Evidence map›Paper›PMID 21228342›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2011

The proximal tubule in the pathophysiology of the diabetic kidney.

Volker Vallon

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed, 2 pooled it
14.3field-weighted citation impact, top 1% 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

200 citing papers in PubMed, 2 syntheses or guidelines pooled it, 386 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. The Human PNPLA3FASEB bioAdvances · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Observational
  11. Urinary biomarkers of diabetic kidney disease.World journal of diabetes · 2026
    Review
  12. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  13. Protective Role of Serum β-Hydroxybutyrate in Early Diabetic Kidney Disease: A Longitudinal Study.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

140 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Volker VallonDepts. of Medicine and Pharmacology, University of California San Diego & VA San Diego Healthcare System, 3350 La Jolla Village Drive, San Diego, CA 92161, USA. vvallon@ucsd.edu
VA San Diego Healthcare System · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
GLOMERULAR AND TUBULAR FUNCTION IN THE DIABETIC KIDNEYR01DK056248 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI THOMSON, SCOTT CULVER · 1999 to 2014
$4.6M
AUTOREGULATION OF GLOMERULAR FILTRATION RATER01DK028602 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI BLANTZ, ROLAND C · 1986 to 2011
$3.9M
Adrenergic and Purinergic Regulation of Target CellsR01GM066232 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI INSEL, PAUL A · 2004 to 2010
$1.9M
Blood Pressure Regulation by OAT3R01HL094728 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ERALY, SATISH A, VALLON, VOLKER · 2010 to 2014
$1.9M
NHLBI NIH HHS R01 HL094728NHLBI NIH HHS R01HL094728NIDDK NIH HHS P30 DK079337NIDDK NIH HHS P30DK079337NIDDK NIH HHS R01 DK028602NIDDK NIH HHS R01 DK056248NIDDK NIH HHS R01DK28602NIDDK NIH HHS R01DK56248NIGMS NIH HHS R01 GM066232NIGMS NIH HHS R01GM66232
6 · The paper itself

Abstract

Diabetic nephropathy is a leading cause of end-stage renal disease. A better understanding of the molecular mechanism involved in the early changes of the diabetic kidney may permit the development of new strategies to prevent diabetic nephropathy. This review focuses on the proximal tubule in the early diabetic kidney, particularly on its exposure and response to high glucose levels, albuminuria, and other factors in the diabetic glomerular filtrate, the hyperreabsorption of glucose, the unique molecular signature of the tubular growth phenotype, including aspects of senescence, and the resulting cellular and functional consequences. The latter includes the local release of proinflammatory chemokines and changes in proximal tubular salt and fluid reabsorption, which form the basis for the strong tubular control of glomerular filtration in the early diabetic kidney, including glomerular hyperfiltration and odd responses like the salt paradox. Importantly, these early proximal tubular changes can set the stage for oxidative stress, inflammation, hypoxia, and tubulointerstitial fibrosis, and thereby for the progression of diabetic renal disease.

Indexed as

Glomerular Filtration RateAbsorptionAnimalsBlood GlucoseCellular SenescenceDiabetic NephropathiesDisease ProgressionFibrosisHumansHyperplasiaHypertrophyInflammation MediatorsKidney Tubules, ProximalNephritis, InterstitialOxidative StressPhenotypeBlood GlucoseInflammation Mediators

Identifiers

PMID21228342
PMCPMC3094037
OpenAlexW2159258864

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.