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Kidney-brain axis inflammatory cross-talk: from bench to bedside.
Aline Silva Miranda1,2, Thiago Macedo Cordeiro2, Thomas Mucida Dos Santos Lacerda Soares2
1Laboratório de Neurobiologia, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais (UFMG), Brazil.
Chronic kidney disease (CKD) increases the risk of brain disorders, including dementia. Beyond cerebrovascular issues, kidney-brain communication involves inflammatory and hormonal pathways that may contribute to cognitive decline in CKD patients.
Area of Science:
- Nephrology
- Neurology
- Neuroscience
Background:
- Chronic kidney disease (CKD) is linked to increased risks of neuropsychiatric disorders, cognitive impairment, and dementia.
- Cerebrovascular lesions are a known contributor, but other mechanisms are implicated, especially in early CKD stages.
Purpose of the Study:
- To review experimental and clinical evidence on kidney-brain cross-talk mechanisms in CKD.
- To explore potential pathways and the pathophysiological role of these interactions in cognitive changes.
- To identify targets for mitigating cognitive decline in CKD patients.
Main Methods:
- Literature review of experimental and clinical studies.
- Discussion of proposed mechanisms including cytokine release, reactive oxygen species (ROS), trophic factors, and renin-angiotensin system (RAS) molecules.
- Hypothesizing pathways for kidney-brain interactions.
Main Results:
- Evidence supports multiple mechanisms beyond cerebrovascular disease contributing to brain dysfunction in CKD.
- Cytokine/chemokine release, ROS, trophic factors, and RAS molecules play roles in kidney-brain communication.
- These interactions are hypothesized to be crucial in the pathophysiology of neuropsychiatric and cognitive changes.
Conclusions:
- Understanding kidney-brain cross-talk is vital for managing cognitive impairment in CKD.
- New therapeutic strategies may target these specific pathophysiological pathways.
- Early intervention can potentially minimize the risk of future cognitive decline.
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