Is obesity a major cause of chronic kidney disease?
Abstract
Excess weight gain is a major risk factor for essential hypertension and for end-stage renal disease (ESRD). Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion because of activation of the sympathetic nervous system and renin-angiotensin system and by physical compression of the kidneys, especially when visceral obesity is present. Obesity also causes renal vasodilation and glomerular hyperfiltration that initially serve as compensatory mechanisms to maintain sodium balance in the face of increased tubular reabsorption. In the long-term, however, these changes, along with the increased systemic arterial pressure, create a hemodynamic burden on the kidneys that causes glomerular injury. With prolonged obesity, there is increasing urinary protein excretion and gradual loss of nephron function that worsens with time and exacerbates hypertension. With the worsening of metabolic disturbances and the development of type II diabetes in some obese patients, kidney disease progresses much more rapidly. Weight reduction is an essential first step in the management of obesity, hypertension, and kidney disease. Special considerations for the obese patient, in addition to adequately controlling the blood pressure, include correction of the metabolic abnormalities and protection of the kidneys from further injury.
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Early in development of obesity and even in obese children, there is often interstitial fibrosis, microalbuminuria or proteinuria, expansion of mesangial matrix, glomerulomegaly, focal segmental glomerular sclerosis, and podocyte disorder associated with glomerular hyperfiltration.
“Early in development of obesity and even in obese children, there is often interstitial fibrosis, microalbuminuria or proteinuria, expansion of mesangial matrix, glomerulomegaly, focal segmental glomerular sclerosis, and podocyte disorder associated with glomerular hyperfiltration142–144.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [143]
With nephron loss there is increasing salt-sensitivity of BP.
“With nephron loss there is increasing salt-sensitivity of BP143.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [143]
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- Authors
- Hall, J. E., Henegar, J. R., Dwyer, T. M., Liu, J., da Silva, A. A., Kuo, J. J., & Tallam, L.
- Affiliations
- University of Mississippi Medical Center (US)
- Corresponding author
- Hall, John E
- Venue
- Advances in Renal Replacement Therapy
- Publisher
- Elsevier BV
- Published
- 2004-01
- Volume
- 11
- Issue
- 1
- Pages
- 41-54
- ISSN
- 1073-4449 (ISSN-L)
- OpenAlex
- W2064497302
- Cited by
- 264
- References
- 79
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 8 · 2023: 28 · 2022: 14 · 2021: 23 · 2020: 10 · 2019: 12 · 2018: 5 · 2017: 6 · 2016: 15 · 2015: 15 · 2014: 12 · 2013: 7 · 2012: 14
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Advances in Renal Replacement Therapy (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL051971)
- 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, chronic kidney disease, end-stage renal disease, essential hypertension, tubular sodium reabsorption, pressure natriuresis, visceral obesity, glomerular hyperfiltration, glomerular injury, proteinuria, type 2 diabetes, weight loss, renin-angiotensin system, sympathetic nervous system, hemodynamic burden
- MeSH terms
- Diabetes Mellitus, Humans, Hypertension, Kidney, Kidney Failure, Chronic, Obesity, Renin-Angiotensin System, Risk Factors, Sympathetic Nervous System, Lipid Peroxidation, Oxidative Stress
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