AIM: The determinants and significance of urinary albumin excretion have been studied in normal subjects and in hypertensive patients; however, they are unknown in patients with primary aldosteronism. PATIENTS AND METHODS: From a population of 114 patients with documented primary aldosteronism, we selected 23 never-treated patients (12 males, 11 females; 11 tumoral, 12 non-tumoral) and compared them to patients with never-treated essential hypertension with low renin (supine plasma renin activity <1 ng/ml per h, n = 23) or normal renin (supine plasma renin activity between 1 and 4 ng/ml per h, n = 23), matched for age, body mass index, mean arterial pressure, renal function and known duration of hypertension. RESULTS: The patients with primary aldosteronism had lower serum potassium and higher plasma aldosterone concentrations than those with essential hypertension. Urinary albumin and beta2-microglobulin excretion were greater in untreated patients with primary aldosteronism than in those with low- or normal-renin essential hypertension. Among the patients with essential hypertension, the renin activity was not a determinant of albuminuria. CONCLUSIONS: These findings indicate that primary aldosteronism is associated with excessive urinary albumin excretion. This albuminuria could be due to impairment of proximal tubular reabsorption caused by hypokalemic nephropathy and/or by high levels of circulating aldosterone; however, it could be an indicator of target-organ damage associated with primary aldosteronism.
AIM: The determinants and significance of urinary albumin excretion have been studied in normal subjects and in hypertensivepatients; however, they are unknown in patients with primary aldosteronism. PATIENTS AND METHODS: From a population of 114 patients with documented primary aldosteronism, we selected 23 never-treated patients (12 males, 11 females; 11 tumoral, 12 non-tumoral) and compared them to patients with never-treated essential hypertension with low renin (supine plasma renin activity <1 ng/ml per h, n = 23) or normal renin (supine plasma renin activity between 1 and 4 ng/ml per h, n = 23), matched for age, body mass index, mean arterial pressure, renal function and known duration of hypertension. RESULTS: The patients with primary aldosteronism had lower serum potassium and higher plasma aldosterone concentrations than those with essential hypertension. Urinary albumin and beta2-microglobulin excretion were greater in untreated patients with primary aldosteronism than in those with low- or normal-renin essential hypertension. Among the patients with essential hypertension, the renin activity was not a determinant of albuminuria. CONCLUSIONS: These findings indicate that primary aldosteronism is associated with excessive urinary albumin excretion. This albuminuria could be due to impairment of proximal tubular reabsorption caused by hypokalemic nephropathy and/or by high levels of circulating aldosterone; however, it could be an indicator of target-organ damage associated with primary aldosteronism.
Authors: Christian Adolf; Evelyn Asbach; Anna Stephanie Dietz; Katharina Lang; Stefanie Hahner; Marcus Quinkler; Lars Christian Rump; Martin Bidlingmaier; Marcus Treitl; Roland Ladurner; Felix Beuschlein; Martin Reincke Journal: Endocrine Date: 2016-05-14 Impact factor: 3.633