Hyporeninemic hypoaldosteronism, sodium wasting and mineralocorticoid-resistant hyperkalemia in two patients with obstructive uropathy.
The renin-aldosterone system and tubular responsiveness to exogenous mineralocorticoid administration was evaluated in 2 hyperkalemic patients with obstructive uropathy. Both patients manifested marked renal sodium wasting and a modest inability to lower urine pH despite systemic acidosis. None of the abnormalities was corrected with supraphysiologic doses of mineralocorticoid. In addition, plasma renin and aldosterone levels were inappropriately low. Thus, both hypoaldosteronism and renal tubular resistance to mineralocorticoids coexisted in these patients. It is likely that an association between these abnormalities is more frequent than previously recognized.
D000450:Aldosterone / Q000097:blood*; D004573:Electrolytes / Q000097:blood / Q000652:urine; D005438:Fludrocortisone / Q000627:therapeutic use*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006869:Hydronephrosis / Q000378:metabolism*; D006947:Hyperkalemia / Q000188:drug therapy* / Q000378:metabolism; D007024:Hypotension, Orthostatic / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood*; D012084:Renin-Angiotensin System; D012964:Sodium / Q000378:metabolism* / Q000652:urine
D004573:Electrolytes; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D005438:Fludrocortisone