape
PubMed indexes 496,690 records tagged with the MeSH heading “Urinary Tract” (counts retrieved 2026-10-31). 61,158 of them (12.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 269,776 records.
Reviews account for 43,330 records (8.7%) and meta-analyses for 1,499. Randomized controlled trials number 5,510 (1.1%) 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 | 269,776 |
| 2000-2009 | 76,524 |
| 2010-2019 | 89,232 |
| 2020 onward | 61,158 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 43,330 | 8.7% |
| Meta-analyses | 1,499 | 0.3% |
| Randomized controlled trials | 5,510 | 1.1% |
Method: PubMed query "Urinary Tract"[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 |
|---|---|---|---|---|
| Brainstem neurons coordinate the bladder and urethral sphincter for urination | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42559936 · DOI · PMC13446904 |
| Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42552307 · DOI · PMC13438567 |
| Acute tubular injury versus acute interstitial nephritis in the kidney precision medicine project | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42579799 · DOI · PMC13464007 |
Brainstem neurons coordinate the bladder and urethral sphincter for urination [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Urination, a vital and conserved process of emptying urine from the urinary bladder in mammals, requires precise coordination between the bladder and external urethral sphincter (EUS) that is tightly controlled by a complex neural network.
- Closing excerpt
- Thus, we identify a cell type in the brainstem that controls the bladder-urethra coordination for urination.
- 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 (188 words)
Urination, a vital and conserved process of emptying urine from the urinary bladder in mammals, requires precise coordination between the bladder and external urethral sphincter (EUS) that is tightly controlled by a complex neural network. However, the specific subpopulation of neurons that accounts for such coordination remains unidentified, limiting the development of target-specific therapies for certain urination disorders, for example, detrusor-sphincter dyssynergia. Here, we find that cells expressing estrogen receptor 1 (ESR1+) in the pontine micturition center (PMC) initiate voiding when activated and suspend ongoing voiding when suppressed, each at 100% reliability. Transection of the pelvic nerve does not impair PMCESR1+ neurons' control of the EUS via the pudendal nerve, whereas transection of the pudendal nerve does not impair their control of the bladder via the pelvic nerve. Anatomically, PMCESR1+ neurons consist of three distinct spinal-projection-based subpopulations: one targeting the sacral parasympathetic nucleus, one innervating the dorsal gray commissure, and a third that projects to both regions, thereby enforcing the coordination of bladder contraction and sphincter relaxation in a rigid temporal sequence. Thus, we identify a cell type in the brainstem that controls the bladder-urethra coordination for urination.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42559936 · DOI · PMC13446904
Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Tubular epithelial cell (TEC)-macrophage crosstalk contributes to aldosterone (Aldo)-dependent renal fibrosis in hypertension.
- Closing excerpt
- Mechanism through which Aldo/MR-induced PANX1-eATP-P2X7 signaling activation promotes macrophage pyroptosis in hypertensive renal injury.
- 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 (301 words)
Tubular epithelial cell (TEC)-macrophage crosstalk contributes to aldosterone (Aldo)-dependent renal fibrosis in hypertension. Extracellular ATP (eATP) can act as a mediator of TEC-macrophage crosstalk. However, whether and how eATP functions in Aldo-induced renal injury remain unknown. A deoxycorticosterone acetate (DOCA)-salt-induced hypertensive mouse model and a primary mouse renal tubular epithelial cell (mTEC)-bone marrow-derived macrophage (BMDM) coculture model were developed. To investigate the relationship between Aldo/MR and eATP signaling in TEC-macrophage crosstalk, specific inhibitors, adeno-associated virus (AAV)-shRNA and small interfering RNA (siRNA) were used. scRNA-seq analysis of kidneys from DOCA-salt mice was performed for verification. Urinary ATP levels and renal pannexin1 (PANX1, an ATP efflux channel) expression increased significantly in DOCA-salt mice, whereas the selective mineralocorticoid receptor (MR) antagonist finerenone treatment reduced urinary ATP levels, PANX1 expression, tubular injury, and macrophage-related inflammation. Inhibiting PANX1-eATP-P2X7 signaling with the PANX1 inhibitor probenecid, specifically knocking down tubular PANX1, or using the eATP ectonucleotidase apyrase or the P2X7 blocker AZ10606120 mitigated renal tubular damage and NLRP3-mediated pyroptosis in the renal cortex of DOCA-salt mice. Similarly, in mTECs, finerenone suppressed Aldo-induced ATP release and PANX1 upregulation. A luciferase assay confirmed the binding site of MR to the PANX1 transcription promoter. Coculture of BMDMs with mTECs under Aldo stimulation significantly increased NLRP3-mediated BMDM pyroptosis and migration. However, these effects were reversed by treating the mTECs with MR or PANX1 siRNA. Similar results were observed after treatment with apyrase or AZ10606120 in the coculture system. scRNA-seq analysis further identified the activation of P2X7/NLRP3-related pyroptosis pathway in macrophages from DOCA-salt mice. In conclusion, TECs play a critical role in macrophage pyroptosis in Aldo-induced renal injury. eATP is a key messenger involved in TEC-macrophage crosstalk. PANX1-eATP-P2X7 signaling mediates TEC‒macrophage interactions to exacerbate Aldo-driven renal inflammation in hypertension. Mechanism through which Aldo/MR-induced PANX1-eATP-P2X7 signaling activation promotes macrophage pyroptosis in hypertensive renal injury.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42552307 · DOI · PMC13438567
Acute tubular injury versus acute interstitial nephritis in the kidney precision medicine project [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BACKGROUNDAcute interstitial nephritis (AIN) is a common cause of acute kidney injury (AKI), but the diagnosis may be missed as kidney biopsies are rarely obtained when acute tubular injury (ATI) is suspected.
- Closing excerpt
- FUNDINGNational Institute of Diabetes and Digestive and Kidney Diseases grants U01DK133081, U01DK133091, U01DK133092, U01DK133093, U01DK133095, U01DK133097, U01DK114866, U01DK114908, U01DK133090, U01DK133113, U01DK133766, U01DK133768, U01DK114907, U01DK114920, U01DK114923, U01DK114933, U24DK114886, UH3DK114926, UH3DK114861, UH3DK114915, and UH3DK114937.
- 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 (236 words)
BACKGROUNDAcute interstitial nephritis (AIN) is a common cause of acute kidney injury (AKI), but the diagnosis may be missed as kidney biopsies are rarely obtained when acute tubular injury (ATI) is suspected.METHODSThe Kidney Precision Medicine Project is a cohort study that obtains kidney biopsies from individuals with AKI, which undergo pathologic and molecular interrogation. We compared ATI and AIN cases among the first 60 AKI participants.RESULTSOn clinicopathologic adjudication, 30 patients (50%) had a primary adjudicated diagnosis of ATI, 13 (22%) patients had AIN, 9 (15%) had diabetic nephropathy, and 3 (5%) had other conditions. There were increased interstitial white blood cells and tubulitis (P < 0.05 for both) in AIN compared with ATI. Prior to biopsy, the treating clinician suspected ATI in 83% of the cases with adjudicated ATI, while the treating clinician suspected AIN in 54% of the cases with AIN. Tissue transcriptomic signatures showed enrichment of proinflammatory signaling and increased expression of CXCL9, a chemokine induced by IFN-γ, in myeloid cells of participants with AIN. CXCL9 localized to inflammatory infiltration in spatial transcriptomic data.CONCLUSIONAdjudication of kidney biopsies revealed distinct pathologic and molecular profiles between ATI and AIN. Kidney biopsy should be considered more frequently in AKI, as AIN is clinically underrecognized.TRIAL REGISTRATIONClinicalTrials.gov NCT04334707.FUNDINGNational Institute of Diabetes and Digestive and Kidney Diseases grants U01DK133081, U01DK133091, U01DK133092, U01DK133093, U01DK133095, U01DK133097, U01DK114866, U01DK114908, U01DK133090, U01DK133113, U01DK133766, U01DK133768, U01DK114907, U01DK114920, U01DK114923, U01DK114933, U24DK114886, UH3DK114926, UH3DK114861, UH3DK114915, and UH3DK114937.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42579799 · DOI · PMC13464007
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 Discovery and prioritization of variants and genes for kidney function in >1.2 million individuals [4]
- Research article Systematic Review and Meta-Analysis of Native Kidney Biopsy Complications [5]
- Research article Efficacy and Tolerability of Mirabegron Compared with Antimuscarinic Monotherapy or Combination Therapies for Overactive Bladder: A Systematic Review and Network Meta-analysis [6]
- Research article Trans-ethnic kidney function association study reveals putative causal genes and effects on kidney-specific disease aetiologies [7]
- Research article Mid- and Long-Term Health Risks in Living Kidney Donors: A Systematic Review and Meta-analysis [8]
- Research article Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline [9]
References
- Li X, Li X, Li J, Qin H, Liang S, Li J, et al.. Brainstem neurons coordinate the bladder and urethral sphincter for urination. . 2026. PMID 42559936 · DOI · PMC13446904
- Wang C, Ma H, Xu J, Tang Y, Feng J, Yang Y, et al.. Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury. . 2026. PMID 42552307 · DOI · PMC13438567
- Schaub JA, Menon R, Melo Ferreira R, Kiernan E, Schmidt IM, Limonte CP, et al.. Acute tubular injury versus acute interstitial nephritis in the kidney precision medicine project. . 2026. PMID 42579799 · DOI · PMC13464007
- Stanzick KJ, Li Y, Schlosser P, Gorski M, Wuttke M, Thomas LF, et al.. Discovery and prioritization of variants and genes for kidney function in >1.2 million individuals. Nat Commun. 2021. PMID 34272381 · DOI · PMC8285412
- Poggio ED, McClelland RL, Blank KN, Hansen S, Bansal S, Bomback AS, et al.. Systematic Review and Meta-Analysis of Native Kidney Biopsy Complications. Clin J Am Soc Nephrol. 2020. PMID 33060160 · DOI · PMC7646247
- Kelleher C, Hakimi Z, Zur R, Siddiqui E, Maman K, Aballéa S, et al.. Efficacy and Tolerability of Mirabegron Compared with Antimuscarinic Monotherapy or Combination Therapies for Overactive Bladder: A Systematic Review and Network Meta-analysis. Eur Urol. 2018. PMID 29699858 · DOI
- Morris AP, Le TH, Wu H, Akbarov A, van der Most PJ, Hemani G, et al.. Trans-ethnic kidney function association study reveals putative causal genes and effects on kidney-specific disease aetiologies. Nat Commun. 2019. PMID 30604766 · DOI · PMC6318312
- O'Keeffe LM, Ramond A, Oliver-Williams C, Willeit P, Paige E, Trotter P, et al.. Mid- and Long-Term Health Risks in Living Kidney Donors: A Systematic Review and Meta-analysis. Ann Intern Med. 2018. PMID 29379948 · DOI
- Gorski M, Jung B, Li Y, Matias-Garcia PR, Wuttke M, Coassin S, et al.. Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline. Kidney Int. 2021. PMID 33137338 · DOI · PMC8010357
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
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