Evidence map›Paper›PMID 20518753›Full record

ReviewActa physiologica (Oxford, England)2010

Tubular reabsorption and diabetes-induced glomerular hyperfiltration.

P Persson, P Hansell, F Palm

Abstract readReview
In one paragraph

Review in Acta physiologica (Oxford, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. PMToxics · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Glomerular Hyperfiltration in Diabetes: Mechanisms, Clinical Significance, and Treatment.Journal of the American Society of Nephrology : JASN · 2017
    Review
  17. Article
  18. Review
  19. The Gomez' equations and renal hemodynamic function in kidney disease research.American journal of physiology. Renal physiology · 2016
    Article
  20. Observational
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

3 authors at 1 institution in 2 countries.

P PerssonDivision of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
P Hansell
F Palm
Uppsala University · SE

Funding

NITRIC OXIDE AND OXYGENATION IN DIABETIC KIDNEYSR00DK077858 · NIDDK · GEORGETOWN UNIVERSITY · PI PALM, NILS AXEL FREDRIK · 2008 to 2010
$747k
NITRIC OXIDE AND OXYGENATION IN DIABETIC KIDNEYSK99DK077858 · NIDDK · GEORGETOWN UNIVERSITY · PI PALM, NILS AXEL FREDRIK · 2007 to 2007
$90k
NIDDK NIH HHS K99 DK077858NIDDK NIH HHS K99/R00 DK077858NIDDK NIH HHS R00 DK077858
6 · The paper itself

Abstract

Elevated glomerular filtration rate (GFR) is a common observation in early diabetes mellitus and closely correlates with the progression of diabetic nephropathy. Hyperfiltration has been explained to be the result of a reduced load of sodium and chloride passing macula densa, secondarily to an increased proximal reabsorption of glucose and sodium by the sodium-glucose co-transporters. This results in an inactivation of the tubuloglomerular feedback (TGF), leading to a reduced afferent arteriolar vasoconstriction and subsequently an increase in GFR. This hypothesis has recently been questioned due to the observation that adenosine A(1)-receptor knockout mice, previously shown to lack a functional TGF mechanism, still display a pronounced hyperfiltration when diabetes is induced. Leyssac demonstrated in the 1960s (Acta Physiol Scand58, 1963:236) that GFR and proximal reabsorption can work independently of each other. Furthermore, by the use of micropuncture technique a reduced hydrostatic pressure in Bowman's space or in the proximal tubule of diabetic rats has been observed. A reduced pressure in Bowman's space will increase the pressure gradient over the filtration barrier and can contribute to the development of diabetic hyperfiltration. When inhibiting proximal reabsorption with a carbonic anhydrase inhibitor, GFR decreases and proximal tubular pressure increases. Measuring intratubular pressure allows a sufficient time resolution to reveal that net filtration pressure decreases before TGF is activated which highlights the importance of intratubular pressure as a regulator of GFR. Taken together, these results imply that the reduced intratubular pressure observed in diabetes might be crucial for the development of glomerular hyperfiltration.

Indexed as

Glomerular Filtration RateAbsorptionAnimalsDiabetic NephropathiesFeedback, PhysiologicalHemodynamicsHumansHydrostatic PressureKidney GlomerulusKidney TubulesMiceMice, TransgenicModels, AnimalUp-Regulation

Identifiers

PMID20518753
PMCPMC2919631
OpenAlexW1672921524

What OpenQuestion holds

Textmetadata
LicenceTDM
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.