title: [Hyperkalemias].
abstract: Hyperkalaemia is a frequent electrolyte disturbance connected with new knowledge and practical routine. It is developed by the disorders of the "external balance" (potassium [K] intake and output) as well as the "internal balance" (distribution of K in the extracellular and intracellular fluid compartments). Factors playing a role in it are: the upright posture, physical activity and hyperosmolality. In the hormonal regulation of K metabolism first of all beta adrenergic agents, insulin and aldosterone have significance; the first two mainly in the internal balance. Hyperkalaemia is occurring especially frequently in renal patients (in acute and chronic renal insufficiency, in dialyzed persons) in patients with diabetes, in adrenal insufficiency (Addison's disease, in selective hypoaldosteronisms and in pseudohypoaldosteronisms) in renal tubular acidosis as well as in response to various drugs (ACE inhibitors, angiotensin receptor antagonists, beta blocking agents, potassium sparing diuretics, NSAID's, anticoagulants etc.). Interactions between illness and drugs as well as between drugs and hormones may have outstanding importance in the development of hyperkalaemia. Physical activity carried out in the upright posture in the presence of hyperosmolality (water restriction together with salt or/and glucose loading) developing in pharmacological hypoaldosteronism accompanied with insulin deficiency, may be especially dangerous with respect to hyperkalaemia. To avoid life-threatening hyperkalaemia it is necessary 1. to stop cardiotoxicity with calcium; 2. to enhance K uptake by the cells by bicarbonate, insulin and beta adrenergic agents; and 3. to remove abnormal quantities of K from the body by enemas and/or ion exchange resins. The quickest and best way of treatment of hyperkalaemia is haemodialysis.
authors.affiliation: Nephrologia-Hypertonia Osztály, Uzsoki utcai Kórház, Budapest.
authors.forename: J
authors.initials: J
authors.lastname: Radó
authors.forename: A
authors.initials: A
authors.lastname: Haris
mesh_terms: D000141:Acidosis, Renal Tubular / Q000150:complications; D058186:Acute Kidney Injury / Q000150:complications; D000224:Addison Disease / Q000150:complications*; D000319:Adrenergic beta-Antagonists / Q000009:adverse effects; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000009:adverse effects; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D004232:Diuretics / Q000009:adverse effects; D006801:Humans; D006947:Hyperkalemia / Q000139:chemically induced / Q000209:etiology* / Q000628:therapy; D006994:Hypoaldosteronism / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000150:complications; D011188:Potassium / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000894:Anti-Inflammatory Agents, Non-Steroidal; D004232:Diuretics; D011188:Potassium