The link between renal failure and Parkinson’s disease: Researchers illuminate the underlying mechanisms

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Deposition of α-synuclein in the kidneys of PD patients. Credit: Yuan et al. Nature Neuroscience (2025). DOI: 10.1038/s41593-024-01866-2.

Lewy body diseases (LBDs) are a class of debilitating neurodegenerative disorders linked to the abnormal aggregation of the protein α-synuclein in nerve cells. When misfolded, this protein can produce clumps known as Lewy bodies, which can adversely impact the functioning of cells, contributing to neurodegeneration.

Recent studies also showed that LBDs, particularly Parkinson’s disease, often initiate in the gut and that, in some cases, kidney failure contributes to their emergence. So far, however, the exact physiological processes connecting kidney failure to PD remain poorly understood.

Researchers at Renmin Hospital of Wuhan University recently carried out a study to better understand these mechanisms by further examining the link between kidney failure and LBDs. Their findings, published in Nature Neuroscience, show that renal dysfunction can cause the accumulation of α-synuclein in the kidneys, which can in turn cause the protein to spread to the brain, in some cases facilitating the development of PD.

“Some studies suggest that in some PD patients, α-synuclein aggregation may originate from peripheral organs but not from the brain,” Zhentao Zhang, senior author of the paper, told Medical Xpress.

“These cases are broadly referred to with the term ‘body-first PD.’ To identify the organs where α-synuclein pathology begins, we stained the peripheral organs and found that the kidneys were positive for α-synuclein pathology in some PD patients.”

Exploring the mechanisms connecting renal failure to Parkinson's disease
α-Syn pathology in the kidneys and CNS of patients with PD and CKD. Credit: Nature Neuroscience (2025). DOI: 10.1038/s41593-024-01866-2

Building on previous studies that unveiled a link between kidney function and the incidence of PD, Zhang and his colleagues carried out experiments to further illustrate the mechanisms behind this connection. To do this, they first stained kidney samples extracted from patients diagnosed with PD and those extracted from people with chronic renal diseases.

“We found that α-synuclein was deposited in the kidneys of these patients,” explained Zhang. “To illustrate the role of renal failure in PD, we induced renal failure in mouse models of PD and found that renal failure exacerbates PD-like pathology. Injection of α-synuclein fibrils into the kidney induced the spread of α-synuclein pathology to the brain, whereas deletion of α-synuclein in blood cells alleviated PD pathology in a mouse model of PD.”

Essentially, the researchers found that the kidneys of patients presenting renal failure contained a large amount of the protein α-synuclein. They were then able to shed light on how this α-synuclein accumulation could lead to PD, specifically following the spread of this protein to the brain.

Zhang and his colleagues also showed that severing the connections between the kidneys and the brain in male mice blocked the accumulation of α-synuclein in the brain following renal failure. In the future, their study could inspire further research exploring the processes they uncovered, which could contribute to the development of therapeutic interventions aimed at slowing down or stopping the progression of PD and potentially other LBDs.

“The most notable finding of our study is that α-synuclein may originate from the kidney and spread to the brain,” added Zhang. “These observations suggest that eliminating circulating α-synuclein may be a possible way to halt the progression of PD. In our next studies, we will study the molecular mechanisms that mediate the deposition of α-synuclein in the kidney as well as the mechanisms that mediate the spread of α-synuclein pathology from the kidney to the brain.”

More information:
Xin Yuan et al, Propagation of pathologic α-synuclein from kidney to brain may contribute to Parkinson’s disease, Nature Neuroscience (2025). DOI: 10.1038/s41593-024-01866-2.

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