The main causes of hyperkalemia are redistribution of potassium from the intracellular to the extracellular space and the delay of potassium in the body. However, so-called false increase potassium in the blood is worth mentioning, which is detected by hemolysis, high leukocytosis (white blood cells including over 200 000/ml of blood) and thrombocytosis. Hyperkalemia in these cases is caused by the release of potassium from the blood cells.
Redistribution of potassium from the intracellular to the extracellular space observed during the development of acidosis, insulin deficiency and the introduction of beta-blockers. Fast exit of potassium from the cells to the development of severe hyperkalemia occurs with severe trauma or crush syndrome. Chemotherapy of lymphoma, leukemia and multiple myeloma is accompanied by increased levels of potassium in the blood serum. Redistribution of potassium can also be caused by alcohol intoxication and the insertion of drugs that change potassium ratio between the cell and its environment. These drugs include cardiac glycosides, depolarizing muscle relaxants (succinylcholine). Hyperkalemia can be caused by severe or long exercise stress.
Hyperkalemia due to the delay of potassium by kidney is one of the most common causes of potassium imbalance with nephrological diseases. Isolation of potassium by the kidney depends on the number of nephrons, adequate delivery of sodium and fluid to the distal nephron, normal aldosterone secretion and condition of distal tubule epithelium. Renal insufficiency on its own doesn’t lead to the development of hyperkalemia until GFR falls to 15-10 ml/min or diuresis decreases to less than 1 l/sec. Under these conditions, homeostasis is maintained by increased secretion of potassium in the remaining nephrons. The exceptions are patients with interstitial nephritis or hyporeninemic hypoaldosteronism. This situation is most commonly seen in elderly patients (diabetics) who use drugs, which directly or indirectly (through the renin) blocking aldosterone synthesis (indomethacin, heparin sodium, captopril, etc.).
The main causes of renal origin hyperkalemia are oliguric renal failure (acute or chronic), mineralocorticoid insufficiency (Addison's disease, hyporeninemic hypoaldosteronism); drugs that violate the renal excretion of potassium (spironolactone, triamterene, amiloride, ACE inhibitors, heparin sodium).
Tubular Defects in Renal Excretion of Potassium
The rapid development of hyperkalemia in acute renal failure and chronic oliguric renal failure due to decreased GFR, reduced intake of fluid in the distal of nephron, direct damage of the distal tubules in acute tubular necrosis.
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Aldosterone stimulates the secretion of potassium in the cortical collecting ducts and increases its cellular uptake. Aldosterone deficiency regardless of the reason of its development predisposes to the development of hyperkalemia. Hypoaldosteronism may be the result of a primary adrenal glands lesion (Addison's disease), or develop as a result of genetic defects in the biosynthesis of aldosterone (adrenal syndrome, or 21-hydroxylase deficiency). During the Addison's disease it often reveals salt depletion and overall reduction in body tone, like with hyperkalemia.
Hypoaldosteronism combined with low plasma renin is known as hyporeninemic hypoaldosteronism. This syndrome is often detected with chronic tubulointerstitial kidney disease, diabetes, obstructive nephropathy, sickle-cell anemia. Drugs may be the cause of hyporeninemic hypoaldosteronism development. We describe the development of this syndrome in the application of indomethacin and heparin sodium. Typically, the syndrome occurs in elderly patients, half of whom developed hyperchloraemic metabolic acidosis as a response to caused by hyperkalemia inhibition of the formation of ammonia in the kidney and impaired secretion of H + because of low level of aldosterone. Doctors detect arterial hypertension in half of the cases; the vast majority of patients are diagnosed with kidney failure.
Drugs that violate the renal potassium excretion
Spironolactone inhibits the secretion of potassium in the cortical collecting ducts. It operates as antagonists of aldosterone binding protein mineralocorticoid receptors in the target cells, forming a spironolactone-receptor complex. This leads to inhibition of dependent on aldosterone sodium reabsorption in the cortical collecting ducts with the corresponding inhibition of distal tubular secretion of potassium. Amiloride and triamterene inhibit the secretion of potassium through aldosterone independent mechanism. ACE inhibitors cause an increase in the level of blood serum potassium through the blockade of the angiotensin II effect and indirect by this suppression of the aldosterone production. Intensity of hyperkalemia, particularly sharp, increases during renal insufficiency. Heparin effects like a direct inhibitor of the synthesis of aldosterone, which requires careful use of this drug to patients with diabetes and renal failure.
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Tubular Potassium Renal Secretion Defects
Tubular potassium renal secretion defects are found in patients with normal or elevated levels of renin and aldosterone in blood serum. These patients haven’t had any effect during mineralocorticoid assigning; normal kaliuresis doesn’t develop as a response to the introduction of sodium sulfate, furosemide or potassium chloride. These defects are detected in patients with sickle cell disease, systemic lupus erythematosus, obstructive nephropathy and patients with transplanted kidney.