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.