Evidence map›Paper›PMID 33547417›Full record

ReviewNature reviews. Nephrology2021

Pathophysiology of diabetic kidney disease: impact of SGLT2 inhibitors.

Ralph A DeFronzo, W Brian Reeves, Alaa S Awad

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05147818 (Risk Factors for Acute Kidney Injury in Diabetic Patients), which is not on this map. Cited by 356 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
356citing papers in PubMed, 9 pooled it
56.1field-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.

NCT05147818 unknown statusnot on this map

Risk Factors for Acute Kidney Injury in Diabetic Patients

TypeobservationalSponsorAssiut UniversityRan2021 to 2023Enrolled400ConditionsDiabete MellitusArmsCBC ,renal function tests , fundus Examination
3 · Its place in the literature

Who cites it

356 citing papers in PubMed, 9 syntheses or guidelines pooled it, 540 citations in OpenAlex.

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296 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

3 authors at 2 institutions in 1 country.

Ralph A DeFronzoDivision of Diabetes, University of Texas Long School of Medicine, San Antonio, TX, USA. defronzo@uthscsa.edu.
W Brian ReevesDivision of Nephrology, University of Texas Long School of Medicine, San Antonio, TX, USA.ORCID http://orcid.org/0000-0001-5191-5866
Alaa S AwadDivision of Nephrology, University of Texas Long School of Medicine, San Antonio, TX, USA.ORCID http://orcid.org/0000-0002-4468-4446
The University of Texas at San Antonio · USTexas Diabetes Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease is the leading cause of kidney failure worldwide; in the USA, it accounts for over 50% of individuals entering dialysis or transplant programmes. Unlike other complications of diabetes, the prevalence of diabetic kidney disease has failed to decline over the past 30 years. Hyperglycaemia is the primary aetiological factor responsible for the development of diabetic kidney disease. Once hyperglycaemia becomes established, multiple pathophysiological disturbances, including hypertension, altered tubuloglomerular feedback, renal hypoxia, lipotoxicity, podocyte injury, inflammation, mitochondrial dysfunction, impaired autophagy and increased activity of the sodium-hydrogen exchanger, contribute to progressive glomerular sclerosis and the decline in glomerular filtration rate. The quantitative contribution of each of these abnormalities to the progression of diabetic kidney disease, as well as their role in type 1 and type 2 diabetes mellitus, remains to be determined. Sodium-glucose co-transporter 2 (SGLT2) inhibitors have a beneficial impact on many of these pathophysiological abnormalities; however, as several pathophysiological disturbances contribute to the onset and progression of diabetic kidney disease, multiple agents used in combination will likely be required to slow the progression of disease effectively.

Indexed as

AutophagyDiabetic NephropathiesEndothelium, VascularGlomerular Filtration RateHumansHyperglycemiaHypertensionHypoglycemic AgentsKidney TubulesObesityPodocytesSodium-Glucose Transporter 2 InhibitorsHypoglycemic AgentsSodium-Glucose Transporter 2 Inhibitors

Identifiers

PMID33547417
OpenAlexW3127916746

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.