title: Abnormal kidney function as a cause and a consequence of obesity hypertension.
abstract: 1. Obesity is the most common nutritional disorder in the US and is a major cause of human essential hypertension. Although the precise mechanisms by which obesity raises blood pressure (BP) are not fully understood, there is clear evidence that abnormal kidney function plays a key role in obesity hypertension. 2. Obesity increases tubular reabsorption and this shifts pressure natriuresis towards higher BP. The increased tubular reabsorption is not directly related to hyperinsulinaemia, but is closely linked to activation of the sympathetic and renin-angiotensin systems, and possible changes in intrarenal physical forces caused by medullary compression due to accumulation of adipose tissue around the kidney and increased extracellular matrix within the kidney. 3. Obesity is also associated with marked renal vasodilation and increased glomerular filtration rate, which are compensatory responses that help overcome the increased tubular reabsorption and maintain sodium balance. However, chronic renal vasodilation causes increased hydrostatic pressure and wall stress in the glomeruli which, along with increased lipids and glucose intolerance, may cause glomerulosclerosis and loss of nephron function in obese subjects. Because obesity is a primary cause of essential hypertension as well as type II diabetes, there is good reason to believe that obesity may also be the most frequent cause of end-stage renal disease. 4. Future research is needed to determine the mechanisms by which excess weight gain activates the neurohumoral systems and alters renal structure and function. Because of the high prevalence of obesity in most industrialized countries, unravelling these mechanisms will likely provide a better understanding of the pathophysiology of human essential hypertension and chronic renal failure.
authors.affiliation: Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson 39216-4505, USA. jeh@fiona.umsmed.edu
authors.forename: J E
authors.initials: JE
authors.lastname: Hall
authors.forename: M W
authors.initials: MW
authors.lastname: Brands
authors.forename: J R
authors.initials: JR
authors.lastname: Henegar
authors.forename: E W
authors.initials: EW
authors.lastname: Shek
mesh_terms: D000818:Animals; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D009765:Obesity / Q000235:genetics / Q000503:physiopathology*