Abstract
Introduction: Primary Aldosteronism (PA) is a secondary form of hypertension characterized by an autonomous and inappropriately high production of aldosterone. Its prevalence is 5-12% and the two main subtypes are the Bilateral Adrenal Hyperplasia (BAH) and the Aldosterone-Producing Adenoma (APA). In this study, we report the results of an evalutation of some patients diagnosed with PA in a Nephrology Unit between 1987-2011. Patients and methods: As much as 54 patients were screened for PA by measuring Plasma Aldosterone Concentration (PAC) and Plasma Renin Activity (PRA), and by calculating the aldosterone/renin ratio (ARR). Confirmation tests were performed on 47 patients with PAC ≥ 15 ng/dL and ARR ≥ 40. Subtype diagnosing was possible through adrenal CT scan, scintigraphy and adrenal venous sampling. Results: As much as 31 patients were diagnosed with PA. In 17 of them, the concordance of CT, scintigraphy and AVS findings made it possible to determine the subtype diagnosis: BAH in 10 and APA in 7 patients. Conclusions: Our results confirm the increasing frequency of diagnosis of PA among patients investigated for resistant hypertension. Early detection of PA in nephrological settings is important because of the relationship between aldosterone and kidney function.
Highlights
Primary Aldosteronism (PA) is a secondary form of hypertension characterized by an autonomous and inappropriately high production of aldosterone
Less common forms are the Unilateral Adrenal Hyperplasia (UAH), that is the micro- or macronodular hyerplasia of the zona glomerulosa of the adrenal cortex, mainly involving one of the adrenal glands (3%); and the bilateral adrenal hyperplasia, micro- or macronodular (1%) [3,4] Even if sporadic, PA may be familial and manifests in at least two forms [5,6]: the Familial Hyperaldosteronism type I (FH-I), or Glucocorticoid-Remediable Aldosteronism (GRA), very rare (< 1%), which has an autosomal dominant mode of transmission and is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/ CYP11B2 gene [7,8]; and the familial hyperaldosteronism type II (FH-II), which is the familial form of Aldosterone-Producing Adenoma (APA) or Bilateral Adrenal Hyperplasia (BAH) or both
During re-examination of cases, using the cutoff values indicated above, aldosterone/renin ratio (ARR) was found to be < 40 ng/dL of Plasma Aldosterone Concentration (PAC) per ng/mL/h of Plasma Renin Activity (PRA) in 7 patients; the diagnosis of PA was excluded in these patients
Summary
Primary Aldosteronism (PA) is a secondary form of hypertension characterized by an autonomous and inappropriately high production of aldosterone. Its prevalence is 5-12% and the two main subtypes are the Bilateral Adrenal Hyperplasia (BAH) and the Aldosterone-Producing Adenoma (APA). Primary Aldosteronism (PA) is a condition characterized by an inappropriately high production of aldosterone, which is relatively autonomous from the renin-angiotensin system, and nonsuppressible by sodium loading [1]. The two main forms, or subtypes, of PA are the Bilateral Adrenal Hyperplasia (BAH), or Idiopatic Hyper Aldosteronism (IHA), with a relative frequency of 65%, and the aldosterone-producing adenoma (APA), with a relative frequency of 30%. Regarding FH-II, linkage studies have implicated a locus at chromosome 7p22 in some of the families studied, allowing a probable genetic heterogeneity [9,10]
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