Evidence map›Paper›PMID 42331866›Full record

ArticleScientific reports2026

Potassium dichromate induces dose-dependent nephrotoxicity through oxidative stress-mediated downregulation of renal aquaporins and upregulation of KIM-1.

Hossam Shehab, Ibrahim El Tantawy El Sayed, Eman A Badr, Nuha Anajirih, Afaf Abdelkader, Eman E ELwakeel, Nagah E Ali, Enas M Kasem, Fatma Al-Zahraa N Al-Shahed, Madaniah O Zakari and 7 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Hossam ShehabDepartment of Chemistry, Faculty of Science, Menoufia University, Shebin El- Koom, 13829, Egypt.
Ibrahim El Tantawy El SayedDepartment of Chemistry, Faculty of Science, Menoufia University, Shebin El- Koom, 13829, Egypt.
Eman A BadrDepartment of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Menoufia University, Shebin El-Koom, 13829, Egypt.
Nuha AnajirihDepartment of Emergency Medical Services, Faculty of Health Sciences, Al Qunfudhah, Umm Al-Qura University, 21912, Makkah, Saudi Arabia.
Afaf AbdelkaderDepartment of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Benha University, Benha, 13518, Egypt.
Eman E ELwakeelDepartment of Anatomy and Embryology, Faculty of Medicine, Benha University, Benha, 13518, Egypt.
Nagah E AliDepartment of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Benha University, Benha, 13518, Egypt.
Enas M KasemDepartment of Physiology, Faculty of Medicine, Benha University, Benha, 13518, Egypt.
Fatma Al-Zahraa N Al-ShahedDepartment of Histology and Cell Biology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
Madaniah O ZakariDepartment of Basic Medical Sciences, College of Medicine, Taibah University, Medina, 41477, Saudi Arabia.
Ekramy M ElmorsyCenter for Health Research, Northern Border University, Arar, 91431, Saudi Arabia.
Samah F IbrahimDepartment of Internal Medicine, College of Medicine, Princess Nourah bint Abdulrahman University, P.O. Box 84428, Riyadh, 11671, Saudi Arabia.
Mustafa ShukryDepartment of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Saudi Arabia, P.O. Box 400, Al-Ahsa, 31982, Saudi Arabia. matta@kfu.edu.sa.
Eman M El NasharDepartment of Anatomy, College of Medicine, King Khalid University, Abha, 62529, Saudi Arabia.
Areej M AlshehriDepartment of Clinical Anatomy, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Ahmad F RawanPre-Clinic Department, Faculty of Veterinary Science, Nangarhar University, Nangarhar, 2603, Afghanistan. afaridrawan@gmail.com.
Ahmed AbdeenDepartment of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Benha University, Toukh, 13736, Egypt. ahmed.abdeen@fvtm.bu.edu.eg.

Funding

Deanship of Scientific Research, King Khalid University RGP2/529/45
6 · The paper itself

Abstract

Potassium dichromate (Cr) is a ubiquitous inorganic chemical reagent, most frequently employed as an oxidizing agent in variety of laboratory and industrial settings and can result in nephrotoxicity. The current study was done to explore the nephrotoxic effects of Cr with a specific focus on alterations in renal aquaporins (AQPs) expression, renal water channel protein, providing insights into how exposure to Cr may compromise renal water homeostasis in a dose-dependent pattern. Thirty-six Wistar albino male rats were assigned into 3 groups evenly; control rats received only distilled water daily, while Cr-Low and Cr-High groups received, 2.5 mg/kg bw, and 7.5 mg/kg bw of Cr i.p for 14 days, respectively. Blood and kidney samples were obtained. Cr induced nephrotoxicity in the current study in a dose-dependent manner, as exhibited by a remarkable deterioration of the renal parameters, oxidative status, histopathological and ultrastructural changes. Renal function registered a significant rise in urea and creatinine, as opposed to total protein and albumin, which decreased substantially. A significant dose dependent rise in malondialdehyde (MDA) level as well as dwindle in the antioxidant enzymes level. Furthermore, hematology divulged a notable reduction in hemoglobin concentration (Hb%) while significant upsurge in white blood cells (WBCs) in exposed groups. In addition, our study demonstrated that Cr, alters the expression level of AQP1 and AQP2 in renal tissue which are salutary for detecting the renal damage early. On the other hand, Cr boosted the upregulation of kidney injury molecule-1 (KIM-1) in kidney tissue confirming its disruption. Interestingly, gene expression of KIM-1, AQP1 and AQP2's in renal membrane correlates well with creatine level, reinforcing their role as sensitive markers of tubular damage and reflect impaired tubular water handling. High exposure produced a severe nephrotoxic profile, distinctly different from controls and far more pronounced than the Cr-Low group.

Indexed as

Aquaporin 2AquaporinsHepatitis A Virus Cellular Receptor 1KidneyKidney DiseasesOxidative StressPotassium DichromateAnimalsAquaporin 1Cell Adhesion MoleculesDose-Response Relationship, DrugDown-RegulationMaleMalondialdehydeRatsRats, WistarAquaporin 1Aquaporin 2AquaporinsCell Adhesion MoleculesHavcr1 protein, ratHepatitis A Virus Cellular Receptor 1MalondialdehydePotassium DichromateAquaporinsDose-dependentKIM-1NephrotoxicityOxidative stressPotassium dichromate

Identifiers

PMID42331866
PMCPMC13287758

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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.