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[Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia].
Schweiz Med Wochenschr. 1982 Dec 04; 112(49):1764-74.SM

Abstract

Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives.

Authors

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Pub Type(s)

English Abstract
Journal Article
Review

Language

ger

PubMed ID

6758113

Citation

Weidmann, P. "[Hyporeninemic Hypoaldosteronism and the Differential Diagnosis of Hyperkalemia]." Schweizerische Medizinische Wochenschrift, vol. 112, no. 49, 1982, pp. 1764-74.
Weidmann P. [Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia]. Schweiz Med Wochenschr. 1982;112(49):1764-74.
Weidmann, P. (1982). [Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia]. Schweizerische Medizinische Wochenschrift, 112(49), 1764-74.
Weidmann P. [Hyporeninemic Hypoaldosteronism and the Differential Diagnosis of Hyperkalemia]. Schweiz Med Wochenschr. 1982 Dec 4;112(49):1764-74. PubMed PMID: 6758113.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia]. A1 - Weidmann,P, PY - 1982/12/4/pubmed PY - 1982/12/4/medline PY - 1982/12/4/entrez SP - 1764 EP - 74 JF - Schweizerische medizinische Wochenschrift JO - Schweiz Med Wochenschr VL - 112 IS - 49 N2 - Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives. SN - 0036-7672 UR - https://www.unboundmedicine.com/medline/citation/6758113/[Hyporeninemic_hypoaldosteronism_and_the_differential_diagnosis_of_hyperkalemia]_ L2 - http://www.diseaseinfosearch.org/result/3627 DB - PRIME DP - Unbound Medicine ER -