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Obesity, kidney dysfunction and hypertension: mechanistic links
John E Hall1,2, Jussara M do Carmo3,4, Alexandre A da Silva3,4
1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA. jehall@umc.edu.
Nature Reviews. Nephrology
|April 25, 2019
Summary
Excessive adiposity (obesity) significantly contributes to primary hypertension, driving cardiovascular and kidney diseases. Understanding the complex interplay of renal and hormonal factors in obesity is crucial for preventing severe health consequences.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
- Obesity Medicine
Background:
- Excessive adiposity is a primary driver of hypertension, accounting for 65-75% of cases.
- Obesity-induced hypertension often begins with abnormal kidney function and increased sodium reabsorption, preceding target organ damage.
- Key factors include kidney compression, elevated renal sympathetic nerve activity (RSNA), and hormonal imbalances (angiotensin II, aldosterone, leptin).
Purpose of the Study:
- To elucidate the intricate mechanisms linking obesity, kidney dysfunction, and hypertension.
- To explore the roles of renal compression, neurohormonal pathways, and adipokines in hypertension development.
- To highlight the challenges in managing obesity-related cardiorenal and metabolic diseases.
Main Methods:
- Review of established literature on obesity, hypertension, and kidney function.
- Analysis of the interplay between visceral fat, renal physiology, and the sympathetic nervous system.
- Examination of hormonal and adipokine signaling pathways involved in sodium balance and blood pressure regulation.
Main Results:
- Obesity initiates hypertension through mechanisms like kidney compression, increased RSNA, and hormonal dysregulation (leptin, angiotensin II, aldosterone).
- Leptin stimulates RSNA, while kidney compression and RSNA activate the renin-angiotensin-aldosterone system, exacerbating hypertension.
- Glucocorticoids and oxidative stress may enhance mineralocorticoid receptor activity, further contributing to hypertension in obesity.
Conclusions:
- The pathogenesis of hypertension in obesity involves complex, interconnected renal, neural, and hormonal pathways.
- Obesity-related hypertension often becomes treatment-resistant, necessitating multifaceted management strategies including addressing comorbidities.
- Effective obesity prevention and control are vital to mitigate the future burden of associated cardiorenal and metabolic diseases.
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