Low-renin hypertension
1974; Elsevier BV; Volume: 5; Issue: 5 Linguagem: Inglês
10.1038/ki.1974.47
ISSN1523-1755
AutoresMichael J. Dünn, Richard L. Tannen,
Tópico(s)Renal function and acid-base balance
ResumoRecently much attention has been focused on patients with essential hypertension and low plasma renin activity (PRA), so-called low-renin In 1964 Conn, Cohen and Rovner [1] showed that patients with primary aldosteronism as a cause of their hypertension had low or undetectable levels of PRA, despite maneuvers which stimulate renin release. As investigators searched for more patients with primary aldosteronism, using low or undetectable PRA as a marker, it became apparent that most patients with low PRA had normal aldosterone secretion (or excretion) and essential hypertension. Since Helmer'ls original series [2] many cases of low-PRA essential hypertension have been reported [3–51]. This burgeoning literature has raised many controversial and unanswered questions about the incidence, etiology, prognosis and therapy of this type of hypertension. Some of the critical issues we will address are whether this represents a volume expansion type of hypertension; whether an unidentified mineralocorticoid accounts for this syndrome; what, if any, its prognostic implications are; and how it should be treated. In addition, the possibility will be considered that low-PRA hypertension does not represent a distinct disease entity with an etiology different from essential hypertension with normal PRA.
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