Chapter 046. Sodium and Water (Part 16)

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Metabolic acidoses, with the exception of those due to the accumulation of organic anions, can be associated with mild hyperkalemia resulting from intracellular buffering of H+ (see above). Insulin deficiency and hypertonicity (e.g., hyperglycemia) promote K+ shift from the ICF to the ECF. The severity of exercise-induced hyperkalemia is related to the degree of exertion. It is due to release of K+ from muscles and is usually rapidly reversible, often associated with rebound hypokalemia. Treatment with beta blockers rarely causes hyperkalemia but may contribute to the elevation in plasma K+ concentration seen with other conditions. Hyperkalemic periodic paralysis (Chap....

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Chapter 046. Sodium and Water (Part 16) Metabolic acidoses, with the exception of those due to the accumulation of organic anions, can be associated with mild hyperkalemia resulting from intracellular buffering of H+ (see above). Insulin deficiency and hypertonicity (e.g., hyperglycemia) promote K+ shift from the ICF to the ECF. The severity of exercise-induced hyperkalemia is related to the degree of exertion. It is due to release of K+ from muscles and is usually rapidly reversible, often associated with rebound hypokalemia. Treatment with beta blockers rarely causes hyperkalemia but may contribute to the elevation in plasma K+ concentration seen with other conditions. Hyperkalemic periodic paralysis (Chap. 382) is a rare autosomal dominant disorder characterized by episodic weakness or paralysis, precipitated by stimuli that normally lead to mild hyperkalemia (e.g., exercise). The genetic defect appears to be a single amino acid substitution due to a mutation in the gene for the skeletal muscle Na+ channel. Hyperkalemia may occur with severe digitalis
toxicity due to inhibition of the Na+,K+-ATPase pump. Depolarizing muscle relaxants such as succinylcholine can increase the plasma K+ concentration, especially in patients with massive trauma, burns, or neuromuscular disease. Chronic hyperkalemia is virtually always associated with decreased renal K+ excretion due to either impaired secretion or diminished distal solute delivery (Table 46-4). The latter is seldom the only cause of impaired K + excretion but may significantly contribute to hyperkalemia in protein-malnourished (low urea excretion) and ECF volume–contracted (decreased distal NaCl delivery) patients. Decreased K+ secretion by the principal cells results from either impaired Na + reabsorption or increased Cl– reabsorption. Table 46-4 Causes of Hyperkalemia I. Renal failure II. Decreased distal flow (i.e., decreased effective circulating arterial volume)
III. Decreased K+ secretion A. Impaired Na+ reabsorption 1. Primary hypoaldosteronism: adrenal insufficiency, adrenal enzyme deficiency (21- hydroxylase, 3β-hydroxysteroid dehydrogenase, corticosterone methyl oxidase) 2. Secondary hypoaldosteronism: hyporeninemia, drugs (ACE inhibitors, NSAIDs, heparin) 3. Resistance to aldosterone: pseudohypoaldosteronism, tubulointerstitial disease, drugs (K+-sparing diuretics, trimethoprim, pentamidine) B. Enhanced Cl- reabsorption (chloride shunt) 1. Gordon's syndrome
2. Cyclosporine Note: ACE, angiotensin-converting enzyme; NSAIDs, nonsteroidal anti- inflammatory drugs. Hyporeninemic hypoaldosteronism is a syndrome characterized by euvolemia or ECF volume expansion and suppressed renin and aldosterone levels (Chaps. 336 and 338). This disorder is commonly seen in mild renal insufficiency, diabetic nephropathy, or chronic tubulointerstitial disease. Patients frequently have an impaired kaliuretic response to exogenous mineralocorticoid administration, suggesting that enhanced distal Cl– reabsorption (electroneutral Na+ reabsorption) may account for many of the findings of hyporeninemic hypoaldosteronism. NSAIDs inhibit renin secretion and the synthesis of vasodilatory renal prostaglandins. The resultant decrease in GFR and K + secretion is often manifest as hyperkalemia. As a rule, the degree of hyperkalemia due to hypoaldosteronism is mild in the absence of increased K+ intake or renal dysfunction. Angiotensin-converting enzyme (ACE) inhibitors block the conversion of angiotensin I to angiotensin II. Angiotensin receptor antagonists directly inhibit the actions of angiotensin II on AT1 angiotensin II receptors. The actions of both of these classes of drugs result in impaired aldosterone release. Patients at increased risk of ACE inhibitor or angiotensin receptor antagonist–induced
hyperkalemia include those with diabetes mellitus, renal insufficiency, decreased effective circulating arterial volume, bilateral renal artery stenosis, or concurrent use of K+-sparing diuretics or NSAIDs.