Review synthesizing evidence that reduced renal function (eGFR, cystatin C) associates with worse PD severity and cognitive decline, proposing uremic toxins, systemic inflammation, oxidative stress, and impaired renal clearance of alpha‑synuclein as mechanistic links in a kidney–brain axis.

Points to accessible renal biomarkers for prognostic stratification and a plausible mechanistic pathway (uremic toxin/alpha‑synuclein clearance) that could be leveraged to design biomarker‑driven trials or explore renal‑targeted repurposing strategies to slow PD progression.

THE OBJECTIVE: Of the study is to evaluate the prognostic significance of renal dysfunction biomarkers in the context of the Parkinson's disease trajectory, with an emphasis on the pathophysiological mechanisms linking renal and brain dysfunction with neurodegeneration, as well as to assess the prognostic potential of specific renal markers for the severity of motor and non-motor symptoms of the disease. MATERIAL AND METHODS: Research papers, mainly published since 2020, from highly cited scientific databases such as Scopus, PubMed, Google Scholar, and eLibrary were included in this review. RESULTS: Studies have found a significant association between decreased renal function, as assessed by the estimated glomerular filtration rate (eGFR) and cystatin C, and the progression of cognitive impairment in PD, as well as the severity of the disease. Uremic toxins, systemic inflammation, and oxidative stress have been identified as key pathophysiological links contributing to alpha-synuclein neurodegeneration and dysregulation in patients with renal dysfunction. The kidneys have been shown to be involved in alpha-synuclein clearance, and renal failure may contribute to its accumulation and distribution to the brain. CONCLUSION: Renal dysfunction biomarkers, in particular eGFR and cystatin C, show potential as prognostic indicators of PD progression, especially for cognitive impairment. The interaction within the kidney-brain axis through uremic toxins, inflammation, oxidative stress, and alpha-synuclein dysregulation represents an important area for further research and development of new therapeutic approaches.