Kidney Week

Abstract: TH-OR078

Integrated In Vitro, Organ-on-a-Chip, and In Vivo Evidence of Microplastic-Induced Kidney Dysfunction

Session Information

• Glomerular Diseases: Novel Mechanisms of Injury
  October 22, 2026 | Location: Room 401, Convention Center
  Abstract Time: 05:20 PM - 05:30 PM

Category: Glomerular Diseases

• 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

• Kasravi, Mohammadreza, Children's Hospital Los Angeles, Los Angeles, California, United States

Mohammadreza Kasravi, MD, MBA

• Alcala, Velia, Children's Hospital Los Angeles, Los Angeles, California, United States

Velia Alcala

• Dedhia, Charmi, Children's Hospital Los Angeles, Los Angeles, California, United States

Charmi Dedhia, MS, MBA

• Rodriguez, Raquel, Children's Hospital Los Angeles, Los Angeles, California, United States

Raquel Rodriguez

• Villani, Valentina, Children's Hospital Los Angeles, Los Angeles, California, United States

Valentina Villani, PhD

• De Filippo, Roger E., Children's Hospital Los Angeles, Los Angeles, California, United States

Roger E. De Filippo, MD

• Perin, Laura, Children's Hospital Los Angeles, Los Angeles, California, United States

Laura Perin, PhD

• Da Sacco, Stefano, Children's Hospital Los Angeles, Los Angeles, California, United States

Stefano Da Sacco, PhD

Background

Microplastics (MP), synthetic polymer particles <5 mm, are emerging environmental contaminants detected in human tissues, including the kidney. Given the kidney's central role in filtration and waste elimination, understanding how chronic MP exposure affects renal cellular integrity and function is critical. However, the mechanistic and physiologic impact of MP on healthy renal systems remains incompletely understood.

Methods

Primary human renal cells, including podocytes, glomerular endothelial cells, mesangial cells, and proximal tubular cells, were exposed to fluorescently labeled 1 µm polystyrene MP in vitro. MP uptake, phenotypic alterations, and injury-associated signaling were assessed using live-cell imaging, flow cytometry, immunofluorescence, and protein array analyses. Functional consequences were evaluated using glomerular and tubular microfluidic organ-on-a-chip platforms. In parallel, healthy wild-type mice were exposed to MP via daily ingestion for 45 days. MP biodistribution was assessed in blood, urine, and kidney tissue, and renal function was evaluated using albumin-to-creatinine ratio (ACR) and histologic analysis.

Results

All renal cell types internalized MP, with podocytes demonstrating the highest uptake in the first hours. MP exposure induced cytoskeletal disruption, loss of endothelial markers, re-expression of injury-associated proteins, and activation of oxidative stress and apoptotic pathways. Organ-on-a-chip studies revealed impaired glomerular barrier integrity, evidenced by increased albumin leakage. In vivo, MP were detected in blood and urine within 2-4 weeks of exposure and accumulated within glomerular and tubular compartments. Chronically exposed mice exhibited a trend toward increased proteinuria, suggesting a path toward early renal dysfunction.

Conclusion

Integrated in vitro, organ-on-a-chip, and in vivo findings demonstrate that MP are systemically absorbed, accumulate within renal tissue, and disrupt renal cellular phenotype and barrier function. These data identify environmental MP exposure as a potential risk factor for renal injury and underscore the need for further investigation into its role in kidney pathophysiology.