This Article Full Text Full Text (PDF) Data Supplement Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fisher, N. D.L. Articles by Williams, G. H. Search for Related Content PubMed PubMed Citation Articles by Fisher, N. D.L. Articles by Williams, G. H. Related Collections Clinical genetics Clinical Studies

(Hypertension. 2002;39:914.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Familial Aggregation of Low-Renin Hypertension

Naomi D.L. Fisher; Shelley Hurwitz; Xavier Jeunemaitre; Paul N. Hopkins; Norman K. Hollenberg; Gordon H. Williams

From the Departments of Medicine and Radiology, Harvard Medical School and Brigham and Women’s Hospital (N.D.L.F., S.H., P.N.H., N.K.H., G.H.W.), Boston, Mass; and Jeunemaitre: Centre d’Investigation Clinique 92401 Inserm/AP, Departement de Genetique, Hopital European Georges Pompidou (X.J.), Paris, France.

Correspondence to Naomi D.L. Fisher, MD, Brigham and Women’s Hospital, 221 Longwood Ave, Boston, MA 02115. E-mail nfisher{at}partners.org

Low-renin hypertension, representing roughly one quarter of all essential hypertension, is widely recognized by distinct physiological features, including salt-sensitivity, diuretic- responsiveness, and a favorable natural history. Although certain demographic features including age, ethnicity, and diabetes mellitus predispose to low-renin hypertension, these factors account for only a minority of cases. We examined familial concordance for renin status in 119 families with 257 hypertensive members. Low-renin was defined rigorously by plasma renin activity 0.69 ng angiotensin I/L per second, drawn when subjects had achieved balance after 5 to 7 days on a 10 mmol sodium diet and had stood upright for at least 1 hour. Given the prevalence of low-renin hypertension in our general population, low-renin hypertension was significantly more concordant among siblings than expected by chance (P=0.01). There were twice as many low-renin families as expected (10.9% versus 5.5%), in sharp contrast to the normal-renin state, in which the observed and expected were similar (61.0% versus 58.6%). These results were independent of age, race, and gender. Variance in renin status attributable to family membership was 35%. Association studies were performed on 8 polymorphisms in 5 candidate genes, and significant association was confirmed with the G460W polymorphism of the adducin gene. Familial determinants, which are probably but not definitely genetic, contribute to the low-renin hypertension state.

Key Words: renin • sodium • siblings • genetics

This article has been cited by other articles:

				H. Sanada, J. Yatabe, S. Midorikawa, S. Hashimoto, T. Watanabe, J. H. Moore, M. D. Ritchie, S. M. Williams, J. C. Pezzullo, M. Sasaki, et al. Single-Nucleotide Polymorphisms for Diagnosis of Salt-Sensitive Hypertension Clin. Chem., March 1, 2006; 52(3): 352 - 360. [Abstract] [Full Text] [PDF]

				G. Bianchi Genetic variations of tubular sodium reabsorption leading to "primary" hypertension: from gene polymorphism to clinical symptoms Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2005; 289(6): R1536 - R1549. [Abstract] [Full Text] [PDF]

				B. A. Young, W. J. Katon, M. Von Korff, G. E. Simon, E. H. B. Lin, P. S. Ciechanowski, T. Bush, M. Oliver, E. J. Ludman, and E. J. Boyko Racial and Ethnic Differences in Microalbuminuria Prevalence in a Diabetes Population: The Pathways Study J. Am. Soc. Nephrol., January 1, 2005; 16(1): 219 - 228. [Abstract] [Full Text] [PDF]

				M. H. Weinberger More on the Sodium Saga Hypertension, November 1, 2004; 44(5): 609 - 611. [Full Text] [PDF]

				G. Bianchi and P. Manunta Adducin, Renal Intermediate Phenotypes, and Hypertension Hypertension, October 1, 2004; 44(4): 394 - 395. [Full Text] [PDF]

				E. M. Freel and J. M.C. Connell Mechanisms of Hypertension: The Expanding Role of Aldosterone J. Am. Soc. Nephrol., August 1, 2004; 15(8): 1993 - 2001. [Abstract] [Full Text] [PDF]

				J. M.C. Connell, R. Fraser, S. MacKenzie, and E. Davies Is Altered Adrenal Steroid Biosynthesis a Key Intermediate Phenotype in Hypertension? Hypertension, May 1, 2003; 41(5): 993 - 999. [Abstract] [Full Text] [PDF]