A subdivision of the type of events according with the subgroup of hypertensive patients is provided in the supplemental table S3. Discussion The main pathological effects of aldosterone excess in the heart and kidney are vascular and perivascular inflammation, fibrosis and cellular hypertrophy (5-8). Thus left ventricular hypertrophy (9), inappropriate left ventricular mass (10,11), microalbuminuria and reduced renal function (12,13) are observed more frequently in patients with PA than in essential hypertensives. In addition, aldosterone excess has been shown to promote insulin resistance, thereby participating in the pathogenesis and progression of metabolic syndrome and diabetes mellitus (14,15). Consistently, in our study we observed a higher prevalence of left ventricular hypertrophy, microalbuminuria and metabolic syndrome in PA patients compared to non-PA hypertensives. Up to 30% of the hypertensive patients display the LREH (44), a clinical condition characterized by suppressed renin and aldosterone levels. The distinction between LREH and mild forms “normal” of PA can be challenging and relies on arbitrary cut-off values chosen to define failure of aldosterone suppression after confirmatory/exclusion testing. According to the Endocrine Society guidelines, no clear recommendations are provided on the optimal cut-off levels that determine positive confirmatory test results (4, 5). In our Hypertension Unit, the saline infusion test was regarded as positive when serum aldosterone levels were >5 ng/dL (or for a captopril challenge test when the ARR was >30 ng/dL/ng·mL-1·h-1). Accordingly, we allocated our low-renin patients into three categories: 1) PA, 2) LREH with a negative ARR test result and 3) LREH with a positive ARR test but with a negative confirmatory test result. Interestingly, patients with LREH and a positive screening test did not differ significantly in terms of clinical, metabolic and biochemical
A subdivision of the type of events according with the subgroup of hypertensive patients is provided in the supplemental table S3. Discussion The main pathological effects of aldosterone excess in the heart and kidney are vascular and perivascular inflammation, fibrosis and cellular hypertrophy (5-8). Thus left ventricular hypertrophy (9), inappropriate left ventricular mass (10,11), microalbuminuria and reduced renal function (12,13) are observed more frequently in patients with PA than in essential hypertensives. In addition, aldosterone excess has been shown to promote insulin resistance, thereby participating in the pathogenesis and progression of metabolic syndrome and diabetes mellitus (14,15). Consistently, in our study we observed a higher prevalence of left ventricular hypertrophy, microalbuminuria and metabolic syndrome in PA patients compared to non-PA hypertensives. Up to 30% of the hypertensive patients display the LREH (44), a clinical condition characterized by suppressed renin and “normal” aldosterone levels. The distinction between LREH and mild forms of PA can be challenging and relies on arbitrary cut-off values chosen to define failure of aldosterone suppression after confirmatory/exclusion testing. According to the Endocrine Society guidelines, no clear recommendations are provided on the optimal cut-off levels that determine positive confirmatory test results (4, 5). In our Hypertension Unit, the saline infusion test was regarded as positive when serum aldosterone levels were >5 ng/dL (or for a captopril challenge test when the ARR was >30 ng/dL/ng·mL-1·h-1). Accordingly, we allocated our low-renin patients into three categories: 1) PA, 2) LREH with a negative ARR test result and 3) LREH with a positive ARR test but with a negative confirmatory test result. Interestingly, patients with LREH and a positive screening test did not differ significantly in terms of clinical, metabolic and biochemical
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