Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP91 | DOI: 10.1530/endoabs.37.EP91

ECE2015 Eposter Presentations Adrenal cortex (94 abstracts)

RNALDO: the effects of blocker withdrawal on renin and angiotensin

Tomas Griffin 1, , Gerard A Browne 1 , Paula M O’Shea 2 & Michael Conall Dennedy 1,


1Discipline of Pharmacology & Therapeutics, NUI Galway, Galway, Ireland; 2Department of Clinical Biochemistry, Galway University Hospital, Galway, Ireland; 3Department of Endocrinology, Galway, Ireland.


Primary hyperaldosteronism (PHA) prevails in up to 20% of individuals with essential hypertension, but often presents a diagnostic challenge due to difficulty in interpreting the aldosterone renin ratio (ARR) largely due to anti-hypertensive medication interference. Interpretation of the ARR in the context of beta blockers presents a particular challenge and may produce false positive results due to renin suppression. We investigated the effects of beta blocker withdrawal on ARR in a cohort taking long term beta blocker therapy for blood pressure (BP) control. Hypertensive individuals with suboptimally controlled BP on a combination of beta blockers, thiazide diuretics and ACEi/ARB were recruited and followed over 8 weeks. Beta blockers were withdrawn at the first visit. Serial measurements of BP were performed and patients had blood drawn serially for measurement of plasma renin activity (PRA), renin mass, aldosterone and electrolytes. BP was optimised at each visit by maximising non-renin-suppressing antihypertensive agents. Main outcome measures were ARR, renin and aldosterone concentrations following beta-blocker withdrawal. 50 individuals were enrolled under informed consent and ethical approval. Interpretation of ARR on beta-blockade gave a false positive diagnosis of PHA in 22%. Beta blocker withdrawal produced a rapid (>50%) recovery of PRA (F=28.6; P<0.0001) and renin mass (F=18.4; P=0.0007) which reached significance within 2 weeks of withdrawal and return of the ARR to normal range in all individuals (F=29.3; P=0.0003). Aldosterone remained unchanged throughout the duration of the study (F=2.5; P=0.1). BP remained unchanged throughout the duration of the study (F=1.0; P=0.4). Both renin mass (r2=0.67; P<0.05) and PRA (r2=0.69; P<0.05) were inversely correlated with beta blocker dose. While clean screens using the ARR are seldom possible, our results demonstrate a high false positive rate for PHA in those taking beta blockers. Beta blocker withdrawal was well tolerated, BP control easily optimised and the ARR more accurate within 2 weeks of withdrawal. We provide convincing data to support beta blocker withdrawal, 2 weeks in advance of screening for PHA.

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