Evidence map›Paper›PMID 30281062›Full record

ReviewJornal brasileiro de nefrologia

Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs.

Guillherme Nobre Cavalcanti Lucas, Ana Carla Carneiro Leitão, Renan Lima Alencar, Rosa Malena Fagundes Xavier, Elizabeth De Francesco Daher, Geraldo Bezerra da Silva Junior

Open access · diamondAbstract readReview
In one paragraph

Review in Jornal brasileiro de nefrologia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 3 pooled it
11.9field-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

99 citing papers in PubMed, 3 syntheses or guidelines pooled it, 296 citations in OpenAlex.

  1. Pooled it
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  6. Article
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39 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

6 authors at 3 institutions in 1 country.

Guillherme Nobre Cavalcanti LucasUniversidade de Fortaleza, Programa de Pós-Graduação em Saúde Coletiva, Centro de Ciências da Saúde, Fortaleza, CE, Brasil.
Ana Carla Carneiro LeitãoUniversidade de Fortaleza, Programa de Pós-Graduação em Saúde Coletiva, Centro de Ciências da Saúde, Fortaleza, CE, Brasil.
Renan Lima AlencarUniversidade de Fortaleza, Programa de Pós-Graduação em Saúde Coletiva, Centro de Ciências da Saúde, Fortaleza, CE, Brasil.
Rosa Malena Fagundes XavierUniversidade de Fortaleza, Programa de Pós-Graduação em Saúde Coletiva, Centro de Ciências da Saúde, Fortaleza, CE, Brasil.
Elizabeth De Francesco DaherUniversidade Federal do Ceará, Faculdade de Medicina, Departamento de Medicina Clínica, Fortaleza, CE, Brasil.
Geraldo Bezerra da Silva JuniorUniversidade de Fortaleza, Programa de Pós-Graduação em Saúde Coletiva, Centro de Ciências da Saúde, Fortaleza, CE, Brasil.ORCID http://orcid.org/0000-0002-8971-0994
Universidade de Fortaleza · BRInstituto de Saúde · BRUniversidade Federal do Ceará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used medications associated with nephrotoxicity, especially when used chronically. Factors such as advanced age and comorbidities, which in themselves already lead to a decrease in glomerular filtration rate, increase the risk of NSAID-related nephrotoxicity. The main mechanism of NSAID action is cyclooxygenase (COX) enzyme inhibition, interfering on arachidonic acid conversion into E2 prostaglandins E2, prostacyclins and thromboxanes. Within the kidneys, prostaglandins act as vasodilators, increasing renal perfusion. This vasodilatation is a counter regulation of mechanisms, such as the renin-angiotensin-aldosterone system works and that of the sympathetic nervous system, culminating with compensation to ensure adequate flow to the organ. NSAIDs inhibit this mechanism and can lead to acute kidney injury (AKI). High doses of NSAIDs have been implicated as causes of AKI, especially in the elderly. The main form of AKI by NSAIDs is hemodynamically mediated. The second form of NSAID-induced AKI is acute interstitial nephritis, which may manifest as nephrotic proteinuria. Long-term NSAID use can lead to chronic kidney disease (CKD). In patients without renal diseases, young and without comorbidities, NSAIDs are not greatly harmful. However, because of its dose-dependent effect, caution should be exercised in chronic use, since it increases the risk of developing nephrotoxicity.

Indexed as

Acute Kidney InjuryAgedAged, 80 and overAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase InhibitorsHumansInfant, NewbornNephritis, InterstitialProstaglandins EProteinuriaRenal Insufficiency, ChronicRisk FactorsAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase InhibitorsProstaglandins E

Identifiers

PMID30281062
PMCPMC6534025
OpenAlexW2894118678

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.