Obesity, hypertension, and chronic kidney disease
Open accessAbstract
Obesity is a major risk factor for essential hypertension, diabetes, and other comorbid conditions that contribute to development of chronic kidney disease. Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion via activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and by physical compression of the kidneys, especially when there is increased visceral adiposity. Other factors such as inflammation, oxidative stress, and lipotoxicity may also contribute to obesity-mediated hypertension and renal dysfunction. Initially, obesity causes renal vasodilation and glomerular hyperfiltration, which act as compensatory mechanisms to maintain sodium balance despite increased tubular reabsorption. However, these compensations, along with increased arterial pressure and metabolic abnormalities, may ultimately lead to glomerular injury and initiate a slowly developing vicious cycle that exacerbates hypertension and worsens renal injury. Body weight reduction, via caloric restriction and increased physical activity, is an important first step for management of obesity, hypertension, and chronic kidney disease. However, this strategy may not be effective in producing long-term weight loss or in preventing cardiorenal and metabolic consequences in many obese patients. The majority of obese patients require medical therapy for obesity-associated hypertension, metabolic disorders, and renal disease, and morbidly obese patients may require surgical interventions to produce sustained weight loss.
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Excess perirenal fat encapsulating the kidneys and excess renal sinus fat may squeeze the kidneys and increase intrarenal pressures.
“excess PRF encapsulating the kidneys and excess RSF may squeeze the kidneys and increase intrarenal pressures10,35.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [10]
In the early phases of obesity, blood pressure may not be salt-sensitive; therefore, hypertension may not be greatly exacerbated by high salt intake.
“In the early phases of obesity, BP may not be salt-sensitive; therefore, hypertension may not be greatly exacerbated by high salt intake10.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [10]
These changes tend to increase fractional NaCl reabsorption in the loop of Henle and decrease delivery of NaCl to the macula densa, causing feedback-mediated reductions in afferent arteriolar resistance, increases in renal blood flow and glomerular filtration rate and stimulation of renin secretion from juxtaglomerular cells.
“These changes tend to increase fractional NaCl reabsorption in the loop of Henle and decrease delivery of NaCl to the macula densa, causing feedback-mediated reductions in afferent arteriolar resistance, increases in RBF and GFR and stimulation of renin secretion from juxtaglomerular cells10.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [10]
Renal vasodilation, increases in renal blood flow and glomerular hyperfiltration occur early after weight gain but are later followed by declines in renal blood flow and glomerular filtration rate as a result of kidney injury and gradual loss of nephrons.
“renal vasodilation, increases in renal blood flow (RBF) and glomerular hyperfiltration occur early after weight gain but are later followed by declines in RBF and glomerular filtration rate (GFR) as a result of kidney injury and gradual loss of nephrons10.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [10]
Physical compression of the kidneys by fat in and around the kidneys is a mediator of abnormal kidney function and increased blood pressure during development of obesity hypertension.
“The mediators of abnormal kidney function and increased blood pressure during development of obesity hypertension include 1) physical compression of the kidneys by fat in and around the kidneys”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
Glomerular hyperfiltration early in obesity may be replaced by a gradual decline in GFR as renal injury and nephron loss occur in association with prolonged hypertension, diabetes and dyslipidemia.
“For example, glomerular hyperfiltration early in obesity may be replaced by a gradual decline in glomerular filtration rate (GFR) as renal injury and nephron loss occur in association with prolonged hypertension, diabetes and dyslipidemia12.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
Increased sympathetic nervous system (SNS) activity is a mediator of abnormal kidney function and increased blood pressure during development of obesity hypertension.
“3) increased sympathetic nervous system (SNS) activity”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
Multiple lines of evidence indicate that increased SNS activity contributes to obesity hypertension.
“Multiple lines of evidence indicate that increased SNS activity contributes to obesity hypertension5,12:”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
In obese dogs, rabbits and humans, retroperitoneal fat often encapsulates the kidney, adheres tightly to the renal capsule, and invades the renal sinuses, causing additional compression and increased intrarenal pressures.
“Also, in obese dogs, rabbits and humans, retroperitoneal fat often encapsulates the kidney, adheres tightly to the renal capsule, and invades the renal sinuses, causing additional compression and increased intrarenal pressures (Figure 3)10,12.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
Increased visceral and retroperitoneal fat may increase BP by physically compressing the kidneys.
“Increased visceral and retroperitoneal fat may increase BP by physically compressing the kidneys.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
Excess fat accumulation in and around the kidneys is associated with increased intrarenal pressures, impaired pressure natriuresis, and hypertension.
“Excess fat accumulation in and around the kidneys is associated with increased intrarenal pressures, impaired pressure natriuresis, and hypertension12.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
Obesity may be an independent risk factor for CKD, beyond its effects to cause hypertension and diabetes.
“there is evidence that obesity may be an independent risk factor for CKD, beyond its effects to cause hypertension and diabetes12.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [12]
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Control of metabolic and cardiovascular function by the leptin–brain melanocortin pathway
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Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms
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Self-citationOverweight and obesity: prevalence, consequences, and causes of a growing public health problem
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Adipose tissue is associated with kidney function parameters
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Examining the evidence for weight management in individuals with type 2 diabetes
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- Authors
- Hall, J., Juncos, L., Wang, Z., Hall, M., do Carmo, J., & da Silva, A.
- Affiliations
- University of Mississippi Medical Center (US)
- Corresponding author
- Hall, Michael
- Venue
- International Journal of Nephrology and Renovascular Disease
- Publisher
- Informa UK Limited
- Published
- 2014-02
- Volume
- 7
- Pages
- 75
- ISSN
- 1178-7058 (ISSN-L)
- PMC
- PMC3933708
- OpenAlex
- W2004830232
- Cited by
- 520
- References
- 100
- Citations by year
- 2026: 29 · 2025: 41 · 2024: 36 · 2023: 41 · 2022: 48 · 2021: 55 · 2020: 54 · 2019: 42 · 2018: 53 · 2017: 47 · 2016: 28 · 2015: 29 · 2014: 15 · 2012: 1
- FWCI
- 5.75
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Nephrology and Renovascular Disease (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Funders
- National Heart, Lung, and Blood Institute (51971, P01-HL-51971, P01HL051971, GM104357)
- National Institute of General Medical Sciences (GM104357, P20GM104357)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Renal and Vascular Pathologies
- Keywords
- obesity, essential hypertension, chronic kidney disease, renal sodium reabsorption, pressure natriuresis, visceral fat, renin-angiotensin-aldosterone system, sympathetic nervous system, glomerular hyperfiltration, renal vasodilation, oxidative stress, lipotoxicity, inflammation, weight loss, bariatric surgery
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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