Evidence map›Paper›PMID 22335797›Full record

ReviewAnnual review of physiology2012

Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.

Volker Vallon, Scott C Thomson

Abstract readReview
In one paragraph

Review in Annual review of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 2 pooled it
8.3field-weighted citation impact, top 2% 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

197 citing papers in PubMed, 2 syntheses or guidelines pooled it, 372 citations in OpenAlex.

  1. Pooled it
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  16. lncRNA TUG1 and kidney diseases.BMC nephrology · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Elucidating the complex interplay between chronic kidney disease and hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review

137 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, La Jolla, California 92093, USA. vvallon@ucsd.edu
Scott C Thomson
University of California, San Diego · USVA 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

Diabetes mellitus affects the kidney in stages. At the onset of diabetes mellitus, in a subset of diabetic patients the kidneys grow large, and glomerular filtration rate (GFR) becomes supranormal, which are risk factors for developing diabetic nephropathy later in life. This review outlines a pathophysiological concept that focuses on the tubular system to explain these changes. The concept includes the tubular hypothesis of glomerular filtration, which states that early tubular growth and sodium-glucose cotransport enhance proximal tubule reabsorption and make the GFR supranormal through the physiology of tubuloglomerular feedback. The diabetic milieu triggers early tubular cell proliferation, but the induction of TGF-β and cyclin-dependent kinase inhibitors causes a cell cycle arrest and a switch to tubular hypertrophy and a senescence-like phenotype. Although this growth phenotype explains unusual responses like the salt paradox of the early diabetic kidney, the activated molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy.

Indexed as

AnimalsDiabetic NephropathiesDisease ProgressionElectrolytesFeedback, PhysiologicalGlomerular Filtration RateGlucoseGlucose Transporter Type 2Glucose Transport Proteins, FacilitativeHumansHypertrophyKidney GlomerulusKidney TubulesKidney Tubules, ProximalSodiumSodium ChlorideElectrolytesGlucoseGlucose Transporter Type 2Glucose Transport Proteins, FacilitativeSodiumSodium Chloride

Identifiers

PMID22335797
PMCPMC3807782
OpenAlexW2112710337

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.