What is the clinical evidence from this study?

Study design: Review. Population: Chronic kidney disease. Intervention: Chronic stress.

What does this research mean for the field?

Chronic stress accelerates renal injury and fibrosis via neuroendocrine dysregulation of the brain-kidney axis through cortisol-mediated aberrant activation of intrarenal mineralocorticoid receptors. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.ESTABLISHES_NEW_DIRECTION.

What question did this study set out to answer?

To delineate the neuroendocrine pathways of the brain-kidney axis that translate chronic stress into direct kidney damage and accelerated renal decline.

September 30, 2026Open Access

Chronic Stress and the Brain-Kidney Axis in Renal Injury: From Neuroendocrine Dysregulation to Kidney Damage.

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Key result

Chronic stress may drive kidney damage via HPA-SNS overactivation and aberrant mineralocorticoid receptor activation.

Why the study?

The neuroendocrine mechanisms by which chronic stress leads to direct kidney damage and chronic kidney disease remain unclear.

Design

Review synthesizing current evidence on brain-kidney axis in stress-induced renal injury

Authors

CZChunyun Zhang CWCheng WanQingdao Eighth People's Hospital JSJing SunXiamen University

Discussion

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Implication

Supports neuroendocrine targeting in stress-related CKD; leaves open whether brain-kidney axis modulation alters progression.

Key Points

To delineate the neuroendocrine pathways of the brain-kidney axis that translate chronic stress into direct kidney damage and accelerated renal decline.
Synthesized findings from large cohort studies and physiological models evaluating chronic stress as an independent contributor to renal deterioration.
Mapped signaling cascades involving the hypothalamic-pituitary-adrenal axis, sympathetic tone, and intrarenal mineralocorticoid receptor pathways.
Chronic stress drives sustained overactivity of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system alongside secondary renin-angiotensin-aldosterone system dysregulation.
Sustained glucocorticoid excess compromises the 11β-HSD2 protective barrier, enabling cortisol to aberrantly activate intrarenal mineralocorticoid receptors.
Glucocortoid cross-activation stimulates profibrotic NOX4/ROS/TGF-β/Smad signaling and activates the complement C5a-C5aR1 axis, promoting fibrosis and defining stress-related kidney disease.

PICO

Population

Chronic kidney disease

Exposure / Comparator

Chronic stress

This review synthesizes evidence on the brain-kidney axis to propose stress-related kidney disease as a distinct clinical entity, highlighting potential precision interventions.

Cite This Study

Zhang et al. (2026) conducted a review in Chronic kidney disease. Chronic stress was evaluated. Chronic stress is hypothesized to induce kidney damage through the brain-kidney axis via HPA and SNS overactivation, leading to aberrant intrarenal mineralocorticoid receptor activation by cortisol.

synapsesocial.com/papers/6abc576efbfca106a1247e70 https://doi.org/10.3390/ijms27188356

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Chronic Stress and the Brain-Kidney Axis in Renal Injury: From Neuroendocrine Dysregulation to Kidney Damage.

Discussion

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Implication

Key Points

PICO

Cite This Study

Chronic Stress and the Brain-Kidney Axis in Renal Injury: From Neuroendocrine Dysregulation to Kidney Damage.

Discussion

Member takes

Implication

Key Points

PICO

Cite This Study

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