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Endocrine Abstracts (2018) 59 P010 | DOI: 10.1530/endoabs.59.P010

SFEBES2018 Poster Presentations Adrenal and steroids (38 abstracts)

Exploring the utility of renin measurements in the routine management of salt-wasting congenital adrenal hyperplasia

Riccardo Pofi 1, , Amalia Cannuccia 3 , Andrea Lenzi 2 , Andrea M Isidori 2 & Jeremy W Tomlinson 1

1Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Oxford, UK; 2Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy; 3Department of Endocrinology, Diabetes and Metabolism, Tor Vergata University, Rome, Italy.

The importance of measuring renin or plasma renin activity (PRA) and aldosterone in establishing mineralocorticoid deficiency is not in doubt. Once mineralocorticoid replacement therapy is initiated, guidance suggests that optimization of mineralocorticoid dose should be based upon measurements of blood pressure, renin (or PRA), and electrolytes. The aim of this study was to explore the relationship between renin and clinically important variables to determine whether measurement of renin can help guide appropriate mineralocorticoid dose titration. We performed an observational, longitudinal, retrospective analysis of data from 55 patients with congenital adrenal hyperplasia (CAH) including 23 patients with salt-wasting (SW) CAH. Multiple regression modelling was used to identify variables contributing to mean arterial blood pressure (MAP), electrolytes and renin. High renin levels were associated with lower sodium concentrations (P=0.01) and sodium and potassium were inversely related (P=0.03). However, there were no relationships between renin and mineralocorticoid dose (P=0.23) or potassium levels (P=0.07). Reflecting the complexities of blood pressure control, multiple regression modelling demonstrated that renin was a weak predictor of MAP (P<0.01) with a low coefficient of relation (B=−0.008) suggesting that a 100-fold variation in renin was associated with a 1 mmHg change in MAP. Glucocorticoid (but not mineralocorticoid) dose (P=0.01) and body mass index (P=0.02) predicted MAP. Renin levels were predicted by MAP (P<0.01), BMI (P=0.02) and glucocorticoid dose (P<0.01), but not by mineralocorticoid dose (P=0.20). Longitudinal analysis (mean follow-up=644±389 days) demonstrated no relationship between changes in mineralocorticoid dose and renin over time. In our small cohort of patients with SW-CAH, the lack of a clinically significant relationship of renin with MAP, or any relationship with mineralocorticoid dose or serum electrolytes calls into question its utility in the optimization of mineralocorticoid replacement. Additional larger studies are now warranted to identify the best strategies and clinical tools to optimize mineralocorticoid replacement.

Volume 59

Society for Endocrinology BES 2018

Glasgow, UK
19 Nov 2018 - 21 Nov 2018

Society for Endocrinology 

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