A patient with diabetes, hyperkalemia, urinary pH<5.5 . Probable cause is -
Pseudohyperaldosteronism is characterized by a clinical picture of hyperaldosteronism with suppression of plasma renin activity and aldosterone. Pseudohyperaldosteronism can be due to a direct mineralocoicoid effect, as with desoxycoicosterone, fluorohydrocoisone, fluoroprednisolone, estrogens, and the ingestion of high amounts of glycyrrhetinic acid. A block of 11-hydroxysteroid-dehydrogenase type 2 (11HSD2), the enzyme that conves coisol into coisone, at the level of epithelial target tissues of aldosterone, is involved in other cases. This mechanism is related either to a mutation of the gene, which encodes 11HSD2 (apparent mineralocoicoid excess syndrome and some cases of low renin hypeension) or to an acquired reduction of the activity of the enzyme due to glycyrrhetinic acid, carbenoxolone, and grapefruit juice. In other cases saturation of 11HSD2 may be involved as in severe Cushing's syndrome and chronic therapy with some coicosteroids. Recently, an activating mutation of the mineralocoicoid receptor gene has been described. Another genetic cause of pseudohyperaldosteronism is the syndrome of Liddle, which is due to a mutation of the gene encoding for beta and gamma subunits of the sodium channels. Causes of Pseudohyperaldosteronism Ref - Researchgate.net
Uremia
Pseudohyperaldosteronism
Type I Renal tubular acidosis
DKA
Endocrinology