Evidence map›Paper›PMID 24049145›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Fluid reabsorption in proximal convoluted tubules of mice with gene deletions of claudin-2 and/or aquaporin1.

Jurgen Schnermann, Yuning Huang, Diane Mizel

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. 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
4.0field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Article
  3. Ion and water permeation through claudin-10b and claudin-15 paracellular channels.Computational and structural biotechnology journal · 2024
    Article
  4. Article
  5. Renal water transport in health and disease.Pflugers Archiv : European journal of physiology · 2022
    Review
  6. Article
  7. Review
  8. Article
  9. Claudin-2: Roles beyond Permeability Functions.International journal of molecular sciences · 2019
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. A model of calcium transport and regulation in the proximal tubule.American journal of physiology. Renal physiology · 2018
    Article
  16. Tight junctions of the proximal tubule and their channel proteins.Pflugers Archiv : European journal of physiology · 2017
    Review
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Jurgen SchnermannNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 10, Rm. 4D51, 9000 Rockville Pike, Bethesda, MD 20892. jurgens@intra.niddk.nih.gov.
Yuning Huang
Diane Mizel
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Renal Function In Transgenic MiceZ01DK043408 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SCHNERMANN, JURGEN B. · 2000 to 2008
$783k
Intramural NIH HHS Z01 DK043408NIDDK NIH HHS DK-043408-12
6 · The paper itself

Abstract

Deletions of claudin-2 (Cldn2) and aquaporin1 (AQP1) reduce proximal fluid reabsorption (PFR) by about 30% and 50%, respectively. Experiments were done to replicate these observations and to determine in AQP1/claudin-2 double knockout mice (DKO) if the effects of deletions of these established water pores are additive. PFR was determined in inactin/ketamine-anesthetized mice by free-flow micropuncture using single-nephron I(125)-iothalamate (io) clearance. Animal means of PFR [% of glomerular filtration rate (GFR)] derived from TF/Piothalamate ratios in 12 mice in each of four groups [wild type (WT), Cldn2(-/-), AQP1(-/-), and DKO) were 45.8 ± 0.85 (51 tubules), 35.4 ± 1 (54 tubules; P < 0.01 vs. WT), 36.8 ± 1 (63 tubules; P < 0.05 vs. WT), and 33.9 ± 1.4 (69 tubules; P < 0.01 vs. WT). Kidney and single-nephron GFRs (SNGFR) were significantly reduced in all mutant strains. The direct relationship between PFR and SNGFR was maintained in mutant mice, but the slope of this relationship was reduced in the absence of Cldn2 and/or AQP1. Transtubular osmotic pressure differences were not different between WT and Cldn2(-/-) mice, but markedly increased in DKO. In conclusion, the deletion of Cldn2, AQP1, or of both Cldn2 and AQP1 reduces PFR by 22.7%, 19.6%, and 26%, respectively. Our data are consistent with an up to 25% paracellular contribution to PFR. The reduced osmotic water permeability caused by absence of AQP1 augments luminal hypotonicity. Aided by a fall in filtered load, the capacity of non-AQP1-dependent transcellular reabsorption is sufficient to maintain PFR without AQP1 and claudin-2 at 75% of control.

Indexed as

AnimalsAquaporin 1ClaudinsGene DeletionKidney Function TestsKidney Tubules, ProximalMaleMiceMice, Inbred C57BLMice, KnockoutOsmolar ConcentrationRNA, MessengerAqp1 protein, mouseAquaporin 1ClaudinsCldn2 protein, mouseRNA, Messengeriothalamatemicropunctureparacellulartranscellulartubular fluid osmolarity

Identifiers

PMID24049145
PMCPMC3840226
OpenAlexW2148622416

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.