Hyperkalaemia secondary to hypo-aldosteronism. A report of 2 cases differentiating hyperreninaemic from hyporeninaemic hypo-aldosteronism.
Hypo-aldosteronism has been considered an important pathophysiological mechanism in the development of hyperkalaemia. This may occur as a consequence of defective regulatory mechanisms in the plasma renin-angiotensin-aldosterone system. Two case reports of hyperkalaemia are described which illustrate the differentiation of hyperreninaemic from hyporeninaemic hypo-aldosteronism. Laboratory investigations, together with measurements of plasma renin activity and aldosterone concentrations during adrenocorticotrophic hormone stimulation and sodium depletion, demonstrated this difference. Appropriate therapy with fludrocortisone (Florinef; Squibb) and furosemide (Lasix; Hoechst) respectively returned the situation to normal.
D000450:Aldosterone / Q000172:deficiency*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006947:Hyperkalemia / Q000209:etiology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood*
D000450:Aldosterone; D012083:Renin; D006854:Hydrocortisone