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Volume 11, Issue 1, Pages 41-54 (January 2004)


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Is obesity a major cause of chronic kidney disease?

John E HallaCorresponding Author Informationemail address, Jeffrey R Henegara, Terry M Dwyera, Jiankang Liua, Alexandre A da Silvaa, Jay J Kuoa, Lakshmi Tallama

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.

a Department of Physiology and Biophysics and Center of Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, Jackson, MS, USA

Corresponding Author InformationAddress correspondence to John E. Hall, PhD, University of Mississippi Medical Center, Department of Physiology and Biophysics, 2500 North State Street, Jackson, MS 39216-4505, USA

 Supported by a grant from the National Heart, Lung and Blood Institute (P01 HL 51971).

PII: S1073-4449(03)00066-9

doi:10.1053/j.arrt.2003.10.007


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