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 (819 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
Blockage in any part of the ureter causing obstruction of urine flow from the kidney to the urinary bladder. The obstruction may be congenital, acquired, unilateral, bilateral, complete, partial, acute, or chronic. Depending on the degree and duration of the obstruction, clinical features vary greatly such as hydronephrosis and obstructive nephropathy.
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: Obstructions, Ureteral; Obstruction, Ureteral; Ureteral Obstructions.
Where it fits in the MeSH classification
- Broader topics
- Ureteral Diseases
Related concepts
Research landscape
PubMed indexes 15,826 records tagged with the MeSH heading “Ureteral Obstruction” (counts retrieved 2026-11-04). 2,365 of them (14.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 7,585 records.
Reviews account for 1,130 records (7.1%) and meta-analyses for 82. Randomized controlled trials number 82 (0.5%) 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 | 7,585 |
| 2000-2009 | 2,679 |
| 2010-2019 | 3,197 |
| 2020 onward | 2,365 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,130 | 7.1% |
| Meta-analyses | 82 | 0.5% |
| Randomized controlled trials | 82 | 0.5% |
Method: PubMed query "Ureteral Obstruction"[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 |
|---|---|---|---|---|
| GSDMD-dependent neutrophil extracellular traps promote macrophage-to-myofibroblast transition and renal fibrosis in obstructive nephropathy | 2022 | Research article Design not recorded in structured metadata | 119 | cc by PMID 35941120 · DOI · PMC9360039 |
| Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis | 2023 | Review article Design not recorded in structured metadata | 106 | cc by PMID 37440209 · DOI · PMC10642920 |
| HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy | 2023 | Research article Design not recorded in structured metadata | 99 | cc by PMID 37463911 · DOI · PMC10354075 |
| Urothelial protein expression in pediatric patients with ureteropelvic junction obstruction | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42429969 · DOI · PMC13672525 |
GSDMD-dependent neutrophil extracellular traps promote macrophage-to-myofibroblast transition and renal fibrosis in obstructive nephropathy [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Renal fibrosis is a common consequence of various progressive nephropathies, including obstructive nephropathy, and ultimately leads to kidney failure.
- Closing excerpt
- Collectively, our findings demonstrate that caspase-11/GSDMD-dependent NETs promote renal fibrosis by facilitating inflammation and MMT, therefore highlighting the role and mechanisms of NETs in renal fibrosis.
- 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 (235 words)
Renal fibrosis is a common consequence of various progressive nephropathies, including obstructive nephropathy, and ultimately leads to kidney failure. Infiltration of inflammatory cells is a prominent feature of renal injury after draining blockages from the kidney, and correlates closely with the development of renal fibrosis. However, the underlying molecular mechanism behind the promotion of renal fibrosis by inflammatory cells remains unclear. Herein, we showed that unilateral ureteral obstruction (UUO) induced Gasdermin D (GSDMD) activation in neutrophils, abundant neutrophil extracellular traps (NETs) formation and macrophage-to-myofibroblast transition (MMT) characterized by α-smooth muscle actin (α-SMA) expression in macrophages. Gsdmd deletion significantly reduced infiltration of inflammatory cells in the kidneys and inhibited NETs formation, MMT and thereby renal fibrosis. Chimera studies confirmed that Gsdmd deletion in bone marrow-derived cells, instead of renal parenchymal cells, provided protection against renal fibrosis. Further, specific deletion of Gsdmd in neutrophils instead of macrophages protected the kidney from undergoing fibrosis after UUO. Single-cell RNA sequencing identified robust crosstalk between neutrophils and macrophages. In vitro, GSDMD-dependent NETs triggered p65 translocation to the nucleus, which boosted the production of inflammatory cytokines and α-SMA expression in macrophages by activating TGF-β1/Smad pathway. In addition, we demonstrated that caspase-11, that could cleave GSDMD, was required for NETs formation and renal fibrosis after UUO. Collectively, our findings demonstrate that caspase-11/GSDMD-dependent NETs promote renal fibrosis by facilitating inflammation and MMT, therefore highlighting the role and mechanisms of NETs in renal fibrosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35941120 · DOI · PMC9360039
Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The kidneys play a key role in maintaining total body homeostasis.
- Closing excerpt
- This review details key concepts and recent advances in the understanding of obstructive nephropathy, highlighting the pathophysiological hallmarks responsible for the functional and architectural changes induced by ureteral obstruction, with a special emphasis on renal fibrosis.
- 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 (212 words)
The kidneys play a key role in maintaining total body homeostasis. The complexity of this task is reflected in the unique architecture of the organ. Ureteral obstruction greatly affects renal physiology by altering hemodynamics, changing glomerular filtration and renal metabolism, and inducing architectural malformations of the kidney parenchyma, most importantly renal fibrosis. Persisting pathological changes lead to chronic kidney disease, which currently affects ∼10% of the global population and is one of the major causes of death worldwide. Studies on the consequences of ureteral obstruction date back to the 1800s. Even today, experimental unilateral ureteral obstruction (UUO) remains the standard model for tubulointerstitial fibrosis. However, the model has certain limitations when it comes to studying tubular injury and repair, as well as a limited potential for human translation. Nevertheless, ureteral obstruction has provided the scientific community with a wealth of knowledge on renal (patho)physiology. With the introduction of advanced omics techniques, the classical UUO model has remained relevant to this day and has been instrumental in understanding renal fibrosis at the molecular, genomic, and cellular levels. This review details key concepts and recent advances in the understanding of obstructive nephropathy, highlighting the pathophysiological hallmarks responsible for the functional and architectural changes induced by ureteral obstruction, with a special emphasis on renal fibrosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37440209 · DOI · PMC10642920
HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Renal inflammation and fibrosis are the common pathways leading to progressive chronic kidney disease (CKD).
- Closing excerpt
- The current study elucidates mechanisms downstream of HCK regulating macrophage activation and polarization via autophagy in CKD and identifies that selective HCK inhibitors could be potentially developed as a new therapy for renal fibrosis.
- 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 (198 words)
Renal inflammation and fibrosis are the common pathways leading to progressive chronic kidney disease (CKD). We previously identified hematopoietic cell kinase (HCK) as upregulated in human chronic allograft injury promoting kidney fibrosis; however, the cellular source and molecular mechanisms are unclear. Here, using immunostaining and single cell sequencing data, we show that HCK expression is highly enriched in pro-inflammatory macrophages in diseased kidneys. HCK-knockout (KO) or HCK-inhibitor decreases macrophage M1-like pro-inflammatory polarization, proliferation, and migration in RAW264.7 cells and bone marrow-derived macrophages (BMDM). We identify an interaction between HCK and ATG2A and CBL, two autophagy-related proteins, inhibiting autophagy flux in macrophages. In vivo, both global or myeloid cell specific HCK-KO attenuates renal inflammation and fibrosis with reduces macrophage numbers, pro-inflammatory polarization and migration into unilateral ureteral obstruction (UUO) kidneys and unilateral ischemia reperfusion injury (IRI) models. Finally, we developed a selective boron containing HCK inhibitor which can reduce macrophage pro-inflammatory activity, proliferation, and migration in vitro, and attenuate kidney fibrosis in the UUO mice. The current study elucidates mechanisms downstream of HCK regulating macrophage activation and polarization via autophagy in CKD and identifies that selective HCK inhibitors could be potentially developed as a new therapy for renal fibrosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37463911 · DOI · PMC10354075
Urothelial protein expression in pediatric patients with ureteropelvic junction obstruction [4]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundPediatric ureteropelvic junction obstruction (UPJO) is the leading cause of congenital obstructive uropathy.
- Closing excerpt
- KRT14/Cr, KRT20/Cr, and UPK2/Cr levels were significantly higher in UPJO urine compared to controls (p ConclusionsWe provide evidence of increased urothelial proteins in urine from children with UPJO in this pilot study, along with evidence of their local expression by obstructed urothelium.
- 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 (174 words)
BackgroundPediatric ureteropelvic junction obstruction (UPJO) is the leading cause of congenital obstructive uropathy. Experimental models have identified local urothelial remodeling in UPJO and implicated this remodeling as a protective adaptation to preserve kidney structural integrity and function. We investigated the expression of urothelial proteins in human urine and resected tissue specimens from children with UPJO in a pilot study.MethodsChildren undergoing pyeloplasty for clinically significant UPJO and healthy age- and sex-matched controls were included. Bladder urine samples were evaluated by ELISA for urothelial proteins (KRT5, KRT14, KRT20, UPK2, UPK3A) and normalized to creatinine (Cr). When available, kidney urine collected at pyeloplasty was compared to bladder urine from the same subject. Urothelial proteins were localized by immunofluorescence microscopy in surgically resected kidney pelvises proximal to the obstruction.ResultsTwenty-three UPJO and 14 control urines were evaluated. KRT14/Cr, KRT20/Cr, and UPK2/Cr levels were significantly higher in UPJO urine compared to controls (p ConclusionsWe provide evidence of increased urothelial proteins in urine from children with UPJO in this pilot study, along with evidence of their local expression by obstructed urothelium.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42429969 · DOI · PMC13672525
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 Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy [5]
- Research article Review. The resistive index in renal Doppler sonography: where do we stand? [6]
- Research article Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments [7]
- Research article Laparoscopic pyeloplasty: current status [8]
- Research article Robot-assisted and laparoscopic repair of ureteropelvic junction obstruction: a systematic review and meta-analysis [9]
- Research article Unilateral ureteral obstruction: beyond obstruction [10]
References
- Wang Y, Li Y, Chen Z, Yuan Y, Su Q, Ye K, et al.. GSDMD-dependent neutrophil extracellular traps promote macrophage-to-myofibroblast transition and renal fibrosis in obstructive nephropathy. . 2022. PMID 35941120 · DOI · PMC9360039
- Nørregaard R, Mutsaers HAM, Frøkiær J, Kwon TH. Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis. . 2023. PMID 37440209 · DOI · PMC10642920
- Chen M, Menon MC, Wang W, Fu J, Yi Z, Sun Z, et al.. HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy. . 2023. PMID 37463911 · DOI · PMC10354075
- Jackson AR, Gupta S, Kercsmar M, Froehlich JW, Lee RS, Becknell B, et al.. Urothelial protein expression in pediatric patients with ureteropelvic junction obstruction. . 2026. PMID 42429969 · DOI · PMC13672525
- Chevalier RL, Forbes MS, Thornhill BA. Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy. Kidney Int. 2009. PMID 19340094 · DOI
- Tublin ME, Bude RO, Platt JF. Review. The resistive index in renal Doppler sonography: where do we stand?. AJR Am J Roentgenol. 2003. PMID 12646425 · DOI
- Martínez-Klimova E, Aparicio-Trejo OE, Tapia E, Pedraza-Chaverri J. Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments. Biomolecules. 2019. PMID 30965656 · DOI · PMC6523883
- Inagaki T, Rha KH, Ong AM, Kavoussi LR, Jarrett TW. Laparoscopic pyeloplasty: current status. BJU Int. 2005. PMID 15720343 · DOI
- Autorino R, Eden C, El-Ghoneimi A, Guazzoni G, Buffi N, Peters CA, et al.. Robot-assisted and laparoscopic repair of ureteropelvic junction obstruction: a systematic review and meta-analysis. Eur Urol. 2014. PMID 23856037 · DOI
- Ucero AC, Benito-Martin A, Izquierdo MC, Sanchez-Niño MD, Sanz AB, Ramos AM, et al.. Unilateral ureteral obstruction: beyond obstruction. Int Urol Nephrol. 2014. PMID 24072452 · DOI
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.