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....
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Chapter 046. Sodium and Water (Part 16) Chapter 046. Sodium and Water (Part 16) Metabolic acidoses, with the exception of those due to the accumulation oforganic anions, can be associated with mild hyperkalemia resulting fromintracellular buffering of H+ (see above). Insulin deficiency and hypertonicity(e.g., hyperglycemia) promote K+ shift from the ICF to the ECF. The severity ofexercise-induced hyperkalemia is related to the degree of exertion. It is due torelease of K+ from muscles and is usually rapidly reversible, often associated withrebound hypokalemia. Treatment with beta blockers rarely causes hyperkalemiabut may contribute to the elevation in plasma K+ concentration seen with otherconditions. Hyperkalemic periodic paralysis (Chap. 382) is a rare autosomaldominant disorder characterized by episodic weakness or paralysis, precipitated bystimuli that normally lead to mild hyperkalemia (e.g., exercise). The genetic defectappears to be a single amino acid substitution due to a mutation in the gene for theskeletal muscle Na+ channel. Hyperkalemia may occur with severe digitalistoxicity due to inhibition of the Na+,K+-ATPase pump. Depolarizing musclerelaxants 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 renalK+ 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 maysignificantly contribute to hyperkalemia in protein-malnourished (low ureaexcretion) 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. Gordons syndrome 2. Cyclosporine Note: ACE, angiotensin-converting enzyme; NSAIDs, nonsteroidal anti-inflammatory drugs. Hyporeninemic hypoaldosteronism is a syndrome characterized byeuvolemia 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 havean 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 renalprostaglandins. The resultant decrease in GFR and K + secretion is often manifestas hyperkalemia. As a rule, the degree of hyperkalemia due to hypoaldosteronismis mild in the absence of increased K+ intake or renal dysfunction. Angiotensin-converting enzyme (ACE) inhibitors block the conversion ofangiotensin I to angiotensin II. Angiotensin receptor antagonists directly inhibitthe actions of angiotensin II on AT1 angiotensin II receptors. The actions of bothof these classes of drugs result in impaired aldosterone release. Patients atincreased risk of ACE inhibitor or angiotensin receptor antagonist–inducedhyperkalemia include those with diabetes mellitus, renal insufficiency, decreasedeffective circulating arterial volume, bilateral renal artery stenosis, or concurrentuse of K+-sparing diuretics or NSAIDs.