Evidence map›Paper›PMID 21849488›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Role of thin descending limb urea transport in renal urea handling and the urine concentrating mechanism.

Tianluo Lei, Lei Zhou, Anita T Layton, Hong Zhou, Xuejian Zhao, Lise Bankir, Baoxue Yang

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Physiological Functions of Urea Transporters.Sub-cellular biochemistry · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Mammalian urine concentration: a review of renal medullary architecture and membrane transporters.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2018
    Review
  11. Article
  12. Emerging Targets of Diuretic Therapy.Clinical pharmacology and therapeutics · 2017
    Review
  13. Article
  14. Urea transport and clinical potential of urearetics.Current opinion in nephrology and hypertension · 2016
    Review
  15. Article
  16. Abnormal Expression of Urea Transporter Protein in a Rat Model of Hepatorenal Syndrome Induced by Succinylated Gelatin.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  17. Article
  18. Review
  19. Thienoquinolins exert diuresis by strongly inhibiting UT-A urea transporters.American journal of physiology. Renal physiology · 2014
    Article
  20. 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

7 authors at 4 institutions in 3 countries.

Tianluo LeiDept. of Pharmacology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Lu, Haidian District, Beijing, China.
Lei Zhou
Anita T Layton
Hong Zhou
Xuejian Zhao
Lise Bankir
Baoxue Yang
Peking University · CNJilin University · CNDuke University · USInserm · FR

Funding

Modeling Solute Transport and Urine Concentrating Mechanism in the Rat KidneyR01DK089066 · NIDDK · DUKE UNIVERSITY · PI LAYTON, ANITA · 2010 to 2014
$1.2M
NIDDK NIH HHS DK089066
6 · The paper itself

Abstract

Urea transporters UT-A2 and UT-B are expressed in epithelia of thin descending limb of Henle's loop and in descending vasa recta, respectively. To study their role and possible interaction in the context of the urine concentration mechanism, a UT-A2 and UT-B double knockout (UT-A2/B knockout) mouse model was generated by targeted deletion of the UT-A2 promoter in embryonic stem cells with UT-B gene knockout. The UT-A2/B knockout mice lacked detectable UT-A2 and UT-B transcripts and proteins and showed normal survival and growth. Daily urine output was significantly higher in UT-A2/B knockout mice than that in wild-type mice and lower than that in UT-B knockout mice. Urine osmolality in UT-A2/B knockout mice was intermediate between that in UT-B knockout and wild-type mice. The changes in urine osmolality and flow rate, plasma and urine urea concentration, as well as non-urea solute concentration after an acute urea load or chronic changes in protein intake suggested that UT-A2 plays a role in the progressive accumulation of urea in the inner medulla. These results suggest that in wild-type mice UT-A2 facilitates urea absorption by urea efflux from the thin descending limb of short loops of Henle. Moreover, UT-A2 deletion in UT-B knockout mice partially remedies the urine concentrating defect caused by UT-B deletion, by reducing urea loss from the descending limbs to the peripheral circulation; instead, urea is returned to the inner medulla through the loops of Henle and the collecting ducts.

Indexed as

Kidney Concentrating AbilityAnimalsFemaleLoop of HenleMembrane Transport ProteinsMiceMice, KnockoutUreaUrea TransportersMembrane Transport ProteinsUreaurea transporter B, mouseUrea Transporters

Identifiers

PMID21849488
PMCPMC3233864
OpenAlexW2076063805

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.