Evidence map›Paper›PMID 39361050›Full record

ArticleArchives of toxicology2024

Thallium reabsorption via NKCC2 causes severe acute kidney injury with outer medulla-specific calcium crystal casts in rats.

Kana Unuma, Shuheng Wen, Sho Sugahara, Shutaro Nagano, Toshihiko Aki, Tadayuki Ogawa, Shino Takeda-Homma, Masakazu Oikawa, Akihiro Tojo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of toxicology, 2024. 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

9 authors.

Kana UnumaDepartment of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan. unumlegm@tmd.ac.jp.ORCID 0000-0002-1241-5217
Shuheng WenDepartment of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Sho SugaharaDepartment of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Shutaro NaganoDepartment of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Toshihiko AkiDepartment of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
Tadayuki OgawaComprehensive Research Facilities for Advanced Medical Science, Dokkyo Medical University, Tochigi, Japan.
Shino Takeda-HommaNational Institute of Radiological Sciences, National Institutes for Quantum Science and Technology, Chiba, Japan.
Masakazu OikawaNational Institute of Radiological Sciences, National Institutes for Quantum Science and Technology, Chiba, Japan.
Akihiro TojoDepartment of Nephrology and Hypertension, Dokkyo Medical University, Tochigi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thallium (Tl) is one of the most toxic heavy metals, associated with accidental poisoning and homicide. It causes acute and chronic systemic diseases, including gastrointestinal and cardiovascular diseases and kidney failure. However, few studies have investigated the mechanism by which Tl induces acute kidney injury (AKI). This study investigated the toxic effects of Tl on the histology and function of rat kidneys using biochemical and histopathological assays after intraperitoneal thallium sulfate administration (30 mg/kg). Five days post-administration, rats exhibited severely compromised kidney function. Low-vacuum scanning electron microscopy revealed excessive calcium (Ca) deposition in the outer medulla of Tl-loaded rats, particularly in the medullary thick ascending limb (mTAL) of the loop of Henle. Tl accumulated in the mTAL, accompanied by mitochondrial dysfunction in this segment. Tl-loaded rats showed reduced expression of kidney transporters and channels responsible for Ca

Indexed as

Acute Kidney InjuryCalciumSolute Carrier Family 12, Member 1ThalliumAnimalsCrystallizationFurosemideKidney MedullaMaleMitochondriaRatsRats, Sprague-DawleyCalciumFurosemideSlc12a1 protein, ratSolute Carrier Family 12, Member 1ThalliumCalcium depositsKidney toxicityMedullary thick ascending limbRat modelThallium

Identifiers

PMID39361050
PMCPMC11496332

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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.