Published online before print May 8, 2006, doi: 10.1161/01.HYP.0000223447.53155.d5
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(Hypertension. 2006;48:25.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
Nephron Number, Uric Acid, and Renal Microvascular Disease in the Pathogenesis of Essential Hypertension
From the Division of Pediatric Nephrology (D.I.F.), Texas Children’s Hospital, Baylor College of Medicine, Houston, Tex; Hospital Universitario and Universidad del Zulia (B.R.-I.), Maracaibo, Venezuela; and the Division of Nephrology, Hypertension and Transplantation (T.N., R.J.J.), University of Florida, Gainesville.
Correspondence to Richard J. Johnson, University of Florida-Gainesville, PO Box 100224, Gainesville, FL 32610. E-mail johnsrj@medicine.ufl.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
One of the world’s greatest epidemics is the epidemic of essential hypertension, which during the last 100 years has increased from a prevalence of 5% to 10% in the European and American population to >30% today. Hypertension was nonexistent in other places of the world but has risen to similar frequencies with the introduction of Western diet and culture. As a major cause of stroke, heart disease, and kidney disease, hypertension is a major underlying cause of morbidity and mortality, and therefore understanding its underlying etiology is critically important.
The groundbreaking studies of Dahl and Guyton led to the recognition of the key role for the kidney in the pathogenesis, but controversy remains on the precise mechanism. The observations that several hereditary causes of hypertension result from genetic mutations that lead to increased sodium reabsorption in the nephron (particularly in the collecting duct) has led to a search for genetic causes.1 However, although genetic polymorphisms are clearly important, most studies suggest genetic mechanisms may only have a modest (20%) influence on the hypertensive phenotype.2
A congenital mechanism, or fetal programming, has also been proposed (the "Barker-Brenner hypothesis").3,4 Low birth weights (LBWs) predispose to the later development of hypertension as well as other cardiovascular diseases, including obesity and diabetes. LBW infants often have impaired kidney development, resulting in a reduced nephron endowment. Following birth, the children have an increased risk for developing endothelial dysfunction and obesity, and by adulthood they have a relatively increased frequency of hypertension, obesity, and diabetes.3,4
Although
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