Evidence map›Paper›PMID 24742475›Full record

ReviewClinical journal of the American Society of Nephrology : CJASN2015

Control of urinary drainage and voiding.

Warren G Hill

Abstract readReview
In one paragraph

Review in Clinical journal of the American Society of Nephrology : CJASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Review
  2. Article
  3. Is occult stress urinary incontinence truly "occult"?Gynecology and pelvic medicine · 2026
    Review
  4. Article
  5. Orai storeoperated CaChannels (Austin, Tex.) · 2025
    Review
  6. Review
  7. The immune mechanisms of the urinary tract against infections.Frontiers in cellular and infection microbiology · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Lead acetate versus cadmium sulfate in the modulation of main physiological pathways controlling detrusor muscle contractility in rat.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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.

Warren G HillLaboratory of Voiding Dysfunction, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts whill@bidmc.harvard.edu.

Funding

Mechanisms of age-related voiding dysfunction defined by systems genetics modelsP20DK097818 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZEIDEL, MARK L. · 2012 to 2014
$1.3M
NIDDK NIH HHS DK08399NIDDK NIH HHS P20 DK097818NIDDK NIH HHS P20-DK097818
6 · The paper itself

Abstract

Urine differs greatly in ion and solute composition from plasma and contains harmful and noxious substances that must be stored for hours and then eliminated when it is socially convenient to do so. The urinary tract that handles this output is composed of a series of pressurizable muscular compartments separated by sphincteric structures. With neural input, these structures coordinate the delivery, collection, and, ultimately, expulsion of urine. Despite large osmotic and chemical gradients in this waste fluid, the bladder maintains a highly impermeable surface in the face of a physically demanding biomechanical environment, which mandates recurring cycles of surface area expansion and increased wall tension during filling, followed by rapid wall compression during voiding. Afferent neuronal inflow from mucosa and submucosa communicates sensory information about bladder fullness, and voiding is initiated consciously through coordinated central and spinal efferent outflow to the detrusor, trigonal internal sphincter, and external urethral sphincter after periods of relative quiescence. Provocative new findings suggest that in some cases, lower urinary tract symptoms, such as incontinence, urgency, frequency, overactivity, and pain may be viewed as a consequence of urothelial defects (either urothelial barrier breakdown or inappropriate signaling from urothelial cells to underlying sensory afferents and potentially interstitial cells). This review describes the physiologic and anatomic mechanisms by which urine is moved from the kidney to the bladder, stored, and then released. Relevant clinical examples of urinary tract dysfunction are also discussed.

Indexed as

HumansInterstitial Cells of CajalMuscle ContractionMuscle, SmoothNeural PathwaysUreterUrethraUrinary BladderUrinationUrotheliumcalciumcell and transport physiologycell signalingepithelialurinary tract

Identifiers

PMID24742475
PMCPMC4348679

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.