Maternally-inherited diabetes with deafness (MIDD) and hyporeninemic
Angiotensin II is essential for the secretion of aldosterone  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