Clinical and experimental nephrology · 2026
The amount of sodium intake may affect the susceptibility to treatment with mineralocorticoid receptor antagonists in patients with primary aldosteronism.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kidoguchi Satoshi, Sugano Naoki, Kawauchi-Hirai Ruri, Yokoo Takashi
Аннотация
BACKGROUND: Patients with primary aldosteronism (PA) have an increased risk of developing cardiovascular disease. In patients with bilateral adrenal aldosterone hypersecretion, mineralocorticoid receptor antagonists (MRAs) are recommended; however, the benefit of these agents is observed only in cases that show a sufficient increase in post-treatment PRA (responders). Because renin secretion can be influenced by sodium intake, the increase in post-treatment PRA may be attributable to sodium restriction.
METHODS: A total of 90 patients who received eplerenone or esaxerenone for PA treatment were included in the study. Patients whose PRA was ≥ 1.0 ng/mL/h at one year after the initiation of MRAs treatment were defined as responders. The predictors of responders and the effect of sodium intake were investigated.
RESULTS: Both baseline and post-treatment PRA and PAC levels were higher in responders. In addition, baseline estimated sodium intake tended to be lower, and post-treatment estimated sodium intake was significantly lower in responders. The post-treatment PRA value was significantly correlated with the post-treatment estimated sodium intake, and the post-treatment estimated sodium intake was an independent predictor of responders, suggesting that post-treatment PRA elevation may be partially attributable to adequate sodium restriction. However, the change in the estimated glomerular filtration rate over the 3-year follow-up period was not different between responders and non-responders.
CONCLUSION: Although sodium restriction is suggested to facilitate attainment of post-treatment PRA ≥ 1.0 ng/mL/h, a marker of adequate aldosterone blockade, it remains uncertain whether achieving PRA ≥ 1.0 ng/mL/h is associated with favorable renal outcomes.
METHODS: A total of 90 patients who received eplerenone or esaxerenone for PA treatment were included in the study. Patients whose PRA was ≥ 1.0 ng/mL/h at one year after the initiation of MRAs treatment were defined as responders. The predictors of responders and the effect of sodium intake were investigated.
RESULTS: Both baseline and post-treatment PRA and PAC levels were higher in responders. In addition, baseline estimated sodium intake tended to be lower, and post-treatment estimated sodium intake was significantly lower in responders. The post-treatment PRA value was significantly correlated with the post-treatment estimated sodium intake, and the post-treatment estimated sodium intake was an independent predictor of responders, suggesting that post-treatment PRA elevation may be partially attributable to adequate sodium restriction. However, the change in the estimated glomerular filtration rate over the 3-year follow-up period was not different between responders and non-responders.
CONCLUSION: Although sodium restriction is suggested to facilitate attainment of post-treatment PRA ≥ 1.0 ng/mL/h, a marker of adequate aldosterone blockade, it remains uncertain whether achieving PRA ≥ 1.0 ng/mL/h is associated with favorable renal outcomes.