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 (621 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
Abnormal enlargement or swelling of a kidney due to dilation of the kidney calices and the kidney pelvis. It is often associated with obstruction of the ureter or chronic kidney diseases that prevents normal drainage of urine into the urinary bladder.
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: Hydronephroses.
Where it fits in the MeSH classification
- Broader topics
- Kidney Diseases
- Narrower topics
- Pyonephrosis
Related concepts
- Kidney
- Kidney Calices
- Kidney Pelvis
- Ureter
- Urinary Bladder
Research landscape
PubMed indexes 11,748 records tagged with the MeSH heading “Hydronephrosis” (counts retrieved 2026-11-04). 1,014 of them (8.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 7,186 records.
Reviews account for 740 records (6.3%) and meta-analyses for 17. Randomized controlled trials number 51 (0.4%) 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 | 7,186 |
| 2000-2009 | 1,694 |
| 2010-2019 | 1,854 |
| 2020 onward | 1,014 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 740 | 6.3% |
| Meta-analyses | 17 | 0.1% |
| Randomized controlled trials | 51 | 0.4% |
Method: PubMed query "Hydronephrosis"[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 |
|---|---|---|---|---|
| Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus | 2017 | Research article Design not recorded in structured metadata | 74 | cc by PMID 28233855 · DOI · PMC5333130 |
| Mechanisms of Developmental Toxicity of Dioxins and Related Compounds | 2019 | Review article Design not recorded in structured metadata | 48 | cc by PMID 30708991 · DOI · PMC6387164 |
| Duplex kidney formation: developmental mechanisms and genetic predisposition | 2020 | Review article Design not recorded in structured metadata | 25 | cc by PMID 32030122 · DOI · PMC6945105 |
| Can ultrasound parameters predict the diagnostic yield of diuretic renal scintigraphy in pediatric hydronephrosis? | 2025 | Research article Design not recorded in structured metadata | 0 | cc by PMID 40388407 · DOI · PMC12088069 |
Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus [1]
Abstract reading summary — source excerpts
- Opening excerpt
- NF-E2-related factor-2 (Nrf2) regulates cellular responses to oxidative and electrophilic stress.
- Closing excerpt
- In addition, tissue-specific ablation of Nrf2 in Keap1-null mice might create useful animal models to uncover novel physiological functions of Nrf2.
- 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 (138 words)
NF-E2-related factor-2 (Nrf2) regulates cellular responses to oxidative and electrophilic stress. Loss of Keap1 increases Nrf2 protein levels, and Keap1-null mice die of oesophageal hyperkeratosis because of Nrf2 hyperactivation. Here we show that deletion of oesophageal Nrf2 in Keap1-null mice allows survival until adulthood, but the animals develop polyuria with low osmolality and bilateral hydronephrosis. This phenotype is caused by defects in water reabsorption that are the result of reduced aquaporin 2 levels in the kidney. Renal tubular deletion of Keap1 promotes nephrogenic diabetes insipidus features, confirming that Nrf2 activation in developing tubular cells causes a water reabsorption defect. These findings suggest that Nrf2 activity should be tightly controlled during development in order to maintain renal homeostasis. In addition, tissue-specific ablation of Nrf2 in Keap1-null mice might create useful animal models to uncover novel physiological functions of Nrf2.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28233855 · DOI · PMC5333130
Mechanisms of Developmental Toxicity of Dioxins and Related Compounds [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Dioxins and related compounds induce morphological abnormalities in developing animals in an aryl hydrocarbon receptor (AhR)-dependent manner.
- Closing excerpt
- TCDD-induced craniofacial malformation in zebrafish is considered to result from the AHR2-dependent reduction in SRY-box 9b (SOX9b), probably partly via the noncoding RNA slincR, resulting in the underdevelopment of chondrocytes and cartilage.
- 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 (202 words)
Dioxins and related compounds induce morphological abnormalities in developing animals in an aryl hydrocarbon receptor (AhR)-dependent manner. Here we review the studies in which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is used as a prototypical compound to elucidate the pathogenesis of morphological abnormalities. TCDD-induced cleft palate in fetal mice involves a delay in palatogenesis and dissociation of fused palate shelves. TCDD-induced hydronephrosis, once considered to be caused by the anatomical obstruction of the ureter, is now separated into TCDD-induced obstructive and non-obstructive hydronephrosis, which develops during fetal and neonatal periods, respectively. In the latter, a prostaglandin E₂ synthesis pathway and urine concentration system are involved. TCDD-induced abnormal development of prostate involves agenesis of the ventral lobe. A suggested mechanism is that AhR activation in the urogenital sinus mesenchyme by TCDD modulates the wingless-type MMTV integration site family (WNT)/β-catenin signaling cascade to interfere with budding from urogenital sinus epithelium. TCDD exposure to zebrafish embryos induces loss of epicardium progenitor cells and heart malformation. AHR2-dependent downregulation of Sox9b expression in cardiomyocytes is a suggested underlying mechanism. TCDD-induced craniofacial malformation in zebrafish is considered to result from the AHR2-dependent reduction in SRY-box 9b (SOX9b), probably partly via the noncoding RNA slincR, resulting in the underdevelopment of chondrocytes and cartilage.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30708991 · DOI · PMC6387164
Duplex kidney formation: developmental mechanisms and genetic predisposition [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Congenital abnormalities of the kidney and urinary tract (CAKUT) are a highly diverse group of diseases that together belong to the most common abnormalities detected in the new-born child.
- Closing excerpt
- We will summarise the molecular programs responsible for ureter induction, review the genes that have been identified as risk factors in duplex kidney formation and discuss molecular and cellular mechanisms that may lead to this malformation.
- 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 (113 words)
Congenital abnormalities of the kidney and urinary tract (CAKUT) are a highly diverse group of diseases that together belong to the most common abnormalities detected in the new-born child. Consistent with this diversity, CAKUT are caused by mutations in a large number of genes and present a wide spectrum of phenotypes. In this review, we will focus on duplex kidneys, a relatively frequent form of CAKUT that is often asymptomatic but predisposes to vesicoureteral reflux and hydronephrosis. We will summarise the molecular programs responsible for ureter induction, review the genes that have been identified as risk factors in duplex kidney formation and discuss molecular and cellular mechanisms that may lead to this malformation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32030122 · DOI · PMC6945105
Can ultrasound parameters predict the diagnostic yield of diuretic renal scintigraphy in pediatric hydronephrosis? [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Diuretic renal scintigraphy (DRS) is a valuable imaging tool for distinguishing obstructive from non-obstructive hydronephrosis, especially in pediatric patients, but non-diagnostic results are not uncommon.
- Closing excerpt
- These findings suggest that while US parameters cannot predict non-diagnostic DRS outcomes, they are effective in identifying obstruction patterns on DRS.
- 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 (168 words)
Diuretic renal scintigraphy (DRS) is a valuable imaging tool for distinguishing obstructive from non-obstructive hydronephrosis, especially in pediatric patients, but non-diagnostic results are not uncommon. In this retrospective analytical study, we examined if kidney ultrasound (US) parameters can predict non-diagnostic DRS, and DRS with an obstruction pattern, potentially guiding patient selection to reduce unnecessary radiation exposure. The study included 67 patients (134 kidneys), 1-month to 4-years of age who underwent both DRS and US. Receiver operating characteristic (ROC) curve analysis of US parameters including parenchymal thickness, cortical thickness, medullary pyramidal thickness, anterior-posterior renal pelvic diameter, was done to assess the predictiveness of these parameters for prediction of DRS results. None of the US parameters reliably predicted non-diagnostic DRS results (AUC range: 0.41-0.61). However, these parameters demonstrated good predictiveness for identifying DRS with an obstruction pattern (AUC range: 0.69-0.87), with anterior-posterior renal pelvic diameter showing the highest performance. These findings suggest that while US parameters cannot predict non-diagnostic DRS outcomes, they are effective in identifying obstruction patterns on DRS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40388407 · DOI · PMC12088069
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 The Society for Fetal Urology consensus statement on the evaluation and management of antenatal hydronephrosis [5]
- Research article Antenatal hydronephrosis as a predictor of postnatal outcome: a meta-analysis [6]
- Research article Postnatal management of antenatal hydronephrosis [7]
- Research article Outcome of isolated antenatal hydronephrosis: a systematic review and meta-analysis [8]
- Research article Consensus on diuresis renography for investigating the dilated upper urinary tract. Radionuclides in Nephrourology Group. Consensus Committee on Diuresis Renography [9]
- Research article Hydronephrosis during pregnancy: a literature survey [10]
References
- Suzuki T, Seki S, Hiramoto K, Naganuma E, Kobayashi EH, Yamaoka A, et al.. Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus. . 2017. PMID 28233855 · DOI · PMC5333130
- Yoshioka W, Tohyama C. Mechanisms of Developmental Toxicity of Dioxins and Related Compounds. . 2019. PMID 30708991 · DOI · PMC6387164
- Kozlov VM, Schedl A. Duplex kidney formation: developmental mechanisms and genetic predisposition. . 2020. PMID 32030122 · DOI · PMC6945105
- Siripongsatian D, Tewattanarat N, Wongsurawat N, Wisanuyotin S, Theerakulpisut D. Can ultrasound parameters predict the diagnostic yield of diuretic renal scintigraphy in pediatric hydronephrosis?. . 2025. PMID 40388407 · DOI · PMC12088069
- Nguyen HT, Herndon CD, Cooper C, Gatti J, Kirsch A, Kokorowski P, et al.. The Society for Fetal Urology consensus statement on the evaluation and management of antenatal hydronephrosis. J Pediatr Urol. 2010. PMID 20399145 · DOI
- Lee RS, Cendron M, Kinnamon DD, Nguyen HT. Antenatal hydronephrosis as a predictor of postnatal outcome: a meta-analysis. Pediatrics. 2006. PMID 16882811 · DOI
- Woodward M, Frank D. Postnatal management of antenatal hydronephrosis. BJU Int. 2002. PMID 11849184 · DOI
- Sidhu G, Beyene J, Rosenblum ND. Outcome of isolated antenatal hydronephrosis: a systematic review and meta-analysis. Pediatr Nephrol. 2006. PMID 16362721 · DOI
- O'Reilly P, Aurell M, Britton K, Kletter K, Rosenthal L, Testa T. Consensus on diuresis renography for investigating the dilated upper urinary tract. Radionuclides in Nephrourology Group. Consensus Committee on Diuresis Renography. J Nucl Med. 1996. PMID 8917195
- Rasmussen PE, Nielsen FR. Hydronephrosis during pregnancy: a literature survey. Eur J Obstet Gynecol Reprod Biol. 1988. PMID 3280355 · 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.