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(Hypertension. 2005;45:326.)
© 2005 American Heart Association, Inc.

Brief Reviews

Subtle Renal Injury Is Likely a Common Mechanism for Salt-Sensitive Essential Hypertension

Richard J. Johnson; Bernardo Rodriguez-Iturbe; Takahiko Nakagawa; Duk-Hee Kang; Dan I. Feig; Jaime Herrera-Acosta

From the Division of Nephrology, Hypertension, and Transplantation (R.J.J., T.N.), University of Florida, Gainesville; Hospital Universitario and Universidad del Zulia (B.R.-I.), Maracaibo, Venezuela; Division of Nephrology (D.-H.K.), Ewha University College of Medicine, Seoul, Korea; Division of Pediatric Nephrology (D.I.F.), Texas Children’s Hospital, Baylor College of Medicine, Houston; and Department of Nephrology (J.H.-A.), Instituto Nacional de Cardiologia I, Mexico City, Mexico.

Correspondence to Richard J. Johnson, MD, Division of Nephrology, Hypertension, and Transplantation, University of Florida, P.O. Box 100224, Gainesville, FL 32610. E-mailjohnsrj@medicine.ufl.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Despite the fact that essential hypertension was originally described as hypertension occurring in the absence of clinical renal disease,¹ Dahl et al later showed by transplantation studies in experimental models of hypertension that the kidney is ultimately responsible for the elevation in blood pressure,² a finding that was verified later in humans.³ Most authorities believe that the mechanism by which the kidney causes hypertension involves a physiological defect in sodium excretion as championed by Guyton et al.⁴ Support for this mechanism is extensive and includes both epidemiological⁵ and physiological⁶ studies.

Several hypotheses have been proposed to explain the mechanism responsible for the defect in renal sodium handling. A favored hypothesis is that hypertension results from a polygenic defect in which there are alterations in the regulation or expression in tubular transport systems involved in sodium reabsorption and excretion.^7,8 The recent discovery that many forms of genetic hypertension are associated with enhanced sodium reabsorption has provided support for this hypothesis.^7,8 However, there are substantial arguments that mitigate this hypothesis as a major mechanism for the renal defect. First, most studies suggest that genetic mechanisms can only account for a minority of cases.^9,10 For example, a study of 1003 identical twins found that when one twin was hypertensive, the other twin was hypertensive only 44% of the time.¹¹ Even more convincing are epidemiological data that demonstrate a dramatic increase in the prevalence of hypertension over the last 100 years. Thus, studies in the early 1900s demonstrated a near absence of hypertension in . . . [Full Text of this Article]

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