Evidence map›Paper›PMID 26701981›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Severity and Frequency of Proximal Tubule Injury Determines Renal Prognosis.

Koji Takaori, Jin Nakamura, Shinya Yamamoto, Hirosuke Nakata, Yuki Sato, Masayuki Takase, Masaaki Nameta, Tadashi Yamamoto, Aris N Economides, Kenji Kohno and 3 more

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 1 pooled it
8.6field-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

152 citing papers in PubMed, 1 synthesis or guideline pooled it, 263 citations in OpenAlex.

  1. Pooled it
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  13. Targeting renal tubular epithelial cellsActa pharmaceutica Sinica. B · 2025
    Article
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  15. Targeting NHypertension (Dallas, Tex. : 1979) · 2025
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92 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

13 authors at 6 institutions in 2 countries.

Koji TakaoriDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
Jin NakamuraDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
Shinya YamamotoDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
Hirosuke NakataDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
Yuki SatoDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
Masayuki TakaseDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;
Masaaki NametaDepartment of Structural Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan;
Tadashi YamamotoDepartment of Structural Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan;
Aris N EconomidesGenome Engineering Technologies and Skeletal Diseases TFA Groups, Regeneron Pharmaceuticals, Inc., Tarrytown, New York;
Kenji KohnoGraduate School of Biological Sciences, Nara Institute of Science and Technology, Nara, Japan;
Hironori HagaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan; and.
Kumar SharmaCenter for Renal Translational Medicine and Institute of Metabolomic Medicine, Department of Medicine, University of California San Diego, Veteran's Administration San Diego HealthCare System, La Jolla, California.
Motoko YanagitaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; motoy@kuhp.kyoto-u.ac.jp.
Kyoto University · JPNiigata University · JPKyoto University Hospital · JPNara Institute of Science and Technology · JPRegeneron (United States) · USVA San Diego Healthcare System · US

Funding

Novel Paradigms in Diabetic ComplicationsDP3DK094352 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHARMA, KUMAR · 2011 to 2011
$6.0M
NIDDK NIH HHS DP3 DK094352
6 · The paper itself

Abstract

AKI increases the risk of developing CKD, but the mechanisms linking AKI to CKD remain unclear. Because proximal tubule injury is the mainstay of AKI, we postulated that proximal tubule injury triggers features of CKD. We generated a novel mouse model to induce proximal tubule-specific adjustable injury by inducing the expression of diphtheria toxin (DT) receptor with variable prevalence in proximal tubules. Administration of high-dose DT in mice expressing the DT receptor consistently caused severe proximal tubule-specific injury associated with interstitial fibrosis and reduction of erythropoietin production. Mild proximal tubule injury from a single injection of low-dose DT triggered reversible fibrosis, whereas repeated mild injuries caused sustained interstitial fibrosis, inflammation, glomerulosclerosis, and atubular glomeruli. DT-induced proximal tubule-specific injury also triggered distal tubule injury. Furthermore, injured tubular cells cocultured with fibroblasts stimulated induction of extracellular matrix and inflammatory genes. These results support the existence of proximal-distal tubule crosstalk and crosstalk between tubular cells and fibroblasts. Overall, our data provide evidence that proximal tubule injury triggers several features of CKD and that the severity and frequency of proximal tubule injury determines the progression to CKD.

Indexed as

Kidney Tubules, ProximalAcute Kidney InjuryAnimalsDisease ProgressionMicePrognosisRenal Insufficiency, ChronicSeverity of Illness Indexacute renal failurechronic kidney diseaseproximal tubule

Identifiers

PMID26701981
PMCPMC4978049
OpenAlexW2267116164

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.