Evidence map›Paper›PMID 33475432›Full record

ArticleClinical toxicology (Philadelphia, Pa.)2021

Neurotoxic effects of nephrotoxic compound diethylene glycol.

Courtney N Jamison, Robert D Dayton, Brian Latimer, Mary P McKinney, Hannah G Mitchell, Kenneth E McMartin

Abstract read
In one paragraph

Article in Clinical toxicology (Philadelphia, Pa.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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.

Courtney N JamisonDepartment of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA, USA.
Robert D DaytonDepartment of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA, USA.
Brian LatimerDepartment of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA, USA.
Mary P McKinneyDepartment of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA, USA.
Hannah G MitchellDepartment of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA, USA.
Kenneth E McMartinDepartment of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA, USA.

Funding

Neurotoxicity and nephrotoxicity of diglycolic acid: a model of calcium chelation-induced mitochondrial dysfunctionR15ES029704 · NIEHS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI MCMARTIN, KENNETH E. · 2018 to 2018
$438k
NIEHS NIH HHS R15 ES029704
6 · The paper itself

Abstract

contextDiethylene glycol (DEG) is an organic compound found in household products but also as an adulterant in medicines by acting as a counterfeit solvent. DEG poisonings have been characterized predominately by acute kidney injury (AKI), but also by delayed neurological sequelae such as decreased reflexes or face and limb weakness.

objectivesCharacterizing the neurological symptoms of DEG poisoning in a subacute animal model would create a clearer picture of overall toxicity and possibly make mechanistic connections between kidney injury and neuropathy.

methodsMale Wistar-Han rats were orally administered doses of 4 - 6 g/kg DEG every 12 or 24 h and monitored for 7 days. Urine was collected every 12 h and endpoint blood and cerebrospinal fluid (CSF) were collected for a renal plasma panel and total protein estimation, respectively. Motor function tests were conducted before and after treatment. Kidney and brain tissue was harvested for metabolic analysis.

resultsOf the 43 animals treated with DEG, 11 developed AKI as confirmed by increased BUN and creatinine levels. Renal and brain DGA accumulation was markedly increased in animals that developed AKI compared to animals without AKI. The total protein content in CSF in animals with kidney injury was markedly elevated compared to control and to treated animals without AKI. Significant decreases in forelimb grip strength and decreases in locomotor and rearing activity were observed in animals with AKI compared to control and to animals without AKI. DISCUSSION: Repeated dosing with DEG in an animal model produced nephrotoxic effects like those in studies with acute DEG administration. The decrease in motor function and increase in CSF protein were only present in animals that developed AKI.

conclusionsThese studies show development of neurotoxicity in this DEG animal model and suggest that neurological symptoms are observed only when DGA accumulation and kidney injury also occur.

Indexed as

Acute Kidney InjuryAdultAnimalsDisease Models, AnimalEthylene GlycolsHumansKidneyMaleNeurotoxicity SyndromesRatsRats, WistarEthylene Glycolscerebrospinal fluidDiethylene glycoldiglycolic acidmetabolite toxicitymotor functionnephrotoxicityneurotoxicity

Identifiers

PMID33475432
PMCPMC8292454

What OpenQuestion holds

Textmetadata
LicenceTDM
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.