Jump to content

Hyperkalemia

From Wikipedia, the free encyclopedia
(Redirected from Hyperkaliemia)

Hyperkalemia
Other namesHyperkalaemia
Electrocardiography showing precordial leads in hyperkalemia.
Pronunciation
SpecialtyCritical care medicine, nephrology
SymptomsPalpitations, muscle pain, muscle weakness, numbness[1][2]
ComplicationsCardiac arrest[1][3]
CausesKidney failure, hypoaldosteronism, rhabdomyolysis, certain medications[1]
Diagnostic methodBlood potassium > 5.5 mmol/L, electrocardiogram[3][4]
Differential diagnosisPseudohyperkalemia[1][2]
TreatmentMedications, low potassium diet, hemodialysis[1]
MedicationCalcium gluconate, dextrose with insulin, salbutamol, sodium bicarbonate[1][3][5]
Frequency~2% (people in hospital)[2]

Hyperkalemia is an elevated level of potassium (K+) in the blood.[1] Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia.[3][4] Typically hyperkalemia does not cause symptoms.[1] Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness.[1][2] Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.[1][3]

Common causes of hyperkalemia include kidney failure, hypoaldosteronism, and rhabdomyolysis.[1] A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors.[1] The severity is divided into mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L), and severe (>6.5 mmol/L).[3] High levels can be detected on an electrocardiogram (ECG).[3] Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.[1][2]

Initial treatment in those with ECG changes is salts, such as calcium gluconate or calcium chloride.[1][3] Other medications used to rapidly reduce blood potassium levels include insulin with dextrose, salbutamol, and sodium bicarbonate.[1][5] Medications that might worsen the condition should be stopped and a low potassium diet should be started.[1] Measures to remove potassium from the body include diuretics such as furosemide, potassium-binders such as polystyrene sulfonate (Kayexalate) and sodium zirconium cyclosilicate, and hemodialysis.[1] Hemodialysis is the most effective method.[3]

Hyperkalemia is rare among those who are otherwise healthy.[6] Among those who are hospitalized, rates are between 1% and 2.5%.[2] It is associated with an increased mortality, whether due to hyperkalaemia itself or as a marker of severe illness, especially in those without chronic kidney disease.[7][6] The word hyperkalemia comes from hyper- 'high' + kalium 'potassium' + -emia 'blood condition'.[8][9]

Signs and symptoms

[edit]

The symptoms of an elevated potassium level are generally few and nonspecific.[10] Nonspecific symptoms may include feeling tired, numbness and weakness.[10] Occasionally palpitations and shortness of breath may occur.[10][11][12] Hyperventilation may indicate a compensatory response to metabolic acidosis, which is one of the possible causes of hyperkalemia.[13] Often, however, the problem is detected during screening blood tests for a medical disorder, or after hospitalization for complications such as cardiac arrhythmia or sudden cardiac death. High levels of potassium (> 5.5 mmol/L) have been associated with cardiovascular events.[13]

Causes

[edit]

Ineffective elimination

[edit]

Decreased kidney function is a major cause of hyperkalemia. This is especially pronounced in acute kidney injury where the glomerular filtration rate and tubular flow are markedly decreased, characterized by reduced urine output.[13] This can lead to a dramatically elevated potassium in conditions of increased cell breakdown as the potassium is released from the cells and cannot be eliminated in the kidney. In chronic kidney disease, hyperkalemia occurs as a result of reduced aldosterone responsiveness and reduced sodium and water delivery in distal tubules.[14]

Medications that interfere with urinary excretion by inhibiting the renin–angiotensin system is one of the most common causes of hyperkalemia. Examples of medications that can cause hyperkalemia include ACE inhibitors, angiotensin receptor blockers,[13] non-selective beta blockers, and calcineurin inhibitor immunosuppressants such as ciclosporin and tacrolimus.[15] For potassium-sparing diuretics, such as amiloride and triamterene; both the drugs block epithelial sodium channels in the collecting tubules, thereby preventing potassium excretion into urine.[14] Spironolactone acts by competitively inhibiting the action of aldosterone.[13] NSAIDs such as ibuprofen, naproxen, or celecoxib inhibit prostaglandin synthesis, leading to reduced production of renin and aldosterone, causing potassium retention.[16] The antibiotic trimethoprim and the antiparasitic medication pentamidine inhibits potassium excretion, which is similar to mechanism of action by amiloride and triamterene.[17]

Mineralocorticoid (aldosterone) deficiency or resistance can also cause hyperkalemia. Primary adrenal insufficiency are: Addison's disease[18] and congenital adrenal hyperplasia (CAH) (including enzyme deficiencies such as 21α hydroxylase, 17α hydroxylase, 11β hydroxylase, or 3β dehydrogenase).[19]

Excessive release from cells

[edit]

Metabolic acidosis can cause hyperkalemia as the elevated hydrogen ions in the cells can displace potassium, causing the potassium ions to leave the cell and enter the bloodstream. However, in respiratory acidosis or organic acidosis such as lactic acidosis, the effect on serum potassium are much less significant although the mechanisms are not completely understood.[14]

Insulin deficiency can cause hyperkalemia as the hormone insulin increases the uptake of potassium into the cells. Hyperglycemia can also contribute to hyperkalemia by causing hyperosmolality in extracellular fluid, increasing water diffusion out of the cells and causes potassium to move alongside water out of the cells also. The co-existence of insulin deficiency, hyperglycemia, and hyperosmolality is often seen in those affected by diabetic ketoacidosis. Apart from diabetic ketoacidosis, there are other causes that reduce insulin levels such as the use of the medication octreotide, and fasting which can also cause hyperkalemia. Increased tissue breakdown such as rhabdomyolysis, burns, or any cause of rapid tissue necrosis, including tumor lysis syndrome can cause the release of intracellular potassium into blood, causing hyperkalemia.[13][14]

Beta2-adrenergic agonists act on beta-2 receptors to drive potassium into the cells. Therefore, beta blockers can raise potassium levels by blocking beta-2 receptors. However, the rise in potassium levels is not marked unless there are other co-morbidities present. Examples of drugs that can raise the serum potassium are non-selective beta-blockers such as propranolol and labetalol. Beta-1 selective blockers such as metoprolol do not increase serum potassium levels.[14][medical citation needed]

Exercise can cause a release of potassium into bloodstream by increasing the number of potassium channels in the cell membrane. The degree of potassium elevation varies with the degree of exercise, which range from 0.3 meq/L in light exercise to 2 meq/L in heavy exercise, with or without accompanying ECG changes or lactic acidosis. However, peak potassium levels can be reduced by prior physical conditioning and potassium levels are usually reversed several minutes after exercise.[14] High levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology because they bind to beta 2 adrenergic receptors, which, when activated, extracellularly decrease potassium concentration.[20]

Hyperkalemic periodic paralysis is an autosomal dominant clinical condition where there is a mutation in gene located at 17q23 that regulates the production of protein SCN4A. SCN4A is an important component of sodium channels in skeletal muscles. During exercise, sodium channels would open to allow influx of sodium into the muscle cells for depolarization to occur. But in hyperkalemic periodic paralysis, sodium channels are slow to close after exercise, causing excessive influx of sodium and displacement of potassium out of the cells.[14][21]

Rare causes of hyperkalemia are discussed as follows. Acute digitalis overdose such as digoxin toxicity may cause hyperkalemia[22] through the inhibition of sodium-potassium-ATPase pump.[14] Massive blood transfusion can cause hyperkalemia in infants due to leakage of potassium out of the red blood cells during storage.[14] Giving succinylcholine to people with conditions such as burns, trauma, infection, prolonged immobilisation can cause hyperkalemia due to widespread activation of acetylcholine receptors rather than a specific group of muscles. Arginine hydrochloride is used to treat refractory metabolic alkalosis. The arginine ions can enter cells and displace potassium out of the cells, causing hyperkalemia. Calcineurin inhibitors such as cyclosporine, tacrolimus, diazoxide, and minoxidil can cause hyperkalemia.[14] Box jellyfish venom can also cause hyperkalemia.[23]

Excessive intake

[edit]

Excessive intake of potassium is not a primary cause of hyperkalemia because the human body usually can adapt to the rise in the potassium levels by increasing the excretion of potassium into urine through aldosterone hormone secretion and increasing the number of potassium secreting channels in kidney tubules.[14] Acute hyperkalemia in infants is also rare even though their body volume is small, with accidental ingestion of potassium salts or potassium medications. Hyperkalemia usually develops when there are other co-morbidities such as hypoaldosteronism and chronic kidney disease.[14]

Pseudohyperkalemia

[edit]

Pseudohyperkalemia occurs when the measured potassium level is falsely elevated.[24] This condition is usually suspected when the patient is clinically well without any ECG changes. Mechanical trauma during blood drawing can cause potassium leakage out of the red blood cells due to haemolysis of the blood sample.[24] Repeated fist clenching during the blood draw can cause a transient rise in potassium levels.[25] Prolonged length of blood storage can also increase serum potassium levels. Hyperkalemia may become apparent when a person's platelet concentration is more than 500,000/microL in a clotted blood sample (serum blood sample). Potassium leaks out of platelets after clotting has occurred. A high white cell count (greater than 120,000/microL) in people with chronic lymphocytic leukemia increases the fragility of red blood cells, thus causing pseudohyperkalemia during blood processing. This problem can be avoided by processing serum samples, because clot formation protects the cells from haemolysis during processing. A familial form of pseudohyperkalemia, a benign condition characterised by increased serum potassium in whole blood stored at cold temperatures, also exists. This is due to increased potassium permeability in red blood cells.[14]

Mechanism

[edit]

Physiology

[edit]

Potassium is the most abundant intracellular cation and about 98% of the body's potassium is found inside cells, with the remainder in the extracellular fluid including the blood. Membrane potential is maintained principally by the concentration gradient and membrane permeability to potassium with some contribution from the Na+/K+ pump. The potassium gradient is critically important for many physiological processes, including maintenance of cellular membrane potential, homeostasis of cell volume, and transmission of action potentials in nerve cells.[13]

Potassium is eliminated from the body through the gastrointestinal tract, kidney and sweat glands. In the kidneys, elimination of potassium is passive (through the glomeruli), and reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone. In sweat glands potassium elimination is quite similar to the kidney; its excretion is also controlled by aldosterone.[medical citation needed]

Regulation of serum potassium is a function of intake, appropriate distribution between intracellular and extracellular compartments, and effective bodily excretion. In healthy individuals, homeostasis is maintained when cellular uptake and kidney excretion naturally counterbalance a patient's dietary intake of potassium.[26][27] When kidney function becomes compromised, the ability of the body to effectively regulate serum potassium via the kidney declines. To compensate for this deficit in function, the colon increases its potassium secretion as part of an adaptive response. However, serum potassium remains elevated as the colonic compensating mechanism reaches its limits.[28][29]

Elevated potassium

[edit]

Hyperkalemia develops when there is excess production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the kidney that impair excretion.[30]

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself; instead, it results in accommodation. Above a certain level of potassium the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction, which can cause ventricular fibrillation and/or abnormally slow heart rhythms.[13]

Diagnosis

[edit]
An ECG of a person with a potassium of 5.7 showing large T waves and small P waves

To gather enough information for diagnosis, the measurement of potassium must be repeated, as the elevation can be due to hemolysis in the first sample. The normal serum level of potassium is 3.5 to 5 mmol/L. Generally, blood tests for kidney function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol are performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia.[medical citation needed]

Also, electrocardiography (ECG) may be performed to determine if there is a significant risk of abnormal heart rhythms.[13] Physicians taking a medical history may focus on kidney disease and medication use (e.g. potassium-sparing diuretics), both of which are known causes of hyperkalemia.[13]

Definitions

[edit]

Normal serum potassium levels are generally considered to be between 3.5 and 5.3 mmol/L.[3] Levels above 5.5 mmol/L generally indicate hyperkalemia, and those below 3.5 mmol/L indicate hypokalemia.[1][3]

ECG findings

[edit]

With mild to moderate hyperkalemia, there is prolongation of the PR interval and development of peaked T waves.[13] Severe hyperkalemia results in a widening of the QRS complex, and the ECG complex can evolve to a sinusoidal shape.[31] There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarisation. Also, (as noted above), hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarisation of the cardiac action potential causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the QRS complex.[medical citation needed] Some of potassium currents are sensitive to extracellular potassium levels, for reasons that are not well understood. As the extracellular potassium levels increase, potassium conductance is increased so that more potassium leaves the myocyte in any given time period.[32] To summarize, classic ECG changes associated with hyperkalemia are seen in the following progression: peaked T wave, shortened QT interval, lengthened PR interval, increased QRS duration, and eventually absence of the P wave with the QRS complex becoming a sine wave. Bradycardia, junctional rhythms and QRS widening are particularly associated with increased risk of adverse outcomes[33]

The serum potassium concentration at which electrocardiographic changes develop is somewhat variable. Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role.[medical citation needed]

ECG findings are not a reliable finding in hyperkalemia. In a retrospective review, blinded cardiologists documented peaked T-waves in only 3 of 90 ECGs with hyperkalemia. Sensitivity of peaked-Ts for hyperkalemia ranged from 0.18 to 0.52 depending on the criteria for peak-T waves.[medical citation needed]

Prevention

[edit]

Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a diuretic (such as furosemide or hydrochlorothiazide).[13] Sodium polystyrene sulfonate and sorbitol (combined as Kayexalate) are occasionally used on an ongoing basis to maintain lower serum levels of potassium though the safety of long-term use of sodium polystyrene sulfonate for this purpose is not well understood.[13]

High dietary sources include vegetables such as avocados,[34][35] tomatoes and potatoes, fruits such as bananas, oranges and nuts.[36]

Treatment

[edit]

Emergency lowering of potassium levels is needed when new arrhythmias occur at any level of potassium in the blood, or when potassium levels exceed 6.5 mmol/L. Several agents are used to temporarily lower K+ levels. The choice depends on the degree and cause of the hyperkalemia, and other aspects of the person's condition.

Myocardial excitability

[edit]

Calcium (calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. A standard ampule of 10% calcium chloride is 10 mL and contains 6.8 mmol of calcium. A standard ampule of 10% calcium gluconate is also 10 mL but has only 2.26 mmol of calcium. Clinical practice guidelines recommend giving 6.8 mmol for typical EKG findings of hyperkalemia.[13] This is 10 mL of 10% calcium chloride or 30 mL of 10% calcium gluconate.[13] Though calcium chloride is more concentrated, it is caustic to the veins and should only be given through a central line.[13] Onset of action is less than one to three minutes and lasts about 30–60 minutes.[13] The goal of treatment is to normalise the EKG and doses can be repeated if the EKG does not improve within a few minutes.[13]

Some textbooks suggest that calcium should not be given in digoxin toxicity as it has been linked to cardiovascular collapse in humans and increased digoxin toxicity in animal models. Recent literature questions the validity of this concern.[medical citation needed]

Temporary measures

[edit]

Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. The effect of these measures tends to be short-lived, but may temporise the problem until potassium can be removed from the body.[37]

  • Insulin (e.g. intravenous injection of 10 units of regular insulin along with 50 mL of 50% dextrose to prevent the blood sugar from dropping too low) leads to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.[38] Its effects last a few hours, so it sometimes must be repeated while other measures are taken to suppress potassium levels more permanently. The insulin is usually given with an appropriate amount of glucose to help prevent hypoglycemia following the insulin administration, though hypoglycaemia remains common especially in the context of acute or chronic renal impairment[39] and capillary blood glucose measurements should be taken regularly after administration to identify this.
  • Salbutamol (albuterol), a β2-selective catecholamine, is administered by nebuliser (e.g. 10–20 mg). This medication also lowers blood levels of K+ by promoting its movement into cells, and will work within 30 minutes.[38] It is recommended to use 20 mg for maximum potassium lowering effect, but to use lower doses if the patient is tachycardic or has ischaemic heart disease. Note that 12-40% of patients do not respond to salbutamol therapy for reasons unknown, especially if on beta-blockers, so it should not be used as monotherapy[40]
  • Sodium bicarbonate may be used with the above measures if it is believed the person has metabolic acidosis,[3] though time to effectiveness is longer and its use is controversial.

Elimination

[edit]

Severe cases require hemodialysis, which are the most rapid methods of removing potassium from the body.[38] These are typically used if the underlying cause cannot be corrected swiftly while temporising measures are instituted or there is no response to these measures.

Loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlortalidone, hydrochlorothiazide, or chlorothiazide) can increase kidney potassium excretion in people with intact kidney function.[38]

Potassium can bind to a number of agents in the gastrointestinal tract.[41][27] Sodium polystyrene sulfonate with sorbitol (Kayexalate) has been approved for this use and can be given by mouth or rectally.[38] However, high quality evidence to demonstrate the effectiveness of sodium polystyrene are lacking, and use of sodium polystyrene sulfonate, particularly with high sorbitol content, is uncommonly but convincingly associated with colonic necrosis.[42][43][44] There are no systematic studies (>6 months) looking at the long-term safety of this medication.[45]

Patiromer is taken by mouth and works by binding free potassium ions in the gastrointestinal tract and releasing calcium ions for exchange, thus lowering the amount of potassium available for absorption into the bloodstream and increasing the amount lost via the feces.[13][46] The net effect is a reduction of potassium levels in the blood serum.[13]

Sodium zirconium cyclosilicate is a medication that binds potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions.[13] Onset of effects occurs in one to six hours.[47] It is taken by mouth.[47]

Epidemiology

[edit]

Hyperkalemia is rare among those who are otherwise healthy.[6] Among those who are in hospital, rates are between 1% and 2.5%.[2]

Society and culture

[edit]

In the United States, hyperkalemia is induced by lethal injection in capital punishment cases. Potassium chloride is the last of the three drugs administered and actually causes death. Injecting potassium chloride into the heart muscle disrupts the signal that causes the heart to beat. This same amount of potassium chloride would do no harm if taken orally and not injected directly into the blood.[citation needed]

References

[edit]
  1. ^ a b c d e f g h i j k l m n o p q r Lehnhardt A, Kemper MJ (March 2011). "Pathogenesis, diagnosis and management of hyperkalemia". Pediatric Nephrology. 26 (3): 377–384. doi:10.1007/s00467-010-1699-3. PMC 3061004. PMID 21181208.
  2. ^ a b c d e f g McDonald TJ, Oram RA, Vaidya B (20 October 2015). "Investigating hyperkalaemia in adults". BMJ. 351: h4762. doi:10.1136/bmj.h4762. PMID 26487322. S2CID 206907572.
  3. ^ a b c d e f g h i j k l Soar J, Perkins GD, Abbas G, Alfonzo A, Barelli A, Bierens JJ, Brugger H, Deakin CD, Dunning J, Georgiou M, Handley AJ, Lockey DJ, Paal P, Sandroni C, Thies KC, Zideman DA, Nolan JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–1433. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045.
  4. ^ a b Pathy MJ (2006). "Appendix 1: Conversion of SI Units to Standard Units". Principles and practice of geriatric medicine. Vol. 2 (4th ed.). Chichester [u.a.]: Wiley. p. Appendix. doi:10.1002/047009057X.app01. ISBN 9780470090558.
  5. ^ a b Mahoney BA, Smith WA, Lo D, Tsoi K, Tonelli M, Clase C (20 April 2005). "Emergency interventions for hyperkalaemia". Cochrane Database of Systematic Reviews. 2005 (2): CD003235. doi:10.1002/14651858.CD003235.pub2. PMC 6457842. PMID 15846652.
  6. ^ a b c Kovesdy CP (March 2017). "Updates in hyperkalemia: Outcomes and therapeutic strategies". Reviews in Endocrine and Metabolic Disorders. 18 (1): 41–47. doi:10.1007/s11154-016-9384-x. PMC 5339065. PMID 27600582.
  7. ^ Einhorn LM, Zhan M, Hsu VD, Walker LD, Moen MF, Seliger SL, Weir MR, Fink JC (22 June 2009). "The Frequency of Hyperkalemia and Its Significance in Chronic Kidney Disease". Archives of Internal Medicine. 169 (12): 1156–1162. doi:10.1001/archinternmed.2009.132. PMC 3544306. PMID 19546417.
  8. ^ Cohen BJ, DePetris A (2013). Medical Terminology: An Illustrated Guide. Lippincott Williams & Wilkins. p. 326. ISBN 9781451187564. Archived from the original on 8 September 2017.
  9. ^ Herlihy B (2014). The Human Body in Health and Illness. Elsevier Health Sciences. p. 487. ISBN 9781455756421. Archived from the original on 8 September 2017.
  10. ^ a b c "What is Hyperkalemia?". National Kidney Foundation. 8 February 2016. Retrieved 23 February 2020.
  11. ^ "High potassium (hyperkalemia)". Mayo Clinic. 18 November 2011. Archived from the original on 28 February 2014. Retrieved 28 February 2014.
  12. ^ "What is Hyperkalemia?". National Kidney Foundation (NKF). 8 February 2016. Retrieved 25 June 2019.
  13. ^ a b c d e f g h i j k l m n o p q r s t u Kovesdy CP (December 2015). "Management of Hyperkalemia: An Update for the Internist". The American Journal of Medicine. 128 (12): 1281–7. doi:10.1016/j.amjmed.2015.05.040. PMID 26093176.
  14. ^ a b c d e f g h i j k l m B Mount D, H Sterns R, P Forman J (5 June 2017). "Causes and evaluation of hyperkalemia in adults". UpToDate. Retrieved 28 September 2017.
  15. ^ Hwa Lee C, Ho Kim G (31 December 2007). "Electrolyte and Acid-Base Disturbances Induced by Clacineurin Inhibitors". Electrolyte Blood Press. 5 (2): 126–130. doi:10.5049/EBP.2007.5.2.126. PMC 3894512. PMID 24459511. Cyclosporine may reduce potassium excretion by altering the function of several transporters, decreasing the activity of the renin-angiotensin-aldosterone system, and impairing tubular responsiveness to aldosterone
  16. ^ Kim S, Joo KW (31 December 2007). "Electrolyte and Acid-Base Disturbances Associated with Non-Steroidal Anti-Inflammatory Drugs". Electrolyte Blood Press. 5 (2): 116–125. doi:10.5049/EBP.2007.5.2.116. PMC 3894511. PMID 24459510.
  17. ^ Karet FE (February 2009). "Mechanisms in Hyperkalemic Renal Tubular Acidosis: Figure 1". Journal of the American Society of Nephrology. 20 (2): 251–254. doi:10.1681/ASN.2008020166. PMID 19193780.
  18. ^ B Mount D, H Sterns R, Lacroix A, Forman P J. "Hyponatremia and hyperkalemia in adrenal insufficiency". UpToDate. Retrieved 6 October 2017.
  19. ^ F Young W, H Sterns R, Forman JP. "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)". UpToDate. Retrieved 12 October 2017. In children, hypoaldosteronism can result from a deficiency of enzymes required for aldosterone synthesis
  20. ^ Lindinger MI (April 1995). "Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle". J. Mol. Cell. Cardiol. 27 (4): 1011–1022. doi:10.1016/0022-2828(95)90070-5. PMID 7563098.
  21. ^ Gutmann L, Conwit R, M shefner J, L Wilterdink J. "Hyperkalemic periodic paralysis". UpToDate. Retrieved 3 October 2017.
  22. ^ Digitalis Toxicity at eMedicine
  23. ^ Haddad V (2016). Medical Emergencies Caused by Aquatic Animals: A Zoological and Clinical Guide. Springer. p. 11. ISBN 9783319202884.
  24. ^ a b Smellie WS (31 March 2007). "Spurious hyperkalaemia". BMJ. 334 (7595): 693–695. doi:10.1136/bmj.39119.607986.47. PMC 1839224. PMID 17395950.
  25. ^ Simon LV, Hashmi MF, Farrell MW (2024), "Hyperkalemia", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29261936, retrieved 27 April 2024
  26. ^ Brown R (5 November 1984). "Potassium Homeostasis and clinical implications". The American Journal of Medicine. 77 (5): 3–10. doi:10.1016/s0002-9343(84)80002-9. PMID 6388326.
  27. ^ a b Weiner ID, Linas SL, Wingo CS (2010). "Chapter 9 Disorder of Potassium Metabolism". In Fluege J, Johnson R, Feehally J (eds.). Comprehensive Clinical Nephrology (4th ed.). Elsevier. pp. 118–129. ISBN 9780323058766.
  28. ^ Mathialahan T, Maclennan KA, Sandle LN, Verbeke C, Sandle GI (2005). "Enhanced large intestinal potassium permeability in end-stage renal disease". Journal of Pathology. 206 (1): 46–51. doi:10.1002/path.1750. PMID 15772943. S2CID 9679428.
  29. ^ Evans KJ, Greenberg A (2005). "Hyperkalemia: A review". J Intensive Care Med. 20 (5): 272–290. doi:10.1177/0885066605278969. PMID 16145218. S2CID 42985122.
  30. ^ Desai A (14 October 2008). "Hyperkalemia Associated With Inhibitors of the Renin-Angiotensin-Aldosterone System: Balancing Risk and Benefit". Circulation. 118 (16): 1609–1611. doi:10.1161/CIRCULATIONAHA.108.807917. PMID 18852376.
  31. ^ "Hyperkalaemia - ECG Features - Management". Archived from the original on 25 March 2016. Retrieved 25 March 2016.
  32. ^ Parham WA, Mehdirad AA, Biermann KM, Fredman CS (2006). "Hyperkalemia Revisited". Tex. Heart Inst. J. 33 (1): 40–47. PMC 1413606. PMID 16572868.
  33. ^ Clase CM, Carrero JJ, Ellison DH, Grams ME, Hemmelgarn BR, Jardine MJ, Kovesdy CP, Kline GA, Lindner G, Obrador GT, Palmer BF, Cheung M, Wheeler DC, Winkelmayer WC, Pecoits-Filho R, Ashuntantang GE, Bakker SJ, Bakris GL, Bhandari S, Burdmann EA, Campbell KL, Charytan DM, Clegg DJ, Cuppari L, Goldsmith D, Hallan SI, He J, Herzog CA, Hoenig MP, Hoorn EJ, Leipziger JG, Leonberg-Yoo AK, Lerma EV, Lopez-Almaraz JE, Małyszko J, Mann JF, Marklund M, McDonough AA, Nagahama M, Navaneethan SD, Pitt B, Pochynyuk OM, Proença de Moraes T, Rafique Z, Robinson BM, Roger SD, Rossignol P, Singer AJ, Smyth A, Sood MM, Walsh M, Weir MR, Wingo CS (January 2020). "Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference". Kidney International. 97 (1): 42–61. doi:10.1016/j.kint.2019.09.018. hdl:10072/392924. PMID 31706619.
  34. ^ Dreher ML, Davenport AJ (2013). "Hass avocado composition and potential health effects". Crit Rev Food Sci Nutr. 53 (7): 738–50. doi:10.1080/10408398.2011.556759. PMC 3664913. PMID 23638933.
  35. ^ Avocado has more potassium than banana Archived 2017-02-03 at the Wayback Machine 5 May 2011, UPI.com
  36. ^ "Potassium And Your CKD Diet". National Kidney Foundation (NKF). Archived from the original on 22 December 2015. Retrieved 21 December 2015.
  37. ^ Elliott MJ, Ronksley PE, Clase CM, Ahmed SB, Hemmelgarn BR (October 2010). "Management of patients with acute hyperkalemia". CMAJ. 182 (15): 1631–5. doi:10.1503/cmaj.100461. PMC 2952010. PMID 20855477.
  38. ^ a b c d e Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A (2 November 2010). "Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18 Suppl 3): S829–61. doi:10.1161/CIRCULATIONAHA.110.971069. PMID 20956228.
  39. ^ Schafers S, Naunheim R, Vijayan A, Tobin G (March 2012). "Incidence of hypoglycemia following insulin-based acute stabilization of hyperkalemia treatment". Journal of Hospital Medicine. 7 (3): 239–242. doi:10.1002/jhm.977. PMID 22489323.
  40. ^ Ahee P, Crowe AV (1 May 2000). "The management of hyperkalaemia in the emergency department". Emergency Medicine Journal. 17 (3): 188–191. doi:10.1136/emj.17.3.188. PMC 1725366. PMID 10819381.
  41. ^ Hollander-Rodriguez JC, Calvert JF (15 January 2006). "Hyperkalemia". American Family Physician. 73 (2): 283–290. PMID 16445274.
  42. ^ Kamel KS, Schreiber M (2012). "Asking the question again: Are cation exchange resins effective for the treatment of hyperkalemia?". Nephrology Dialysis Transplantation. 27 (12): 4294–7. doi:10.1093/ndt/gfs293. PMID 22989741.
  43. ^ Watson M, Abbott KC, Yuan CM (2010). "Damned if You Do, Damned if You Don't: Potassium Binding Resins in Hyperkalemia". Clinical Journal of the American Society of Nephrology. 5 (10): 1723–6. doi:10.2215/CJN.03700410. PMID 20798253.
  44. ^ Sterns RH, Rojas M, Bernstein P, Chennupati S (May 2010). "Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective?". J. Am. Soc. Nephrol. 21 (5): 733–5. doi:10.1681/ASN.2010010079. PMID 20167700.
  45. ^ Harel Z, Harel S, Shah PS, Wald R, Perl J, Bell CM (March 2013). "Gastrointestinal Adverse Events with Sodium Polystyrene Sulfonate (Kayexalate) Use: A Systematic Review". The American Journal of Medicine. 126 (3): 264.e9–264.e24. doi:10.1016/j.amjmed.2012.08.016. PMID 23321430.
  46. ^ "FDA approves new drug to treat hyperkalemia". Food and Drug Administration (FDA) (Press release). 22 October 2015. Archived from the original on 7 November 2015. Retrieved 1 November 2015.
  47. ^ a b "Sodium Zirconium Cyclosilicate Monograph for Professionals". Drugs.com. Retrieved 11 October 2019.
[edit]
Retrieved from "https://en.wikipedia.org/w/index.php?title=Hyperkalemia&oldid=1258770801"