Maternally-inherited diabetes with deafness (MIDD) and
hyporeninemic hypoaldosteronism.
Angiotensin II is essential for the secretion of aldosterone [5] with ACE-I can produce a variable degree of
hyporeninemic hypoaldosteronism or type IV renal tubular acidosis [6-10] characterized by metabolic acidosis and hyperkalaemia due to aldosterone deficiency.
In the primary or
hyporeninemic hyperaldosteronism, autonomous hypersecretion of aldosterone is held by neoplastic tissue, adrenocortical adenomas or adenocarcinomas, or by nodular hyperplasia of the zona glomerulosa of the adrenal cortex, also known as primary hyperaldosteronism or non neoplastic hyperaldosteronism.
These findings may be attributable to
hyporeninemic hypoaldosteronism, subsequent to lead intoxication, as well as to inhibition of distal tubular Na-K-ATPase (100).
(6, 17) This may result in the inhibition of renin-angiotensin system and decreased aldosterone synthesis as
hyporeninemic hypoaldosteronism or
hyporeninemic normoaldosteronism.
