It is based on the administration of 50 mg of losartan. In cases of primary hyperaldosteronism, after 2 hours the ARR is >35 ng/dL of aldosterone/ng/mL/h PRA and plasma aldosterone concentration is >10 ng/dL.

Once the diagnosis of primary hyperaldosteronism has been confirmed, the cause must be identified. CT scanning is the most commonly used test for this purpose.

All patients with primary hyperaldosteronism who have to undergo surgical treatment (unilateral adrenalectomy) should perform adrenal venous sampling (AVS) to distinguish between unilateral and bilateral adrenal disease. This distinction is fundamental because adrenalectomy is indicated only in unilateral forms, while bilateral forms must be treated with medical therapy. AVS involves the determination of aldosterone and cortisol plasma concentrations in the two adrenal veins and in the inferior vena cava or in another peripheral vein; there are three different protocols:

• Unstimulated sequential or simultaneous sampling of the two adrenal veins

 • Basal, unstimulated, sequential, or simultaneous sampling of the two adrenal veins, followed by another simi lar sampling stimulated by intravenous injection of a bolus of ACTH (or tetracosactide)

 • Continuous ACTH infusion with sequential bilateral adrenal venous sampling

The ratio of plasma aldosterone concentration to plasma cortisol concentration in blood collected from the adrenal vein is termed the aldosterone corrected for cortisol ratio (A/C ratio).

When AVS is performed without ACTH stimulation, an A/C ratio of the adrenal veins of the two sides >2:1 indicates an unilateral form. Similarly, a diagnosis of lateralization can be made if the ratio of the A/C ratio of one side to the simultaneous A/C ratio of a peripheral vein is >2:1 and if, at the same time, the contralateral A/C ratio is less than or equal to the A/C ratio of a peripheral vein or inferior vena cava.

With the continuous infusion of ACTH, an A/C ratio of the two adrenal veins >4:1 , indicates unilateral disease; a ratio <3:1 is suggestive of bilateral excess secretion of aldo sterone and, therefore, the absence of lateralization; finally, a ratio between 3:1 and 4:1 may indicate either monolaterality or bilaterality of excess aldosterone production.

On the other hand, bolus infusion involves AVS being per formed before and after intravenous injection of a 250 μg bolus of ACTH. However, this technique has shown poor diagnostic accuracy.

Finally, genetic testing for familial forms is recommended in subjects with primary hyperaldosteronism <20 years or with a family history of primary hyperaldosteronism or a cerebrovascular event occurring at <40 years. The diagnosis of familial hyperaldosteronism type I is based on detecting the chimeric gene CYP11B1/CYP11B2 by Southern blotting or PCR (Polymerase Chain Reaction). In the case of familial type II hyperaldosteronism, the diagnosis is based on confirmation of primary hyperaldosteronism in at least two family members and the exclusion of type I in hypertensive family members. Finally, tests for mutations in the KCNJ5 gene are not yet commercially available for familial type III.

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