Xenobiotics and Kidney Health: Emerging Challenges in Toxicology and Therapeutics

A special issue of Journal of Xenobiotics (ISSN 2039-4713).

Deadline for manuscript submissions: 25 June 2026 | Viewed by 454

Special Issue Editors


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Guest Editor
Unit of Nephrology and Dialysis, Department of Clinical and Experimental Medicine, University of Messina, 98122 Messina, Italy
Interests: clinical nephrology; chronic kidney disease; glomerulonephritis; diabetic kidney disease; renal tubular acidosis; acute kidney injury; dialysis
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Guest Editor
Department of Medical Sciences and Public Health, University of Cagliari, 09100 Cagliari, Italy
Interests: onconephrology; acute and chronic kidney injury; hemodialysis and extracorporeal blood purification (including hemoadsorption) in acute and chronic patients; nephrotoxicity of anticancer therapies and dose optimization; vascular access in dialysis; uremic toxins and middle molecules; patient-reported outcomes and symptom burden in renal disease; clinical epidemiology in nephrology

Special Issue Information

Dear Colleagues,

The kidney plays a central role in xenobiotic elimination, making it both a critical detoxification organ and a vulnerable target for chemical-induced injury. As our environment becomes increasingly complex with pharmaceuticals, industrial chemicals, environmental pollutants, and emerging contaminants, understanding the interplay between xenobiotics and renal health has never been more urgent.

Over the last two decades, nephrotoxicology has evolved from descriptive pathology to mechanistic investigation, incorporating advances in molecular biology, toxicogenomics, and computational modeling. We now recognize that xenobiotic-induced kidney injury involves complex interactions between transport systems, metabolic pathways, oxidative stress responses, and repair mechanisms. Simultaneously, the kidney's role in drug disposition has profound implications for therapeutic efficacy and safety, particularly in vulnerable populations with impaired renal function.

This Special Issue aims to address the emerging challenges at the intersection of xenobiotics, toxicology, and renal therapeutics. We welcome contributions that advance our understanding of how environmental and pharmaceutical agents affect kidney structure and function, and how we can better predict, prevent, and treat xenobiotic-induced nephrotoxicity.

We are particularly interested in studies exploring novel mechanisms of nephrotoxicity, including mitochondrial dysfunction, endoplasmic reticulum stress, epigenetic modifications, and immune-mediated injury. Research on renal transporters and their role in xenobiotic disposition, drug–drug interactions, and inter-individual variability is highly encouraged. We also seek investigations into emerging renal threats, including novel psychoactive substances, nanomaterials, microplastics, PFAS compounds, and combination exposures.

Additionally, we welcome work on therapeutic innovations, such as novel biomarkers for early detection of kidney injury, protective strategies against nephrotoxicants, regenerative approaches, and personalized risk assessment tools. Studies utilizing in vitro models (kidney organoids, microphysiological systems), in silico approaches , and translational investigations linking preclinical findings to clinical outcomes are of particular value.

We invite original research articles, comprehensive reviews, and perspective pieces that advance the field of renal toxicology and therapeutics, from molecular mechanisms to clinical applications. Together, we can build a more complete understanding of how to protect kidney health in an increasingly xenobiotic-laden world.

Dr. Guido Gembillo
Dr. Matteo Floris
Guest Editors

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Keywords

  • chronic kidney disease
  • renal pathology
  • hemodialysis
  • xenobiotics
  • toxins: pharmacology
  • renal replacement therapy

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Published Papers (1 paper)

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Research

14 pages, 1220 KB  
Article
Environmental Exposure to Cadmium and Lead Exacerbates Kidney Function in People with Diabetes
by Soisungwan Satarug, David A. Vesey, Tanaporn Khamphaya, Donrawee Waeyeng and Supabhorn Yimthiang
J. Xenobiot. 2025, 15(6), 199; https://doi.org/10.3390/jox15060199 - 1 Dec 2025
Viewed by 316
Abstract
This study investigates the relationship between kidney function and exposure to low-level cadmium (Cd) and lead (Pb) in individuals with and without diabetes. Specifically, it tests the hypothesis that the nephrotoxicity of Cd and Pb reduces the tubular degradation of filtered proteins, namely [...] Read more.
This study investigates the relationship between kidney function and exposure to low-level cadmium (Cd) and lead (Pb) in individuals with and without diabetes. Specifically, it tests the hypothesis that the nephrotoxicity of Cd and Pb reduces the tubular degradation of filtered proteins, namely β2-microglobulin (β2M). Data were obtained from a Thai cohort of 137 people, of which 65 were diagnosed with diabetes. Blood Cd, blood Pb, and urinary excretion of Cd (ECd) were used as exposure indicators, while urinary N-acetylglucosaminidase (ENAG) and fractional tubular degradation of β2M (FrTDβ2M) reflected kidney tubular cell injury and the function of tubular cells, respectively. Spearman’s rank correlation revealed that FrTDβ2M varied directly with the estimated glomerular filtration rate (eGFR; r = 0.434), and inversely with fasting plasma glucose (r = −0.215), ECd (r = −0.527), ENAG (r = −0.536), and Cd/Pb exposure (r = −0.249). In a multiple regression model analysis adjusting for potential confounders, the association between FrTDβ2M and eGFR in those with diabetes was particularly strong (β = 0.476) compared to controls (β = 0.360), whereas an inverse association of FrTDβ2M and ECd (β = −0.295) was found only in those with diabetes, along with a positive association of ENAG with ECd (R2 = 0.071). A mediation analysis has revealed that tubular injury (ENAG) mediated 26% of the FrTDβ2M decrease associated with Cd/Pb exposure. These findings suggested that tubular protein degradation pathways may be compromised under combined metabolic and environmental stressors, Cd, and Pb. Full article
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