Evidence map›Paper›PMID 27525285›Full record

ReviewJournal of diabetes research2016

Oxidative Stress in Diabetic Nephropathy with Early Chronic Kidney Disease.

Alejandra Guillermina Miranda-Díaz, Leonardo Pazarín-Villaseñor, Francisco Gerardo Yanowsky-Escatell, Jorge Andrade-Sierra

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 3 pooled it
18.2field-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

114 citing papers in PubMed, 3 syntheses or guidelines pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
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  12. Targeting p66Shc to restore KFrontiers in physiology · 2025
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  13. Review
  14. Nutrition research and practice · 2024
    Article
  15. Article
  16. Therapeutic Effect of Desmodium caudatum Extracts on Alleviating Diabetic Nephropathy Mice.Plant foods for human nutrition (Dordrecht, Netherlands) · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

54 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 1 country.

Alejandra Guillermina Miranda-DíazDepartment of Physiology, University Health Sciences Centre (Centro Universitario de Ciencias de la Salud), University of Guadalajara, 44150 Guadalajara, JAL, Mexico.ORCID 0000-0002-3635-6135
Leonardo Pazarín-VillaseñorNephrology Service, Civil Hospital of Guadalajara "Dr. Juan I. Menchaca", Guadalajara, JAL, Mexico.ORCID 0000-0001-8755-9058
Francisco Gerardo Yanowsky-EscatellNephrology Service, Civil Hospital of Guadalajara "Dr. Juan I. Menchaca", Guadalajara, JAL, Mexico.ORCID 0000-0002-0621-5075
Jorge Andrade-SierraNephrology Service, Civil Hospital of Guadalajara "Dr. Juan I. Menchaca", Guadalajara, JAL, Mexico.
Hospital Civil de Guadalajara · MXUniversidad de Guadalajara · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increase in the prevalence of diabetes mellitus (DM) and the secondary kidney damage produces diabetic nephropathy (DN). Early nephropathy is defined as the presence of microalbuminuria (30-300 mg/day), including normal glomerular filtration rate (GFR) or a mildly decreased GFR (60-89 mL/min/1.73 m(2)), with or without overt nephropathy. The earliest change caused by DN is hyperfiltration with proteinuria. The acceptable excretion rate of albumin in urine is <30 mg/day. Albuminuria represents the excretion of >300 mg/day. Chronic kidney disease (CKD) is characterized by abnormalities in renal function that persist for >3 months with health implications. Alterations in the redox state in DN are caused by the persistent state of hyperglycemia and the increase in advanced glycation end products (AGEs) with ability to affect the renin-angiotensin system and the transforming growth factor-beta (TGF-β), producing chronic inflammation and glomerular and tubular hypertrophy and favoring the appearance of oxidative stress. In DN imbalance between prooxidant/antioxidant processes exists with an increase in reactive oxygen species (ROS). The overproduction of ROS diminishes expression of the antioxidant enzymes (manganese superoxide dismutase, glutathione peroxidase, and catalase). The early detection of CKD secondary to DN and the timely identification of patients would permit decreasing its impact on health.

Indexed as

Oxidative StressAlbuminuriaCatalaseDiabetic NephropathiesEarly DiagnosisGlutathione PeroxidaseGlycation End Products, AdvancedHumansReactive Oxygen SpeciesRenal Insufficiency, ChronicRenin-Angiotensin SystemSuperoxide DismutaseTransforming Growth Factor betaCatalaseGlutathione PeroxidaseGlycation End Products, AdvancedReactive Oxygen SpeciesSuperoxide DismutaseTransforming Growth Factor beta

Identifiers

PMID27525285
PMCPMC4971321
OpenAlexW2498616159

What OpenQuestion 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 OpenQuestion graph.