Dietary salt restriction in primary aldosteronism

Primary aldosteronism (PA) is caused by the overproduction of aldosterone, a mineralocorticoid hormone produced in the adrenal cortex [1]. Aldosterone is a main regulator of sodium and water reabsorption, as well as potassium excretion, in the kidneys. Thus, aldosterone has a central physiological role in regulating salt and water balance, and consequently blood pressure. For this reason, patients with PA have increased blood pressure, and circulating concentrations of potassium are often low. Once considered to be a rare disease, PA is now known to be the cause of high blood pressure in approximately 5% of patients with hypertension and up to 20% of patients with therapy-resistant hypertension [1]. PA is a serious disorder that is associated with a greatly increased risk for cardiovascular diseases, impaired renal function and increased mortality if left untreated. Importantly, patients with PA have a twofold increased risk of developing coronary artery disease, a two to three times increased risk of stroke, a twofold increased risk of heart failure, and a fourfold increased risk of atrial fibrillation, as compared to patients with essential hypertension and comparable blood pressure levels [2]. Fortunately, however, administration of disease-specific treatment—either unilateral adrenalectomy for patients with PA localized to one of the adrenals, or mineralocorticoid receptor antagonist treatment in patients with bilateral disease—reduces these risks substantially [3, 4]. Nevertheless, a large proportion of patients with PA still have high blood pressure despite successful disease-specific treatment and need antihypertensive treatment. More than half of patients who have been operated with adrenalectomy for unilateral PA thus still have hypertension at long-term postoperative follow-up [4]. In this context, a paper recently published in the Journal of Internal Medicine by Schneider et al. in Munich, Germany, is of special interest [5]. The effect of a 12-week dietary salt restriction on blood pressure was assessed in 41 patients with PA who were all receiving medical treatment with a mineralocorticoid receptor antagonist. The patients received personal and structured education aimed at reducing dietary salt intake. Dietary sodium intake was assessed every fourth week and decreased from 9.1 to 5.2 g/day, linked to a decrease in 24-h sodium excretion from 156 to 90 mmol/day. This had a powerful effect on systolic blood pressure that decreased from 130 to 121 mmHg. Diastolic blood pressure also decreased significantly, although more modestly, from 84 to 81 mmHg. Randomized controlled trials have shown that dietary salt restriction lowers blood pressure. The effect is largest in persons with severe hypertension, where low-salt food is delivered to participants and adherence monitored with measurement of sodium excretion in the urine [6]. A large systematic review in persons without known PA—including 133 randomized controlled trials intervening with education on salty food and feedback from urine sodium excretion—found significant blood pressure-lowering effects during the first months, but very little after 6 months [7]. Moreover, the effect was only about 1 mmHg in systolic blood pressure in normotensive subjects with a systolic blood pressure below 130 mmHg. Giving advice to lower salt intake on one occasion without giving education or feedback has minimal effects on blood pressure [8]. The effect of sodium restriction on blood pressure in persons with PA in the study by Schneider et al. is thus substantially larger than in studies on primary hypertension [5]. This is a very interesting and encouraging finding. However, the effects could partly be explained by improved drug adherence and lifestyle habits. Several other findings are also of interest in the study by Schneider et al. [5]: (a) A mean weight loss of 1.4 kg was achieved after 12 weeks of dietary salt reduction, reflecting loss of body water; (b) pulse pressure, a surrogate variable used to evaluate arterial stiffness, decreased from 46 to 40 mmHg; (c) symptoms of depression and anxiety, evaluated with validated questionnaires, improved; and (d) salt taste threshold decreased from 32 to 21 mmol/L. Salt taste threshold was evaluated by letting the patients taste solutions containing different concentrations of NaCl and compare to distilled water. The solution with the lowest NaCl concentration in which the patients sensed a salty taste was defined as the salt taste threshold. The group in Munich has previously shown that patients with PA have a significantly higher salt taste threshold (32 mmol/L) compared to patients with essential hypertension (24 mmol/L) and normotensive controls (16 mmol/L), and that treatment with either adrenalectomy or mineralocorticoid receptor antagonist lowers the threshold (from 32 to 16 mmol/L) [9]. In conclusion, given the positive effect on blood pressure in the study by Schneider et al., as well as positive effects on symptoms of depression and anxiety, a moderate dietary sodium restriction should be considered in patients with PA [5]. The results from trials in persons with primary hypertension show the importance of comprehensive counseling about salty food and feedback from 24-h sodium excretion when salt restriction is used for therapeutic purposes. Future randomized controlled trials are of major interest to confirm the positive effect of dietary salt restriction in patients with PA. Writing—original draft; writing—review and editing: Oskar Ragnarsson. Writing—original draft; writing—review and editing: Bo Carlberg. Writing—review and editing: Tommy Olsson. The authors have nothing to disclose.