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Hypokalaemia and Hyperkalaemia

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Hypokalaemia and Hyperkalaemia Postgrad Med J 2001;77:759–764 759 Postgrad Med J: first published as 10.1136/pgmj.77.914.759 on 1 December 2001. Downloaded from Hypokalaemia and hyperkalaemia A Rastergar, M Soleimani Abstract compartments. Humans, as carnivorous ani- Disturbances in potassium homoeostasis mals, consume large amount of potassium presenting as low or high serum potas- intermittently. Dietary potassium, which is sium are common, especially among hos- rapidly absorbed by the gut, could increase pitalised patients. Given the fact that serum potassium dramatically. However, sev- untreated hypokalaemia or hyperkalae- eral physiological mechanisms quickly shift the mia is associated with high morbidity and potassium intracellularly, allowing slow excre- mortality, it is critical to recognise and tion of potassium by the kidney, and mainte- treat these disorders promptly. In this nance of normal potassium homoeostasis.1 article, normal potassium homoeostasis is Normal physiological regulators, insulin and reviewed initially and then a pathophysi- catecholamines, are stimulated by ingestion of ological approach to work-up and man- food containing glucose and potassium. These agement of hypokalaemia and hyper- hormones are essential in shift of potassium kalaemia is presented. Recent advances intracellularly, depositing it primarily in the liver 2 with respect to the role of kidney in and striated muscle cells. Catecholamines, by handling of the potassium, the regulation acting through diVerent receptors, have diVerent of renal ion transporters in hypokalaemia, eVect on potassium deposition. â2-stimulation and treatment of hypokalaemia and hy- results in a shift of potassium into the cell, while 3 perkalaemia will be discussed. á-stimulation has the opposite eVect. The eVect (Postgrad Med J 2001;77:759–764) of mineralocorticoids and parathyroid hormone in internal potassium homoeostasis is minimal at Keywords: hypokalaemia; hyperkalaemia; potassium best. In addition to these physiological regula- tors, internal potassium homoeostasis is also Potassium homoeostasis aVected by changes in acid-base and osmolarity. Potassium is the most abundant cation in the Sudden changes in osmolarity, by shifting the body. It is predominantly restricted to the water out of cell, creates a solvent drag phenom- intracellular space, such that only 2% is located enon, and helps push potassium out of the cell, extracellularly and the remaining 98% is in the resulting in a rise in serum potassium (table 1). intracellular compartment. The ratio of intra- The eVect of acid-base status is much more Department of cellular to extracellular potassium (Ki/Ke) is complicated and depends on the nature of the Internal Medicine, the major determinant of resting membrane disorder (box 1). Although, the rule of thumb Yale University School potential, and is regulated primarily by the has been that for each 0.1 unit change in pH, of Medicine, New sodium-potassium ATPase pump located on there is a 0.6 mmol/l change in serum potas- http://pmj.bmj.com/ Haven, Connecticut the plasma membrane of most cells. Although sium, this is a very crude approximation and A Rastergar extracellular potassium accounts for only 2% varies greatly by the nature of acid-base Department of of total body potassium, it has a major eVect on disorders. For example organic acidosis as seen Internal Medicine, the ratio of Ki/Ke and through that on the rest- in diabetic ketoacidosis or lactic acidosis result University of ing membrane potential. As a result, serum in little or no change in serum potassium while Cincinnati, Cincinnati, potassium is normally regulated around the non-organic (mineral) acidosis, such as acidosis Ohio narrow range of 3.5–5.0 mmol/l. of renal failure, has the greatest eVect. Other M Soleimani on September 27, 2021 by guest. Protected copyright. The daily intake of potassium in the western acid-base disorders shift potassium minimally.45 Correspondence to: diet is between 80–120 mmol. The kidney is Dr M Soleimani, Division of the major route of potassium excretion, Nephrology and Hypertension, University of accounting for 90% of potassium loss daily. Cincinnati Medical Center, The remaining 10% is excreted through the Box 1: EVect of acid-base disorders on 231 Albert Sabin Way, MSB gastrointestinal tract. The kidney is, therefore, serum potassium 5502, Cincinnati, OH 45267–0585, USA responsible for long term potassium homoeos- x For any pH change the eVect of acidae- [email protected] tasis, as well as the serum potassium concentra- mia is greater than alkalaemia. tion. On short term basis, serum potassium is Submitted 8 September x Non-organic (mineral acidosis) results in 2000 also regulated by the shift of potassium a shift of 0.24–1.7 mmol/l per 0.1 unit pH Accepted 14 June 2001 between the intracellular and extracellular change. Table 1 Regulators of potassium distribution between intracellular and extracellular x Organic acidosis has little to no eVect on compartment potassium shift. x Respiratory and metabolic alkalosis and Regulators Mechanism of action Potassium shift into cells respiratory acidosis result in similar small Insulin Activation of sodium-potassium Increase shift of potassium into and out of cell ATPase respectively (0.1–0.4 mmol/l on average). Catecholamines Activation of â receptors Increase 2 x In chronic acid-base disorders the final Activation of á receptors Decrease Mineralocorticoids Unknown Mild increase potassium reflects primarily the eVect on Parathormone Unknown Mild decrease renal handling of potassium and to lesser Acid-base changes Exchange of H+ for K+ See table 2 extent of transcellular shift. Hyperosmolality Solvent drags Shifts potassium extracellularly www.postgradmedj.com 760 Rastergar, Soleimani Postgrad Med J: first published as 10.1136/pgmj.77.914.759 on 1 December 2001. Downloaded from Renal handling of potassium The filtered potassium (around 700–800 Box 2: Classification of hyperkalaemia mmol/day) is largely reabsorbed by proximal (1) Spurious hyperkalaemia nephron segments, including proximal convo- x Due to high platelet and/or leucocyte luted tubules and thick limb of Henle. The count. potassium that is excreted is, therefore, a result x Due to muscular activity during of secretion by distal segments, predominantly venepuncture. distal convoluted tubule and the collecting duct. Transport studies in these latter tubule (2) Transcellular shift of potassium segments have demonstrated that potassium x Acidaemia (for example, acute renal fail- secretion is accomplished via apical potassium ure). channels. The secretion of potassium in these x Hyperosmolality (for example, severe nephron segments is indirectly but tightly cou- hyperglycaemia). -blockers (for example, propranolol). pled to sodium reabsorption via the amiloride- x â2 sensitive sodium channel; increased sodium x Insulin deficiency (for example, type I reabsorption increases whereas decreased so- diabetes mellitus). dium reabsorption decreases potassium secre- (3) Increase intake tion. It is this secretory ability of the potassium x Infusion of potassium containing solu- channels in the distal segments which regulates tions. the excretion of potassium. As a result, any x Increase potassium intake in patients with condition that decreases the activity of renal defect in potassium excretion. potassium channels results in hyperkalaemia (4) Decrease renal excretion (for example, amiloride intake or aldosterone x Mineralocorticoid deficiency: (a) Addi- deficiency) whereas their increased activity son’s disease, (b) isolated aldosterone results in hypokalaemia (for example, primary deficiency, (c) renin deficiency (for exam- aldosteronism or Liddle’s syndrome). ple, diabetic nephropathy), (d) angio- In summary, kidney is the major regulator of tensin II receptor blockers, (e) angio- long term potassium homoeostasis and serum tensin converting enzyme inhibitors, (f) potassium. However, on short term basis, insu- use of non-steroidal anti-inflammatory lin and catecholamines, among others, regulate drugs. serum potassium through changes in transcel- x Resistance to mineralocorticoids eVect: lular distribution of potassium. (a) tubulointerstitial disease, (b) high dose mineralocorticoids antagonists (for Hyperkalaemia example, spironolactone, trimethoprim). Hyperkalaemia is defined as serum potassium x Severe renal failure. greater than 5.0 mmol/l. True hyperkalaemia should however be distinguished from pseudo- hyperkalaemia, a rise in serum potassium secondary to release of intracellular potassium metabolic acidosis; however, a sudden rise in during phlebotomy or storage of blood sample. osmolality, especially in association with insu- During phlebotomy the combination of venous lin deficiency, could result in significant hyper- http://pmj.bmj.com/ occlusions and hand clinching could result in kalaemia. â-blockers alone are rarely associated potassium release locally. If this is suspected, a with significant hyperkalaemia, however, they blood sample should be drawn from a free could play a contributory part. flowing vein without fist clinching. Potassium Given the renal ability to excrete large can also be released in test tube by haemolysis, amount of potassium, increase in intake could severe thrombocytosis (usually >900 × 1010/l result in hyperkalaemia, only if associated with × 9 platelets) or leucocytosis (leucocytes >70 10 / subtle or overt defect in potassium excretion. on September 27, 2021 by guest. Protected copyright. l). If this is suspected the measurement should Salt substitutes,
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