Disease relevance of Hypoaldosteronism

• Plasma renin activity (PRA) and aldosterone are decreased in diabetic with nephropathy and hypertension, in those with neuropathy including orthostatic hypotension, and in those with hypoaldosteronism [1].
• It is concluded that hyporeninemic hypoaldosteronism is responsible for hyperkalemia in some patients with AIDS and that treatment with fludrocortisone is effective in these cases [2].
• Thus, selective hypoaldosteronism in the presence of high renin levels exists in a substantial percentage of hypotensive critically ill patients [3].
• Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism [4].
• The renal-adrenal group also had normal ratios regardless of plasma renin concentration and K levels [patients with aldosterone-producing adenomas, 2.85 +/- 0.15; idiopathic hyperaldosteronism, 2.14 +/- 0.19; salt-losing nephropathy, 3.06 +/- 0.54; Bartter's syndrome, 2.89 +/- 0.20; isolated (hyporeninemic) hypoaldosteronism, 3.20 +/- 0.39] [5].

High impact information on Hypoaldosteronism

• Selective hypoaldosteronism and impairment of angiotensin II production [6].
• Evidence of prostacyclin deficiency in the syndrome of hyporeninemic hypoaldosteronism [7].
• The results suggest that hypoaldosteronism in diabetic patients may result from combined defects in both renin and aldosterone biosynthesis [8].
• Heparin-induced hypoaldosteronism. Report of a case [9].
• Indomethacin-induced hyporeninaemic hypoaldosteronism [10].

Chemical compound and disease context of Hypoaldosteronism

• Possible role for impaired renal prostaglandin production in pathogenesis of hyporeninaemic hypoaldosteronism [11].
• These findings suggest that glucose-induced hyperkalemia is not infrequent in diabetics and that it is not usually associated with hypoaldosteronism [12].
• In an attempt to evaluate deficiencies of renin activation and adrenal zona glomerulosa biosynthesis in hyporeninemic hypoaldosteronism (HH), we studied active and inactive renin (AR and IR, respectively) responses to the dopamine antagonist metoclopramide, furosemide, and graded dose infusion of ACTH in 10 HH patients and 6 normal subjects [13].
• Inactive renin and prostaglandin E2 production in hyporeninemic hypoaldosteronism [14].
• Studies of renin activation and regulation of aldosterone and 18-hydroxycorticosterone biosynthesis in hyporeninemic hypoaldosteronism [13].

Biological context of Hypoaldosteronism

• A missense mutation (GGC[435Gly]-->AGC[Ser]) in exon 8 of the CYP11B2 gene inherited in Japanese patients with congenital hypoaldosteronism [15].
• Up-regulation of the adrenomedullin system mediates hypotension and hypoaldosteronism induced by simulated microgravity [16].
• The aldosterone synthase activities of the mutants were decreased to varying degrees indicating that point mutations at positions 296, 301, 302, and 335 could potentially cause hypoaldosteronism [17].

Anatomical context of Hypoaldosteronism

• This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis, both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture) [18].

Gene context of Hypoaldosteronism

• Congenital hyperreninemic hypoaldosteronism unlinked to the aldosterone synthase (CYP11B2) gene [19].
• TGF beta production is increased in the diabetic state so that this peptide as well as the insulin family may be involved in hyporeninemic hypoaldosteronism [20].
• A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism [21].
• We conclude that hyporeninemic hypoaldosteronism plays a key role in the pathogenesis of hyperkalemia in SLE [22].
• Endogenous ANP levels in the hyperkalemic patients with hypoaldosteronism were markedly elevated at 1186 +/- 340 pmol/L (compared to 93 +/- 10 pmol/L in healthy elderly controls), a level that would be capable of suppressing the potassium-mediated aldosterone response [23].

Analytical, diagnostic and therapeutic context of Hypoaldosteronism

• Urinary kallikrein excretion rates in the patients with isolated hypoaldosteronism were significantly lower than in the control groups, but increased in response to therapy with fludrocortisone [24].
• Intravenous infusion of hypertonic glucose induced a transitory paradoxical serum potassium elevation in 3 nondiabetic patients with selective hypoaldosteronism [25].

References