This Article Full Text Full Text (PDF) All Versions of this Article: 51/3/609    most recent HYPERTENSIONAHA.107.101915v1 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 Quack, I. Articles by Rump, L. C. Search for Related Content PubMed PubMed Citation Articles by Quack, I. Articles by Rump, L. C.

(Hypertension. 2008;51:609.)
© 2008 American Heart Association, Inc.

Hypertension Grand Rounds

A Tale of Two Patients With Mendelian Hypertension

Ivo Quack; Oliver Vonend; Lorenz Sellin; Johannes Stegbauer; Gabriele Dekomien; Lars Christian Rump

From the Department of Nephrology, Heinrich-Heine-University (I.Q., L.S., J.S., L.C.R.), Düsseldorf, Germany; the Department of Internal Medicine I (O.V.), Ruhr University, Bochum, Germany; Marienhospital (G.D.), Herne, Germany; and the Department of Human Genetics (G.D.), Ruhr University, Bochum, Germany.

Correspondence to Lars Christian Rump, MD, Department of Nephrology, Heinrich-Heine-University Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany. E-mail christian.rump@med.uni-duesseldorf.de

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

	Introduction

 
Conn emphasized the triad of hypertension, hypokalemia, and metabolic alkalosis in his seminal account of patients with primary aldosteronism.¹ He believed that primary aldosteronism was a very common cause of hypertension. Kaplan introduced the discussion as to the actual prevalence of primary aldosteronism, a topic still debated today.^2,3 Suffice it to say that hypokalemic hypertension is a fixed entity in the minds of clinicians as synonymous with primary aldosteronism, and perhaps this reaction is appropriate. Nonetheless, there are other diagnostic considerations. For instance, licorice gluttony looks exactly like primary aldosteronism clinically; the diagnosis requires a particularly high grade of detective work.⁴ However, Mendelian disorders have become increasingly recognized, especially because elucidation of their molecular mechanisms provides reliable diagnostic tools.⁵ Another confounder is the fact that contrary to prevailing clinical opinion, electrolyte and acid-base abnormalities are absent in many patients with primary aldosteronism.⁶ We describe 2 remarkable patients who were clinical adventures for us and provided several important lessons.

	Case 1

 
An 18-year-old male student was admitted for further evaluation of suspected primary aldosteronism. A routine examination at the age of 15 years revealed a blood pressure of 150/90 mm Hg; however, no further workup was done at that time and no therapeutic consequences were drawn. Three years later, the patient’s concerned mother consulted a nephrologist. Family history revealed hypertension in his father and brother. At that time, a 24-hour ambulatory blood pressure measurement (ABPM) revealed an average 24 h blood pressure of 156/98 mm Hg without a nocturnal dip. The nephrologist’s attention . . . [Full Text of this Article]

This article has been cited by other articles:

				P. W. Sanders Dietary Salt Intake, Salt Sensitivity, and Cardiovascular Health Hypertension, March 1, 2009; 53(3): 442 - 445. [Full Text] [PDF]

				J. Y. Lee, R. J. Prineas, and J. W. Eaton Heritability of Erythrocyte Sodium Permeability: A Possible Genetic Marker for Hypertension Ann. Clin. Lab. Sci., January 1, 2009; 39(3): 241 - 250. [Abstract] [Full Text] [PDF]