There is a growing concern within the medical community about the potential burden of microplastics on human organs and tissues. In this study, we investigated by microRaman spectroscopy the presence of microplastics in human kidneys and urine. Moreover, an open-access software was developed and validated for the project, which enabled the comparison between the investigated spectra and a self-created spectral database, thus enhancing the ability to characterize polymers and pigments in biological matrices. Healthy portions of ten kidneys obtained from nephrectomies, as well as ten urine samples from healthy donors were analyzed: 26 particles in both kidney and urine samples were identified, with sizes ranging from 3 to 13 μm in urine and from 1 to 29 μm in kidneys. The most frequently determined polymers are polyethylene and polystyrene, while the most common pigments are hematite and Cu-phthalocyanine. This preclinical study proves the presence of microplastics in renal tissues and confirms their presence in urine, providing the first evidence of kidney microplastics deposition in humans.

Rare earth-doped ceria systems form one of the most thoroughly studied materials classes to be employed as solid electrolytes in solid oxide cells. In order to unveil the structural details ruling the ionic conductivity properties, the (Ce_1-xRE_x)O_2-x/2 series with RE = (Nd_0.63Dy_0.37), (Nd_0.74Tm_0.26), and (Sm_0.67Gd_0.33), and x ranging between 0.05 and 0.60, have been synthesized and characterized by means of synchrotron X-ray powder diffraction and pair distribution function analyses. By coupling the mentioned techniques, the whole spectrum of structural order and disorder characterizing these compounds at different scale lengths could be revealed and discussed in detail. With reference to the average scale, for x ≥ 0.40 or 0.50, depending on the system, the Fm3 @#x0305;m crystal structure of the CeO₂-based solid solution is accompanied by defect aggregates with Ia3 @#x0305; structure growing within the ceria matrix. The local structure (r < 10 Å), on the contrary, even at the lowest doping degree can be described as a disordered fluctuation between the average structures characterizing the Fm3 @#x0305;m and Ia3 @#x0305; phases, which explains the reduction in ionic conductivity observed even within the stability range of the CeO₂-based solid solution.

Microplastics (MPs) are widespread environmental contaminants, but their potential effects on kidney health remain poorly defined. As an organ continuously exposed to circulating particles and involved in their urinary elimination, the kidney may represent both a target of MP toxicity and a route of excretion. In this narrative review, we examine current evidence linking MPs to kidney injury, integrating experimental, mechanistic, and human data. Particular attention is given to the early events governing particle–cell interactions. After exposure, micro- and nanoplastics acquire an eco- and biomolecular corona that modifies their surface properties, cellular recognition, uptake, and biodistribution. Following internalization through phagocytic and endocytic pathways, particles may accumulate within endolysosomal compartments and interact with intracellular structures, disrupting cellular homeostasis. In renal cells, these events converge on mitochondrial dysfunction, reactive oxygen species generation, endoplasmic reticulum stress, inflammatory signaling, altered autophagy, and regulated cell death. Several interconnected pathways have been implicated, including Keap1–Nrf2/ARE and NF-κB signaling, MAPK and IRE1/XBP1-mediated stress responses, ACSL4–GPX4-related ferroptosis, and TGF-β1-related profibrotic signaling. Human studies have detected MPs in urine and kidney tissue and provide preliminary evidence linking MP burden with early markers of kidney damage, although current findings remain limited by small study populations and substantial methodological heterogeneity. Patients with chronic kidney disease, particularly those receiving dialysis, may represent a population of special interest because potentially altered renal handling may coexist with repeated exposure to polymer-based medical devices and dialysis fluids. Despite this potential relevance, data on MP exposure and accumulation in CKD and dialysis patients remain remarkably scarce. We finally discuss the limitations of current experimental models and analytical methods and the need for standardized biomonitoring, more environmentally relevant particles and exposure concentrations, and detection strategies capable of reaching the nanoscale, including artificial intelligence-assisted analysis. Overall, available evidence provides a mechanistic basis for MP-induced kidney injury, but its clinical relevance and contribution to human kidney disease remain to be established.