Key result
Primary aldosteronism is associated with ~9-fold higher 19-nor-DOC excretion than normotensives, but matches low renin hypertension.
Why the study?
Nonaldosterone mineralocorticoids such as 19-nor-deoxycorticosterone may contribute to the mineralocorticoid activity in primary aldosteronism, but their urinary excretion has not been well characterized.
Are urinary free 19-nor-deoxycorticosterone levels elevated in patients with primary aldosteronism compared to those with low renin hypertension or normotensive subjects?
Cross-Sectional (n=24)
Are urinary free 19-nor-deoxycorticosterone levels elevated in patients with primary aldosteronism compared to those with low renin hypertension or normotensive subjects?
Patients with primary aldosteronism may have elevated levels of UF 19-nor-DOC proportional to aldosterone excess, which could contribute to the hypertension and hypokalemia seen in this disease.
Elevated urinary 19-nor-DOC versus normotensives but not low-renin hypertension; hypothesis-generating for its role in mineralocorticoid excess and requires prospective study.
Nonaldosterone mineralocorticoids, such as deoxycorticosterone (DOC) and 18-hydroxy-DOC, have been reported to be elevated in some patients with primary aldosteronism (PA). Since DOC is a probable precursor of a more potent mineralocorticoid, 19-nor-deoxycorticosterone (19-nor-DOC), this study evaluated urinary free (UF) 19-nor-DOC excretion in 6 patients with PA and compared the results to those from 11 patients with low renin hypertension (LRH) and 7 normotensive subjects. PA was due to either an aldosterone-producing adenoma (APA; 4 patients) or bilateral adrenal hyperplasia (2 patients) diagnosed by adrenal venous catheterization or surgery. Compared to LRH subjects, patients with PA had a higher mean blood pressure (137 +/- 9 vs. 114 +/- 3 mm Hg), a lower plasma potassium level (3.1 +/- 0.2 vs. 3.9 +/- 0.1 meq/1) and greater renin suppression (0.3 +/- 0.1 vs. 0.6 +/- 0.1 ng angiotensin I/ml . h). UF 19-nor-DOC levels were elevated in PA subjects compared to those in normotensives (3,716 +/- 1,517 vs. 428 +/- 112 ng/day) but not compared to those in LRH patients (1,237 +/- 471). Two patients with APA had distinctly elevated UF 19-nor-DOC levels (11,137 and 7,744 ng/day), but another APA patient had the lowest value (305 ng/day). UF 19-nor-DOC positively correlated with the aldosterone secretion rate in PA (r = 0.75) but not LRH subjects. In conclusion, this study demonstrates that patients with PA may have elevated levels of UF 19-nor-DOC which are proportional to the aldosterone excess and could be a contributing factor to the hypertension, hypokalamia, and excess mineralocorticoid activity of this disease.
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Griffing et al. (1983) conducted a cross-sectional in Primary aldosteronism and low renin hypertension (n=24). Primary aldosteronism vs. Normotensive subjects and low renin hypertension patients was evaluated on Urinary free 19-nor-deoxycorticosterone (19-nor-DOC) excretion. Patients with primary aldosteronism had elevated urinary free 19-nor-deoxycorticosterone excretion compared to normotensive subjects (3,716 vs 428 ng/day), but not compared to low renin hypertension.
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