Evidence map›Paper›PMID 40164775›Full record

ReviewNature reviews. Nephrology2025

Ureter development and associated congenital anomalies.

Andreas Kispert

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Complete ureteral duplication with occult calculi: A case report.Experimental and therapeutic medicine · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The kidney stroma in development and disease.Nature reviews. Nephrology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Andreas KispertInstitute of Molecular Biology, Hannover Medical School, Hannover, Germany. kispert.andreas@mh-hannover.de.ORCID http://orcid.org/0000-0002-8154-0257

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malformations of the ureter are among the most common birth defects in humans. Although some of these anomalies are asymptomatic, others are clinically relevant, causing perinatal lethality or progressing to kidney failure in childhood. The genetic causes and developmental aetiology of ureteral anomalies are difficult to study in humans; however, embryological and genetic analyses in the mouse have provided insights into the complex developmental programmes that govern ureter formation from simple tissue primordia, and the pathological consequences that result from disruption of these programmes. Abnormalities in the formation of the nephric duct and ureteric bud lead to changes in the number of ureters (and kidneys), whereas the formation of ectopic ureteric buds, failure of the nephric duct to target the cloaca or failure of the distal ureter to mature underlie vesicoureteral reflux, ureter ectopia, ureterocoele and subsequent hydroureter. Alterations in ureter specification, early growth or cyto-differentiation programmes have now also been associated with various forms of perinatal hydroureter and hydronephrosis as a consequence of functional obstruction. The characterization of cellular processes and molecular drivers of ureterogenesis in the mouse may not only aid understanding of the aetiology of human ureteral anomalies, improve prognostication and benefit the development of therapeutic strategies, but may also prove important for efforts to generate a bioartificial organ.

Indexed as

UreterAnimalsHumansMice

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.