There is evidence that primary aldosteronism (PA) may be common in patients
with essential hypertension (EH) when determinations of serum aldosterone
(SA), plasma renin activity(PRA), and the SA/PRA ratio are used as screenin
g. An inherited form of primary hyperaldosteronism is the glucocorticoid-re
mediable aldosteronism (GRA) caused by an unequal crossing over between the
CYP11B1 and CYP11B2 genes that results in a chimeric gene, which has aldos
terone synthase activity regulated by ACTH. The aim of this study was to ev
aluate the prevalence of PA and the GRA in 305 EH patients and 205 normoten
sive controls. We measured SA (1-16 ng/dL) and PRA (1-2.5 ng/mL . h) and ca
lculated the SA/PRA ratio in all patients. A SA/PRA ratio level greater tha
n 25 was defined as being elevated. PA was diagnosed in the presence of hig
h SA levels (>16 ng/dL), low PRA levels (<0.5 ng/mL . h), and very high SA/
PRA ratio (>50). Probable PA was diagnosed when the SA/PRA ratio was more t
han 25 but the other criteria were not present. A Fludrocortisone test was
done to confirm the diagnosis. GRA was differentiated from other forms of P
A by: the aldosterone suppression test with dexamethasone, the high levels
of 18-hydroxycortisol, and the genetic detection of the chimeric gene. In E
H patients, 29 of 305 (9.5%) had PA, 13 of 29 met all the criteria for PA,
and 16 of 29 were initially diagnosed as having a probable PA and confirmed
by the fludrocortisone test. Plasma potassium was normal in all patients.
The dexamethasone suppression test was positive for GRA in 10 of 29 and 18-
hydroxycortisol levels were high in 2 of 29 patients who had also a chimeri
c gene. In normotensive subjects, 3 of 205 (1.46%) had PA, and 1 of 205 had
a GRA. In summary, we found a high frequency of normokalemic PA in EH pati
ents. A high proportion of PA suppressed SA with dexamethasone, but only a
few had a chimeric gene or high levels of 18-hydroxycortisol. These results
emphasize the need to further investigate EH patients.