Obesity-associated hypertension and kidney disease
Abstract
PURPOSE OF REVIEW: The worldwide prevalence of obesity and its associated metabolic and cardiovascular disorders has risen dramatically during the past two decades. Our objective is to review the mechanisms that link obesity with hypertension and altered kidney function. RECENT FINDINGS: Current evidence suggests that excess weight gain may be responsible for 65-75% of the risk for essential hypertension. Abnormal renal pressure natriuresis, due initially to increased renal tubular sodium reabsorption, is a key factor linking obesity with hypertension. Obesity increases renal sodium reabsorption by activating the renin-angiotensin and sympathetic nervous systems, and by altering intrarenal physical forces. Adipose tissue functions as an endocrine organ, secreting hormones/cytokines (e.g. leptin) that may activate the sympathetic nervous system and alter kidney function. Excess visceral adipose tissue may physically compress the kidneys, increasing intrarenal pressures and tubular reabsorption. Sustained obesity eventually causes structural changes in the kidneys and loss of nephron function, further increasing arterial pressure and leading to severe renal disease in some cases. SUMMARY: Despite considerable progress in understanding the pathophysiology of obesity, there are still no specific guidelines for the treatment of obesity hypertension other than weight reduction. Special considerations for obese hypertensive patients, in addition to controlling blood pressure, are correcting the metabolic abnormalities and protecting the kidneys from injury. This remains an important area for further research, especially in view of the current 'epidemic' of obesity in most industrialized countries.
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Obesity may lead to compression of the kidneys, resulting in increased intrarenal pressures and tending to reduce blood flow rates in the vasa recta and loop of Henle.
“obesity may lead to compression of the kidneys, resulting in increased intrarenal pressures and tending to reduce blood flow rates in the vasa recta and loop of Henle35,45 (FIG. 2).”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [45]
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- Authors
- Hall, J. E., Kuo, J. J., da Silva, A. A., de Paula, R. B., Liu, J., & Tallam, L.
- Affiliations
- University of Mississippi Medical Center (US)
- Corresponding author
- Hall, John E.
- Venue
- Current Opinion in Nephrology and Hypertension
- Published
- 2003-03
- Volume
- 12
- Issue
- 2
- Pages
- 195-200
- ISSN
- 1062-4821 (ISSN-L)
- OpenAlex
- W2077179567
- Cited by
- 187
- References
- 32
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 8 · 2021: 10 · 2020: 4 · 2019: 6 · 2018: 3 · 2017: 11 · 2016: 7 · 2015: 7 · 2014: 14 · 2013: 14 · 2012: 7
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Nephrology & Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01-HL-51971, P01HL051971)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- obesity, obesity-related hypertension, essential hypertension, kidney disease, renal sodium reabsorption, renin-angiotensin system, sympathetic nervous system, adipose tissue hormones, leptin, visceral adipose tissue, intrarenal pressure, nephron function, weight loss
- MeSH terms
- Female, Humans, Hypertension, Kidney Diseases, Kidney Function Tests, Male, Obesity, Prognosis, Severity of Illness Index, Comorbidity, Incidence, Risk Assessment
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