Evidence map›Paper›PMID 23733640›Full record

ReviewComprehensive Physiology2011

Pathophysiology of the diabetic kidney.

Volker Vallon, Radko Komers

Abstract readReview
In one paragraph

Review in Comprehensive Physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 2 pooled it
–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

146 citing papers in PubMed, 2 syntheses or guidelines pooled it, 256 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Tie2 activator 4E2 ameliorates diabetic nephropathy and synergizes with dapagliflozin in a mouse model.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. A new mechanism of diabetic kidney disease progression by Piezo proteins: mediators between mechanical stimuli and fibrosis.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  18. Article
  19. Review
  20. Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025
    Review

86 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

2 authors at 2 institutions in 1 country.

Volker VallonDepartment of Medicine, University of California San Diego & VA San Diego Healthcare System, San Diego, California, USA. vvallon@ucsd.edu
Radko Komers
Oregon Health & Science University · USUniversity of California, San Diego · 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

Diabetes mellitus contributes greatly to morbidity, mortality, and overall health care costs. In major part, these outcomes derive from the high incidence of progressive kidney dysfunction in patients with diabetes making diabetic nephropathy a leading cause of end-stage renal disease. A better understanding of the molecular mechanism involved and of the early dysfunctions observed in the diabetic kidney may permit the development of new strategies to prevent diabetic nephropathy. Here we review the pathophysiological changes that occur in the kidney in response to hyperglycemia, including the cellular responses to high glucose and the responses in vascular, glomerular, podocyte, and tubular function. The molecular basis, characteristics, and consequences of the unique growth phenotypes observed in the diabetic kidney, including glomerular structures and tubular segments, are outlined. We delineate mechanisms of early diabetic glomerular hyperfiltration including primary vascular events as well as the primary role of tubular growth, hyperreabsorption, and tubuloglomerular communication as part of a "tubulocentric" concept of early diabetic kidney function. The latter also explains the "salt paradox" of the early diabetic kidney, that is, a unique and inverse relationship between glomerular filtration rate and dietary salt intake. The mechanisms and consequences of the intrarenal activation of the renin-angiotensin system and of diabetes-induced tubular glycogen accumulation are discussed. Moreover, we aim to link the changes that occur early in the diabetic kidney including the growth phenotype, oxidative stress, hypoxia, and formation of advanced glycation end products to mechanisms involved in progressive kidney disease.

Indexed as

AnimalsDiabetic NephropathiesHumansKidney

Identifiers

PMID23733640
PMCPMC6029262
OpenAlexW1540594287

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.