Evidence map›Paper›PMID 28840540›Full record

ReviewJournal of nephrology2017

A more tubulocentric view of diabetic kidney disease.

Letizia Zeni, Anthony G W Norden, Giovanni Cancarini, Robert J Unwin

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 1 pooled it
13.2field-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

138 citing papers in PubMed, 1 synthesis or guideline pooled it, 253 citations in OpenAlex.

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78 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

4 authors at 2 institutions in 3 countries.

Letizia ZeniDepartment of Medical and Surgical Specialities, Radiological Sciences and Public Health, University of Brescia, Piazza del Mercato 15, 25121, Brescia, Italy. l.zeni@ucl.ac.uk.ORCID http://orcid.org/0000-0001-9221-5698
Anthony G W NordenUCL Centre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK.
Giovanni CancariniDepartment of Medical and Surgical Specialities, Radiological Sciences and Public Health, University of Brescia, Piazza del Mercato 15, 25121, Brescia, Italy.
Robert J UnwinUCL Centre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill Street, London, NW3 2PF, UK.
Azienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia · ITThe Royal Free Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is a common complication of Diabetes Mellitus (DM) Types 1 and 2, and prevention of end stage renal disease (ESRD) remains a major challenge. Despite its high prevalence, the pathogenesis of DN is still controversial. Initial glomerular disease manifested by hyperfiltration and loss of glomerular size and charge permselectivity may initiate a cascade of injuries, including tubulo-interstitial disease. Clinically, 'microalbuminuria' is still accepted as an early biomarker of glomerular damage, despite mounting evidence that its predictive value for DN is questionable, and findings that suggest the proximal tubule is an important link in the development of DN. The concept of 'diabetic tubulopathy' has emerged from recent studies, and its causative role in DN is supported by clinical and experimental evidence, as well as plausible pathogenetic mechanisms. This review explores the 'tubulocentric' view of DN. The recent finding that inhibition of proximal tubule (PT) glucose transport (via SGLT2) is nephro-protective in diabetic patients is discussed in relation to the tubule's potential role in DN. Studies with a tubulocentric view of DN have stimulated alternative clinical approaches to the early detection of diabetic kidney disease. There are tubular biomarkers considered as direct indicators of injury of the proximal tubule (PT), such as N-acetyl-β-D-glucosaminidase, Neutrophil Gelatinase-Associated Lipocalin and Kidney Injury Molecule-1, and other functional PT biomarkers, such as Urine free Retinol-Binding Protein 4 and Cystatin C, which reflect impaired reabsorption of filtered proteins. The clinical application of these measurements to diabetic patients will be reviewed in the context of the need for better biomarkers for early DN.

Indexed as

AlbuminuriaAnimalsBiomarkersDiabetic NephropathiesGlomerular Filtration RateHumansKidney Tubules, ProximalSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsBiomarkersSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsDiabetic kidney diseaseDiabetic tubulopathyHyperfiltrationMicroalbuminuriaSGLT2 nephro-protectionTubular biomakers

Identifiers

PMID28840540
PMCPMC5698396
OpenAlexW2745568596

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.