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Results for “hyperaldosteronism”

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PubMed1980

Familial, dexamethasone-suppressible, normokalemic hyperaldosteronism.

An 8-year-old boy was found to be hypertensive on routine exam (144/88). His brother (age 6) and father (age 31) were also found to have elevated blood pressure. Detailed investigations first revealed a low renin level without hypokalemia. Further study revealed that all three patients had low plasma renin activity and nonsuppresible plasma aldosterone levels after saline infusion. Serum potassium was almost always normal. A trial of dexamethasone therapy normalized blood pressure, and plasma and urinary aldosterone decreased to low levels and renin levels increased. Therapy with spironolactone and prednisone also normalized blood pressure. However, the amount of prednisone required to maintain normotension resulted in Cushingoid features and has been discontinued. Studies in the father suggest that the aldosterone production by his adrenals is hyperresponsive to adrenocorticotropic hormone (ACTH). Renin levels should be determined in all hypertensive children and their hypertensive parents. If renin is low and plasma aldosterone fails to be suppressed by saline infusion, a trial of dexamethasone would seem indicated before other investigations are carried out.

Adult↗
PubMed1981

Hypokalemic metabolic alkalosis in normotensive infants with elevated plasma renin activity and hyperaldosteronism: role of dietary chloride deficiency.

The role of chloride deficiency in the generation of hypokalemic metabolic alkalosis with elevated plasma renin activity and plasma aldosterone levels, normal blood pressure, and a renal concentrating defect was studied in six infants given a soy formula that was deficient in chloride. A deceleration in linear growth, weight gain, and head circumference with age and delayed neurologic development were noted in every infant during the first six months of life. Microscopic hematuria and persistent elevation of plasma creatinine were noted in four of the infants. A renal biopsy in two infants revealed no juxtaglomerular hyperplasia, but interstitial tubular calcification was observed in one, and interstitial fibrosis was found in both. The generation of the hypokalemic metabolic alkalosis in these infants was explained by the reduced intake of chloride, and the addition of chloride alone to the diet resulted in a correction of the electrolyte abnormalities and the alkalosis.

Alkalosis↗