Hyperparathyroidism secondary to hyperaldosteronism

Introduction: Hyperparathyroidism has been associated with essential hypertension. In rats, volume expansion, the deoxycorticosterone (DOC)-salt hypertension model and primary aldosteronism cause a reduction in plasma calcium levels and secondary hyperparathyroidism. In these rats, urinary calcium decreases with thiazides and/or aldosterone antagonists, while furosemide gives the opposite effect. Also, licorice causes an increase in parathyroid hormone and urinary calcium excretion. Aim: To report clinical observations on different clinical cases of aldosteronism, with and without nephrolithiasis, and to elucidate the mechanism causing lithogenesis in patients affected by this pathology. Methods: In our hypertension unit, we studied 11 patients with primary aldosteronism: 4 with adenomas and 7 with bilateral adrenal cortex hyperplasia. Only 6 of 11 showed calcium oxalate stones. In all patients we measured parathormone (PTH), calcium, potassium and phosphorus levels in serum and urine before and after treatment with aldosterone antagonists. None of the patients showed either chronic renal insufficiency or any pathologies at the parathyroid glands. No patients received diuretics in the month before the study. Results: All patients affected by primary aldosteronism showed an increased PTH level, which was reduced following therapy with aldosterone antagonists. Calcium and phosphorus serum levels remained unchanged, while the treatment reduced urinary calcium and phosphorus levels and increased serum potassium levels in a statistically significant manner (t-test = p < 0.01). Conclusions: Our data support the hypothesis of a hyperparathyroidism secondary to aldosteronism. In fact, the aldosterone antagonist normalizes all the values we measured. Therefore, we conclude that (i) aldosterone seems to play a new and important role in the pathogenesis of calcium nephrolithiasis; (ii) aldosterone antagonists may efficiently reduce calcium loss and PTH activation, thus preventing nephrolithiasis in aldosteronism, and most probably also in osteopenia; and (iii) nephrolithiasis is not automatically caused by these conditions, but it requires the contemporary presence of lithogenic factors or the absence of protective factors or it needs a prolonged stimulus.