Hyperkalemia

No Results

No Results

processing….

Hyperkalemia is defined as a serum potassium concentration greater than approximately 5.0-5.5 mEq/L in adults; the range in infants and children is age-dependent. Levels higher than 7 mEq/L can lead to significant hemodynamic and neurologic consequences, whereas levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. See the image below.

Many individuals with hyperkalemia are asymptomatic. When present, symptoms are nonspecific and predominantly related to muscular or cardiac function. Weakness and fatigue are the most common complaints. Occasionally, patients may report the following:

Frank muscle paralysis

Dyspnea

Palpitations

Chest pain

Nausea or vomiting

Paresthesias

In general, the results of the physical examination alone do not alert the physician to the diagnosis of hyperkalemia, except when severe bradycardia is present or muscle tenderness accompanies muscle weakness, suggesting rhabdomyolysis. Examination findings in patients with hyperkalemia include the following:

Vital signs usually normal, except occasionally in bradycardia due to heart block or tachypnea due to respiratory muscle weakness

Muscle weakness and flaccid paralysis

Depressed or absent deep tendon reflexes

When hyperkalemia is discovered, investigate potential pathophysiologic mechanisms. Hyperkalemia can result from any of the following, which often occur in combination:

Excessive intake

Decreased excretion

A shift of potassium from the intracellular to the extracellular space

See Clinical Presentation for more detail.

In a patient who does not have a predisposition to hyperkalemia, repeat the blood test before taking any actions to bring down the potassium level, unless ECG changes are present. Other tests include the following:

ECG

Urine potassium, sodium, and osmolality

Complete blood count (CBC)

Metabolic profile

If the BUN and serum creatinine levels suggest renal insufficiency, using the MDRD or CKD-EPI equation to determine the estimated glomerular filtration rate (eGFR) is recommended. ^[1] Chronic kidney disease alone generally will not cause hyperkalemia until the eGFR is less than 20-25 mL/min.

Depending on the clinical findings and the results of the above laboratory work, the following may be indicated:

Glucose level – In patients with known or suspected diabetes mellitus

Digoxin level – If the patient is on a digitalis medication

Arterial or venous blood gas – If acidosis is suspected

Urinalysis – If signs of renal insufficiency without an already known cause are present (to look for evidence of glomerulonephritis)

Serum cortisol and aldosterone levels – To check for mineralocorticoid deficiency when other causes are eliminated

Serum uric acid and phosphorus tests – For tumor lysis syndrome

Serum creatinine phosphokinase (CPK) and calcium measurements – For rhabdomyolysis

Urine myoglobin test – For crush injury or rhabdomyolysis; suspect if urinalysis reveals blood in the urine but no red blood cells are seen on urine microscopy

ECG

Vital for assessing the physiologic significance of the hyperkalemia

ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia

In patients with organic heart disease and an abnormal baseline ECG, bradycardia may be the only new ECG abnormality

ECG changes have a sequential progression, which roughly correlate with the potassium level, but with the caveats mentioned above ^[2]

Early ECG changes of hyperkalemia, typically seen at a serum potassium level of 5.5-6.5 mEq/L, include the following:

Tall, peaked T waves with a narrow base, best seen in precordial leads ^[3]

Shortened QT interval

ST-segment depression

At a serum potassium level of 6.5-8.0 mEq/L, the ECG typically shows the following:

Peaked T waves

Prolonged PR interval

Decreased or disappearing P wave

Widening of the QRS

Amplified R wave

At a serum potassium level higher than 8.0 mEq/L, the ECG shows the following:

Absence of P waves

Progressive QRS widening

Intraventricular/fascicular/bundle branch blocks

The progressively widened QRS eventually merges with the T wave, forming a sine wave pattern. Ventricular fibrillation or asystole follows.

See Workup for more detail.

The aggressiveness of therapy is directly related to the rapidity with which hyperkalemia has developed, the absolute level of hyperkalemia, and the evidence of toxicity. The faster the rise of potassium, the higher the level, and the stronger the evidence of cardiotoxicity, the more aggressive therapy should be.

If the patient has only a moderate elevation in potassium level and no ECG abnormalities, treatment is as follows:

Increase potassium excretion using a cation exchange resin or diuretics

Correct the source of excess potassium (eg, increased intake or inhibited excretion)

In patients with severe hyperkalemia, treatment is as follows:

IV calcium to ameliorate cardiac toxicity, if present

Identify and remove sources of potassium intake

IV glucose and insulin infusion to enhance potassium uptake by cells

Correct severe metabolic acidosis with sodium bicarbonate

Consider beta-adrenergic agonist therapy (eg, nebulized albuterol, 10 mg, administered by a respiratory therapist); preferred over alkali therapy in patients with renal failure

Increase potassium excretion by administering diuretics or gastrointestinal cation-exchange medications

Emergency dialysis for patients with potentially lethal hyperkalemia that is unresponsive to more conservative measures or with complete renal failure

Medications for increasing potassium excretion include the following:

IV saline and a loop diuretic (eg, furosemide), in patients with normal renal function

An aldosterone analogue, such as 9-alpha fluorohydrocortisone acetate (Florinef), in patients with hyporeninemia or hypoaldosteronism or solid organ transplant patients with chronic hyperkalemia from calcineurin inhibitor use

Potassiuim binders include cation exchange resins such as sodium polystyrene sulfonate (SPS; Kayexalate), patiromer, or sodium zirconium cyclosilicate (Lokelma); an SPS retention enema may be used for hyperkalemic emergencies, oral products have slower onset of action, but may be considered for patients with advanced renal failure who are not yet on dialysis or are transplant candidates

Surgery

Surgery is typically unnecessary, but the following scenarios may involve surgical intervention:

Patients with metabolic acidosis and consequent hyperkalemia due to ischemic gut: Exploration required

Patients with hyperkalemia due to rhabdomyolysis: Surgical decompression of swollen ischemic muscle compartments may be needed

Patients without end-stage renal disease who require hemodialysis for control of hyperkalemia: Placement of a hemodialysis catheter for emergent dialysis needed ^[4]

See Treatment and Medication for more detail.

Hyperkalemia is defined as a serum potassium concentration higher than the upper limit of the normal range; the range in infants and children is age-dependent, whereas the range for adults is approximately 3.5-5.5 mEq/L. The upper limit may be considerably higher in young or premature infants, as high as 6.5 mEq/L. ^[5] Degrees of hyperkalemia are generally defined as follows (however, note that not all sources agree on these levels) ^[6] :

5.5-6.0 mEq/L – Mild

6.1-7.0 mEq/L – Moderate

≥7.0 mEq/L – Severe

Levels higher than 7 mEq/L can lead to significant hemodynamic and neurologic consequences. Levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal.

Because of a paucity of distinctive signs and symptoms, hyperkalemia can be difficult to diagnose. Indeed, it is frequently discovered as an incidental laboratory finding. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. (See Etiology.) However, any single laboratory study demonstrating hyperkalemia must be repeated to confirm the diagnosis, especially if the patient has no changes on electrocardiography (ECG).

Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether ECG signs of electrolyte imbalance are present (see Workup). Continuous ECG monitoring is essential if hyperkalemia is confirmed. Other testing is directed toward uncovering the condition or conditions that led to the hyperkalemia (see Workup).

The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise of the potassium level, the higher it has reached, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be.

In severe cases, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued. (See Treatment.)

Potassium is the primary intracellular cation; 95-98% of the total body potassium is found in the intracellular space, primarily in muscle. Total body potassium stores amount to approximately 50 mEq/kg (3500 mEq in a 70-kg person).

Normal homeostatic mechanisms precisely maintain the serum potassium level within a narrow range (3.5-5.0 mEq/L). The primary mechanisms for maintaining this balance are the buffering of extracellular potassium against a large intracellular potassium pool (via the sodium-potassium pump), which provides minute-to-minute control, and urinary excretion of potassium, which determines total body potassium balance.

Potassium is obtained through the diet. Common potassium-rich foods include meats, beans, tomatoes, potatoes, and fruits such as bananas. Gastrointestinal (GI) absorption is complete, resulting in daily excess intake of about 1 mEq/kg (60-100 mEq).

Under normal conditions, approximately 90% of potassium excretion occurs in the urine, with less than 10% excreted through sweat or stool. Within the kidneys, potassium excretion occurs mostly in the principal cells of the cortical collecting duct (CCD). Urinary potassium excretion depends on adequate luminal sodium delivery to the distal convoluted tubule (DCT) and the CCD, as well as the effect of aldosterone and other adrenal corticosteroids with mineralocorticoid activity.

Sodium reabsorption through epithelial sodium channels (ENaC) located on the apical membrane of cortical collecting tubule cells is driven by aldosterone and generates a negative electrical potential in the tubular lumen, driving the secretion of potassium at this site through the renal outer medullary potassium (ROMK) channels. Aldosterone also regulates sodium transport in the thick ascending limb of the loop of Henle, the DCT, and the connecting tubule.

A family of signaling molecules, the WNK (with no K [lysine]) kinases, plays a critical role in the regulation of sodium and potassium transport in the distal nephron. ^[7] The WNK kinases are suspected of playing a role in the pathogenesis of several forms of hypertension. ^{[4, 8]}

WNK1 and WNK4 regulate the expression and function of the NaCl cotransporter and ROMK in the distal tubule. Increased WNK4 activity results in decreased NaCl cotransporter expression, permitting greater delivery of sodium to the cortical collecting tubule, thus facilitating potassium secretion.  Conversely, lesser WNK4 activity results in increased NaCl cotransporter expression, diminishing distal sodium delivery, thus limiting cortical collecting tubule potassium secretion. ^{[9, 10]}

Renal potassium excretion is increased by the following:

Renal potassium excretion is decreased by the following:

Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion also is increased. Even in the absence of potassium intake, however, obligatory renal losses amount to 10-15 mEq/day. Thus, chronic losses occur in the absence of any ingested potassium.

In chronic kidney disease, renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate (GFR) decreases to less than 15-20 mL/min. Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut is thought to increase, though evidence for this compensatory mechanism has been elusive.

The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load. An excess of only 100-200 mEq will increase the serum potassium concentration by about 1 mEq/L. ^[11]

Potassium is predominantly an intracellular cation; thus, serum potassium levels do not always accurately reflect total body potassium stores. Serum potassium levels are determined by the shift of potassium between intracellular and extracellular fluid compartments, as well as by total-body potassium homeostasis.

Several factors regulate the distribution of potassium between the intracellular and extracellular spaces, including glucoregulatory hormones, adrenergic stimuli, and pH. Insulin enhances potassium entry into cells, whereas glucagon impairs it. Beta-adrenergic agonists enhance potassium entry into cells, whereas beta-blockers and alpha-adrenergic agonists inhibit it.

Alkalosis enhances potassium entry into cells. Acidosis causes a shift of potassium from intracellular space into extracellular space. Inorganic or mineral acid acidoses are more likely to cause a shift of potassium out of the cells than organic acidosis is.

In addition, an acute increase in osmolality, such as may result from hyperglycemia, causes potassium to exit from cells. Acute cell-tissue breakdown (eg, hemolysis or rhabdomyolysis) releases potassium into the extracellular space.

The 2 sets of regulatory factors—those that regulate total-body homeostasis and those that regulate distribution of potassium between intracellular and extracellular spaces—meld to create smooth control of potassium levels throughout the day. Thus, serum concentrations can remain stable even in the face of acute intake or loss of potassium.

For example, although a high-potassium meal might contain enough potassium to raise the serum potassium acutely to lethal levels if the potassium remained in the extracellular space, Na⁺ -K⁺ -ATPase rapidly takes up the potassium into cells, thus preventing the development of hyperkalemia. Adrenergic stimulation and insulin are important in maintaining the activity of Na⁺ -K⁺ -ATPase. The excess potassium then can be excreted by the kidneys, allowing serum potassium levels to return to normal.

Recent studies point toward a gastrointestinal-renal signal that is aldosterone-independent and causes enhanced renal potassium excretion after a meal. The mechanisms have not been fully determined. ^[12]

This integrated regulatory process is manifested in the diurnal rhythm for renal potassium excretion. The highest excretion occurs at midday, approximately 18 hours after peak potassium ingestion at the evening meal. ^[13]

Hyperkalemia can result from any of the following:

In many cases a combination of these factors is involved. For example, a person with a GFR of less than 45 mL/min who consistently eats large amounts of high-potassium foods and is taking a medication that blocks the rennin-angiotensin-aldosterone system is at very high risk for hyperkalemia due to limitations in renal excretion of potassium in the face of high intake.

A person with diabetes mellitus who has hyporeninemic hypoaldosteronism associated with diabetic nephropathy is at high risk for hyperkalemia due to a diminished ability to shift potassium into the intracellular space (insulin deficiency) and impaired renal excretion (aldosterone deficiency). A third circumstance is acute kidney injury from rhabdomyolysis or tumor lysis syndrome, in which hyperkalemia results from impaired renal excretion in addition to the release of large amounts of potassium from intracellular to extracellular fluid compartments.

Excessive intake

Excessive potassium intake alone is a very uncommon cause of hyperkalemia in anyone with an estimated GFR higher than 60 mL/min. The mechanisms for shifting potassium intracellularly and for renal excretion allow a person with normal potassium homeostatic mechanisms to ingest very high quantities of potassium. Even parenteral administration of as much as 60 mEq/hr for several hours creates only a minimal increase in serum potassium concentration in healthy individuals.

The most common source of increased potassium intake is intravenous (IV) or oral potassium supplementation. Packed red blood cells (PRBCs) may also carry high concentrations of potassium that can lead to hyperkalemia during PRBC transfusion. ^[14]

Decreased excretion

Decreased excretion of potassium, especially when coupled with excessive intake, is the most common cause of hyperkalemia. The most common causes of decreased renal potassium excretion include the following:

Renal failure (most common) ^[15]

Medications that interfere with potassium excretion (eg, potassium-sparing diuretics, angiotensin-converting enzyme [ACE] inhibitors, ^{[16, 17, 18, 19]} and nonsteroidal anti-inflammatory drugs [NSAIDs])

Reduced aldosterone production

Impaired responsiveness of the distal tubule to the action of aldosterone (eg, type IV renal tubular acidosis observed with diabetes mellitus, sickle cell disease, or chronic partial urinary tract obstruction) ^{[20, 21]}

Primary adrenal disease (eg, Addison disease or salt-wasting forms of congenital adrenal hyperplasia)

Hyporeninemic hypoaldosteronism or renal tubular disease (pseudohypoaldosteronism I ^[22] or II)

Shift from intracellular to extracellular space

A number of factors can influence the shift of potassium from the intracellular to the extracellular space (see table below). By itself, this mechanism is a relatively uncommon cause of hyperkalemia, but it can exacerbate hyperkalemia produced by high intake or impaired renal excretion of potassium. A common scenario is that insulin deficiency or acute acidosis produces mild-to-moderate impairment of intracellular shifting of potassium.

Table. Selected Factors Affecting Plasma Potassium (Open Table in a new window)

Factor

Effect on Plasma K⁺

Mechanism

Aldosterone

Decrease

Increases sodium resorption, and increases K⁺ excretion

Insulin

Decrease

Stimulates K⁺ entry into cells by increasing sodium efflux (energy-dependent process)

Beta-adrenergic agents

Decrease

Increases skeletal muscle uptake of K⁺

Alpha-adrenergic agents

Increase

Impairs cellular K⁺ uptake

Acidosis (decreased pH)

Increase

Impairs cellular K⁺ uptake

Alkalosis (increased pH)

Decrease

Enhances cellular K⁺ uptake

Cell damage

Increase

Intracellular K⁺ release

Succinylcholine

Increase

Cell membrane depolarization

Clinical situations in which this mechanism is the major cause of hyperkalemia include the following:

Hyperkalemia may also be caused by IV administration of epsilon aminocaproic acid (EACA), a synthetic amino acid. EACA has been found to cause hyperkalemia in studies conducted in dogs. The mechanism of action is presumed to be a structural similarity between EACA and arginine and lysine. These latter amino acids enter the muscle cell in exchange for potassium, thereby leading to an increase in extracellular potassium. ^{[27, 28]}

High levels of potassium cause abnormal heart and skeletal muscle function by lowering cell-resting action potential and preventing repolarization, leading to muscle paralysis. Classic ECG findings begin with tenting of the T wave, followed by lengthening and eventual disappearance of the P wave and widening of the QRS complex. ^[29] However, varying degrees of heart block are also common.

Just before the heart stops, the QRS and T wave merge to form a sinusoidal wave.

Hyperkalemia can result from increased potassium intake, decreased potassium excretion, or a shift of potassium from the intracellular to the extracellular space. The most common causes involve decreased excretion. Alone, excessive intake or an extracellular shift is distinctly uncommon. Often, several disorders are present simultaneously.

Alone, increased intake of potassium is a rare cause of hyperkalemia, because the mechanisms for renal excretion and intracellular disposition are very efficient. In general, a relatively high potassium intake contributes to hyperkalemia in individuals who have impaired renal excretion or intracellular-to-extracellular shift.

Increased intake may result from the following:

High-potassium, low-sodium diets

Ingestion of potassium supplements – Ingested amounts would have to be massive to be the sole cause of hyperkalemia, but even relatively small amounts can produce hyperkalemia in a patient with impaired renal excretion

High concentrations of potassium in IV fluid preparations (eg, total parenteral nutrition formulas)

Dietary salt substitutes – Several “no-salt” or “low-salt” substitutes contain about 10-12 mEq of potassium per gram of salt and can be dangerous, especially with diminished renal function

Penicillin G potassium therapy

PRBC transfusion (risk peaks at 2-3 weeks of cell storage)

Cardioplegia solutions – These contain 20-30 mmol/L of potassium chloride

Almost all patients who present with persistent hyperkalemia have impaired renal excretion of potassium. Mild degrees of renal failure generally do not result in resting hyperkalemia, because of compensation by adaptive mechanisms in the kidneys and GI tract. However, once the GFR falls below 15-20 mL/min, significant hyperkalemia can occur, even in the absence of an abnormally large potassium load. The simple lack of nephron mass prevents normal potassium homeostasis.

Other mechanisms, such as drug effects or renal tubular acidosis, can decrease renal potassium excretion and cause hyperkalemia even in individuals with normal or only mildly decreased renal function. Two other causes of decreased excretion of potassium are reduced distal sodium delivery and reduced tubular fluid flow rate.

Medications that can decrease potassium excretion include the following:

Disorders that can cause type IV renal tubular acidosis, resulting in hyperkalemia, include the following:

Like increased intake, this is rarely the sole cause of hyperkalemia, because the mechanisms for renal excretion are very efficient. However, the inability to transport potassium intracellularly exacerbates hyperkalemia in individuals who have impaired renal excretion.

Factors that can shift potassium into the extracellular space include the following:

Hypertonicity may lead to hyperkalemia by the following 2 mechanisms:

Loss of intracellular water, resulting in an increased intracellular potassium concentration, favoring a gradient for potassium to move out of the cells

As water exits the cells, “solvent drag,” which sweeps potassium along

The most common cause of hyperosmolality is hyperglycemia in uncontrolled diabetes mellitus. Other conditions with hypertonicity are hypernatremia, hypertonic mannitol, and high-osmolarity contrast media..

Aldosterone deficiency is somewhat controversial as a cause of hyperkalemia. There is some evidence that long-term aldosterone deficiency impairs cell potassium uptake.

Toad venom, which is used in traditional Chinese medicine and in folk medicine in southeastern Asia, contains cardiac glycosides whose structure and biochemical activity are similar to those of digitalis. These cause hyperkalemia by binding to the alpha subunit of Na⁺ -K⁺ -ATPase and thus inhibiting reuptake of potassium from the extracellular space. ^[35]

Toad venom is prepared from dried secretions, typically from the Asiatic toad (Bufo gargarizans). In addition being an ingredient in Chinese medications (eg, Chan Su, Lu-Shen Wan), toad venom has also turned up in purported aphrodisiacs. Digoxin Fab fragments have been used to treat toad venom poisoning. ^[36]

Genetic disorders that can result in hyperkalemia include the following:

Glomerulopathy with fibronectin deposits

GFND is a genetically heterogeneous autosomal dominant disorder which manifests as proteinuria, hypertension, type IV renal tubular acidosis. It eventually leads to end-stage renal failure, in the second to fifth decade of life. Type 1 GFND maps to chromosome 1q32, but the gene is unknown at this time. Type 2 GFND is caused by mutations in the FN1 gene located on chromosome 2q34.

Disorders of steroid metabolism and mineralocorticoid receptors

21-hydroxylase deficiency in its classic form and aldosterone synthase deficiency result in hyperkalemia due to low aldosterone levels. 11-Beta hydroxylase deficiency, 3-beta hydroxysteroid dehydrogenase deficiency, and 17 alpha-hydroxylase/17,20-lyase deficiency are generally not characterized by the development of hyperkalemia.

Congenital hypoaldosteronism

Congenital hypoaldosteronism is caused by mutations in the CYP11B2 gene, which encodes the type II corticosterone methyloxidase enzyme. It is inherited in an autosomal recessive manner. Patients with this disorder have decreased aldosterone and salt wasting. They will have an increased serum ratio of 18-hydroxycorticosterone to aldosterone.

Pseudohypoaldosteronism

Type I pseudohypoaldosteronism (PHAI) can be caused by an inactivating mutation of 1 of 3 encoding subunits of the epithelial sodium channel (SCNN1A, SCNN1G, or SCNN1B). PHAI is inherited in an autosomal recessive manner. These mutations result in impaired potassium secretion due to impaired sodium reabsorption in the distal tubule. ^[38]

PHAI tends to be most severe in the neonatal period, causing renal salt wasting and respiratory tract infections. Sweat, stool, and saliva have high sodium concentrations. Sometimes this disorder can be mistaken for cystic fibrosis.

Another form of PHAI is caused by mutations in the NR3C2 gene and is inherited in an autosomal dominant manner. Patients with this disorder may present in the neonatal period with renal salt wasting and hyperkalemic acidosis similar to those seen in the autosomal recessive form. Patients with this form of PHAI generally improve with age and are typically asymptomatic in adulthood. ^[39]

Gordon syndrome, or pseudohypoaldosteronism type II (PHAII), characterized by hyperkalemia and hypertension, is caused by mutations in several genes. The following 5 loci are known to be associated with PHAII:

The genes causing this disorder code for protein kinases that are localized to the distal tubule and that regulate ion transport in this nephron segment. WNK4 appears to have several roles in regulating sodium, potassium, and chloride transport through transcellular and paracellular pathways. ^[40] Interestingly, PHAII from mutations in WNK1 is significantly less severe than PHAII from mutations in WNK4 or KLHL3, whereas PHAII from mutations in CUL3 is more severe. ^[41] All forms of PHII generally respond to treatment with thiazide diuretics.

Disorders of chloride homeostasis

Disorders of chloride homeostasis can also result in hyperkalemia. Isolated hyperchlorhidrosis is caused by mutations in the CA12 gene, and is inherited in an autosomal recessive manner. This disorder can cause excessive salt wasting in sweat, which can result in severe hyponatremic dehydration and hyperkalemia. ^[42]

Nephronophthisis

Nephronophthisis is characterized by enlargement of the kidneys, inflammatory portal fibrosis of the liver, and variable development of end-stage renal disease (ESRD). Patients with the infantile form of this disease generally reach ESRD before the age of 2 years. Patients with the juvenile form reach ESRD at a median age of 13 years. Patients with other forms of the disease have variable natural history.

Ultimately, this disorder causes a progressive interstitial fibrosis and tubulopathy. Routine laboratory evaluation will show increased creatinine and potassium.

Hyperkalemic periodic paralysis

HYPP is caused by mutations in the SCN4A gene and is inherited in an autosomal dominant manner. During attacks (which can be precipitated by administration of potassium), individuals with HYPP have flaccid generalized weakness and increased serum potassium levels. In addition, patients with HYPP can also have myotonia, which is not typically a feature of hypokalemic periodic paralysis (HOKPP). A number of similar disorders involving myotonia or muscular weakness are allelic to HYPP. ^[43]

Patients with diabetes constitute a unique high-risk group for hyperkalemia, in that they develop defects in all aspects of potassium metabolism. ^{[16, 17]} The typical healthy diabetic diet often is high in potassium and low in sodium. Diabetic persons frequently have underlying renal disease and often develop hyporeninemic hypoaldosteronism (ie, decreased aldosterone secondary to suppressed renin levels), impairing renal excretion of potassium. ^{[20, 21]}

Many patients with diabetes are placed on ACE inhibitor or ARB therapy for treatment of hypertension or diabetic nephropathy, exacerbating the defect in potassium excretion. Finally, persons with diabetes have insulin deficiency or resistance to insulin action, limiting their ability to shift potassium intracellularly.

Hyperkalemia, defined as a serum potassium concentration greater than 5.0–5.3 mEq/L, is rare in a general population of healthy individuals. In hospitalized patients, the incidence of hyperkalemia has ranged from 1% to 10%, depending on how the condition is defined. In hospitalized patients, drugs are implicated in the development of hyperkalemia in as many as 75% of cases. Decreased renal function, ^[15] genitourinary disease, cancer, severe diabetes, and polypharmacy may also predispose to hyperkalemia.

The incidence of hyperkalemia in the pediatric population is unknown, though the prevalence of hyperkalemia in extremely low birth weight premature infants can exceed 50%. ^[44] Hyperkalemia in pediatric patients is most commonly associated with renal insufficiency, acidosis, and diseases that involve defects in mineralocorticoid, aldosterone, and insulin function. ^[22]

Military recruits, individuals with sickle cell traits, and people who abuse drugs are at risk for hyperkalemia because of acute rhabdomyolysis. These cases disproportionately occur in males, probably reflecting the higher muscle mass of males, though an underlying hormonal predisposition cannot be absolutely excluded.

Patients with diabetes mellitus are at increased risk for hyperkalemia. In one review of an unselected group of diabetes clinic patients, 15% (270 of 1764) had a serum potassium level higher than 5 mEq/L; however, fewer than 4% had levels higher than 5.4 mEq/L. ^[45] Clinical risk factors significant in predicting the occurrence of hyperkalemia included renal insufficiency, duration of diabetes mellitus, age, glycosylated hemoglobin levels, and retinopathy—but not the serum glucose level or the drugs used for diabetes treatment.

Use of ACE inhibitors as a risk factor for hyperkalemia is a significant concern, particularly because the indications for these agents in high-risk populations are broad. In a 1998 study, 11% of patients at a Veterans Affairs general medicine outpatient clinic had hyperkalemia; risk factors included elevated blood urea nitrogen (BUN) and serum creatinine, severe diabetes mellitus, heart failure, peripheral vascular disease, and the use of a long-acting drug. Hyperkalemia occurred in less than 6% of patients with normal renal function. ^[46]

As cardiovascular therapy has evolved, the growing population of patients with chronic heart failure also has come to constitute a high-risk group. The factors promoting the development of hyperkalemia in these patients include underlying renal insufficiency due to poor cardiac output and reduced renal blood flow, as well as the high prevalence of diabetes mellitus in patients with heart failure and the growing use of ACE inhibitors, ARBs, aldosterone inhibitors (eg, spironolactone), and direct renin inhibitors (eg, aliskiren), alone and in combination. ^{[20, 21, 47, 48, 49]}

Initial studies examining the risk of hyperkalemia in patients with heart failure who were treated with aldosterone inhibitors revealed only a minor increase in hyperkalemia. However, later studies showed that as the treatment became more widespread, morbidity and mortality from hyperkalemia increased. ^[50]

Hyperkalemia has been reported in less than 5% of the general population worldwide. Hospitalized patients in countries as diverse as England, Australia, and Israel experience hyperkalemia approximately 10% of the time. No racial differences in the incidence of hyperkalemia appear to exist.

As in the United States, risk factors include advanced age, significant prematurity, and the presence of renal failure, diabetes mellitus, and heart failure. Additionally, one series documented an increased incidence of hyperkalemia with cancer and GI disease. ^[51] Polypharmacy, particularly the use of potassium supplements and potassium-sparing diuretics, in patients with underlying renal insufficiency contributed to hyperkalemia in almost 50% of the cases.

Several series document the increasing tendency for hyperkalemia in patients at the extremes of life—that is, small premature infants and elderly people. Renal insufficiency plays a significant role in both groups.

Studies in small premature infants indicate that the incidence of hyperkalemia is increased in infants with a lower GFR, as estimated on the basis of endogenous creatinine clearance. In these cases, hyperkalemia often occurs within the first 48 hours of life. Even full-term infants may have transient hyperkalemia and hyponatremia due to decreased responsiveness to aldosterone (PHAI). ^[22]

Several factors contribute to the increased propensity for elderly people to become hyperkalemic. Renal function tends to deteriorate with age, even in relatively healthy individuals. The GFR decreases by approximately 1 mL/min each year in people older than 30 years. Renal blood flow also decreases. Oral intake declines, resulting in decreased urine flow rates. Plasma renin activity and aldosterone levels also tend to decrease with age, reducing the ability of the distal nephron to secrete potassium.

Elderly patients are more likely to be taking medications that could interfere with potassium secretion, such as NSAIDs, ACE inhibitors, and potassium-sparing diuretics. Elderly individuals who are bedridden often are placed on subcutaneous heparin, which can decrease aldosterone production.

Men are significantly more prone to hyperkalemia than women are. This difference has been noted in several series and stands in contrast to the increased incidence of hypokalemia in women. The reasons for this discrepancy are unknown. However, neuromuscular disorders, including myotonic and muscular dystrophies and related disorders that can predispose patients to hyperkalemia with succinylcholine administration, are more prevalent in males. ^[52]

For patients with a defined and transient cause of hyperkalemia, the prognosis is excellent. With correction of the underlying causative condition, full resolution can be expected. However, patients who have ongoing risk factors for hyperkalemia are likely to experience recurrent episodes.

Sudden and rapid onset of hyperkalemia can be fatal. With slow or chronic increase in potassium levels, adaptation occurs via renal excretion, with fractional potassium excretion increasing by as much as 5-10 times the reference range.

Complications of hyperkalemia range from mild ECG changes to cardiac arrest. Weakness is common as well. The primary cause of morbidity and mortality is potassium’s effect on cardiac function. ^[53] The mortality can be as high as 67% if severe hyperkalemia is not treated rapidly. ^[54]

In hospitalized patients, hyperkalemia is an independent risk factor for death. In one series, 406 (1.4%) of 29,063 patients who were hospitalized developed hyperkalemia; 58 (14.3%) of the 406 died, with the risk increasing as the potassium level increased. ^[51]

Whereas 28% of patients with a serum potassium level above 7 mEq/L died, only 9% of those with a potassium level below 6.5 mEq/L died. ^[51] In 7 of the 58 deaths, the cause of death was directly attributable to hyperkalemia. Most cases resulting in death were complicated by renal failure. It is noteworthy that all of the patients who died of hyperkalemia had normal potassium levels within the 36 hours preceding death.

Interestingly, in a large study of individuals living in the community, serum potassium leveles greater than 5.0 mEq/L correlated with increased mortality, although the mechanisms were not clear. ^[55]

Murata K, Baumann NA, Saenger AK, Larson TS, Rule AD, Lieske JC. Relative performance of the MDRD and CKD-EPI equations for estimating glomerular filtration rate among patients with varied clinical presentations. Clin J Am Soc Nephrol. 2011 Aug. 6(8):1963-72. [Medline]. [Full Text].

Diercks DB, Shumaik GM, Harrigan RA. Electrocardiographic manifestations: electrolyte abnormalities. J Emerg Med. 2004. 27:153-160. [Medline].

Chew HC, Lim SH. Electrocardiographical case. A tale of tall T’s. Hyperkalaemia. Singapore Med J. 2005 Aug. 46(8):429-32; quiz 433. [Medline].

San-Cristobal P, de los Heros P, Ponce-Coria J, et al. WNK kinases, renal ion transport and hypertension. Am J Nephrol. 2008. 28(5):860-70. [Medline].

Shaffer SG, Kilbride HW, Hayen LK, Meade VM, Warady BA. Hyperkalemia in very low birth weight infants. J Pediatr. 1992 Aug. 121(2):275-9. [Medline].

Tran HA. Extreme hyperkalemia. South Med J. 2005 Jul. 98(7):729-32. [Medline].

Kahle KT, Ring AM, Lifton RP. Molecular physiology of the WNK kinases. Annu Rev Physiol. 2008. 70:329-55. [Medline].

Huang CL, Kuo E. Mechanisms of disease: WNK-ing at the mechanism of salt-sensitive hypertension. Nat Clin Pract Nephrol. 2007 Nov. 3(11):623-30. [Medline].

Hoorn EJ, Nelson JH, McCormick JA, Ellison DH. The WNK kinase network regulating sodium, potassium, and blood pressure. J Am Soc Nephrol. 2011 Apr. 22 (4):605-14. [Medline].

Hadchouel J, Ellison DH, Gamba G. Regulation of Renal Electrolyte Transport by WNK and SPAK-OSR1 Kinases. Annu Rev Physiol. 2016. 78:367-89. [Medline].

Marino PL. Potassium. The ICU Book. Baltimore: Williams & Wilkins; 1998.

Preston RA, Afshartous D, Rodco R, Alonso AB, Garg D. Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans. Kidney Int. 2015 Dec. 88 (6):1383-1391. [Medline].

Gumz ML, Rabinowitz L, Wingo CS. An Integrated View of Potassium Homeostasis. N Engl J Med. 2015 Jul 2. 373 (1):60-72. [Medline].

Bhananker SM, Ramamoorthy C, Geiduschek JM, Posner KL, Domino KB, Haberkern CM, et al. Anesthesia-related cardiac arrest in children: update from the Pediatric Perioperative Cardiac Arrest Registry. Anesth Analg. 2007 Aug. 105(2):344-50. [Medline].

Einhorn LM, Zhan M, Hsu VD, Walker LD, Moen MF, Seliger SL, et al. The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med. 2009 Jun 22. 169(12):1156-62. [Medline]. [Full Text].

Raebel MA, Ross C, Xu S, et al. Diabetes and Drug-Associated Hyperkalemia: Effect of Potassium Monitoring. J Gen Intern Med. 2010 Jan 20. [Medline]. [Full Text].

Johnson ES, Weinstein JR, Thorp ML, et al. Predicting the risk of hyperkalemia in patients with chronic kidney disease starting lisinopril. Pharmacoepidemiol Drug Saf. 2010 Mar. 19(3):266-72. [Medline].

Lin HH, Yang YF, Chang JK, et al. Renin-angiotensin system blockade is not associated with hyperkalemia in chronic hemodialysis patients. Ren Fail. 2009. 31(10):942-5. [Medline].

Weir MR, Rolfe M. Potassium homeostasis and Renin-Angiotensin-aldosterone system inhibitors. Clin J Am Soc Nephrol. 2010 Mar. 5(3):531-48. [Medline].

Preston RA, Afshartous D, Garg D, et al. Mechanisms of impaired potassium handling with dual renin-angiotensin-aldosterone blockade in chronic kidney disease. Hypertension. 2009 Mar 23. [Medline].

Khanna A, White WB. The management of hyperkalemia in patients with cardiovascular disease. Am J Med. 2009 Mar. 122(3):215-21. [Medline].

Schweiger B, Moriarty MW, Cadnapaphornchai MA. Case report: severe neonatal hyperkalemia due to pseudohypoaldosteronism type 1. Curr Opin Pediatr. 2009 Apr. 21(2):269-71. [Medline].

Papaioannou V, Dragoumanis C, Theodorou V, Pneumatikos I. The propofol infusion ‘syndrome’ in intensive care unit: from pathophysiology to prophylaxis and treatment. Acta Anaesthesiol Belg. 2008. 59(2):79-86. [Medline].

Matthews JM. Succinylcholine-induced hyperkalemia. Anesthesiology. 2006 Aug. 105(2):430; author reply 431. [Medline].

Piotrowski AJ, Fendler WM. Hyperkalemia and cardiac arrest following succinylcholine administration in a 16-year-old boy with acute nonlymphoblastic leukemia and sepsis. Pediatr Crit Care Med. 2007 Mar. 8(2):183-5. [Medline].

Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology. 1975 Jul. 43(1):89-99. [Medline]. [Full Text].

Perazella MA, Biswas P. Acute hyperkalemia associated with intravenous epsilon-aminocaproic acid therapy. Am J Kidney Dis. 1999 Apr. 33(4):782-5. [Medline].

Carroll HJ, Tice DA. The effects of epsilon amino-caproic acid upon potassium metabolism in the dog. Metabolism. 1966 May. 15(5):449-57. [Medline].

Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. 2000 Oct. 18(6):721-9. [Medline].

Sánchez-Carpintero I, Ruiz-Rodriguez R, López-Gutiérrez JC. [Propranolol in the treatment of infantile hemangioma: clinical effectiveness, risks, and recommendations]. Actas Dermosifiliogr. 2011 Dec. 102(10):766-79. [Medline].

Pavlakovic H, Kietz S, Lauerer P, Zutt M, Lakomek M. Hyperkalemia complicating propranolol treatment of an infantile hemangioma. Pediatrics. 2010 Dec. 126(6):e1589-93. [Medline].

Cummings CC, McIvor ME. Fluoride-induced hyperkalemia: the role of Ca2+-dependent K+ channels. Am J Emerg Med. 1988 Jan. 6(1):1-3. [Medline].

Suzuki H, Terai M, Hamada H, Honda T, Suenaga T, Takeuchi T, et al. Cyclosporin A treatment for Kawasaki disease refractory to initial and additional intravenous immunoglobulin. Pediatr Infect Dis J. 2011 Oct. 30(10):871-6. [Medline].

Nowicki TS, Bjornard K, Kudlowitz D, Sandoval C, Jayabose S. Early recognition of renal toxicity of high-dose methotrexate therapy: a case report. J Pediatr Hematol Oncol. 2008 Dec. 30(12):950-2. [Medline].

Gowda RM, Cohen RA, Khan IA. Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications. Heart. 2003 Apr. 89(4):e14. [Medline]. [Full Text].

New MI. Inborn errors of adrenal steroidogenesis. Mol Cell Endocrinol. 2003. 211:75-83. [Medline].

White PC. Aldosterone synthase deficiency and related disorders. Mol Cell Endocrinol. 2004. 217:81-87. [Medline].

Sartorato P, Khaldi Y, Lapeyraque AL, et al. Inactivating mutations of the mineralocorticoid receptor in Type I pseudohypoaldosteronism. Mol Cell Endocrinol. 2004 Mar 31. 217(1-2):119-25. [Medline].

Geller DS, Rodriguez-Soriano J, Vallo Boado A, Schifter S, Bayer M, Chang SS, et al. Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I. Nat Genet. 1998 Jul. 19(3):279-81. [Medline].

Gamba G. Role of WNK kinases in regulating tubular salt and potassium transport and in the development of hypertension. Am J Physiol Renal Physiol. 2005. 288:F245-52. [Medline]. [Full Text].

Boyden LM, Choi M, Choate KA, Nelson-Williams CJ, Farhi A, Toka HR, et al. Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities. Nature. 2012 Jan 22. 482(7383):98-102. [Medline]. [Full Text].

Muhammad E, Leventhal N, Parvari G, Hanukoglu A, Hanukoglu I, Chalifa-Caspi V, et al. Autosomal recessive hyponatremia due to isolated salt wasting in sweat associated with a mutation in the active site of Carbonic Anhydrase 12. Hum Genet. 2011 Apr. 129(4):397-405. [Medline].

Jurkat-Rott K, Mitrovic N, Hang C, Kouzmekine A, Iaizzo P, Herzog J, et al. Voltage-sensor sodium channel mutations cause hypokalemic periodic paralysis type 2 by enhanced inactivation and reduced current. Proc Natl Acad Sci U S A. 2000 Aug 15. 97(17):9549-54. [Medline]. [Full Text].

Lorenz JM, Kleinman LI, Markarian K. Potassium metabolism in extremely low birth weight infants in the first week of life. J Pediatr. 1997 Jul. 131(1 Pt 1):81-6. [Medline].

Jarman PR, Kehely AM, Mather HM. Hyperkalaemia in diabetes: prevalence and associations. Postgrad Med J. 1995 Sep. 71(839):551-2. [Medline]. [Full Text].

Reardon LC, Macpherson DS. Hyperkalemia in outpatients using angiotensin-converting enzyme inhibitors. How much should we worry?. Arch Intern Med. 1998 Jan 12. 158(1):26-32. [Medline]. [Full Text].

Maggioni AP, Greene SJ, Fonarow GC, Böhm M, Zannad F, Solomon SD, et al. Effect of aliskiren on post-discharge outcomes among diabetic and non-diabetic patients hospitalized for heart failure: insights from the ASTRONAUT trial. Eur Heart J. 2013 Oct. 34(40):3117-27. [Medline]. [Full Text].

Gheorghiade M, Böhm M, Greene SJ, Fonarow GC, Lewis EF, Zannad F, et al. Effect of aliskiren on postdischarge mortality and heart failure readmissions among patients hospitalized for heart failure: the ASTRONAUT randomized trial. JAMA. 2013 Mar 20. 309(11):1125-35. [Medline].

Mann JF, Anderson C, Gao P, Gerstein HC, Boehm M, Rydén L, et al. Dual inhibition of the renin-angiotensin system in high-risk diabetes and risk for stroke and other outcomes: results of the ONTARGET trial. J Hypertens. 2013 Feb. 31(2):414-21. [Medline].

Juurlink DN, Mamdani MM, Lee DS. Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study. N Engl J Med. 2004. 351:543-551. [Medline]. [Full Text].

Paice B, Gray JM, McBride D. Hyperkalaemia in patients in hospital. Br Med J (Clin Res Ed). 1983 Apr 9. 286(6372):1189-92. [Medline]. [Full Text].

Gurnaney H, Brown A, Litman RS. Malignant hyperthermia and muscular dystrophies. Anesth Analg. 2009 Oct. 109(4):1043-8. [Medline].

Segura J, Ruilope LM. Hyperkalemia risk and treatment of heart failure. Heart Fail Clin. 2008 Oct. 4(4):455-64. [Medline].

Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec. 36(12):3246-51. [Medline].

Hughes-Austin JM, Rifkin DE, Beben T, Katz R, Sarnak MJ, Deo R, et al. The Relation of Serum Potassium Concentration with Cardiovascular Events and Mortality in Community-Living Individuals. Clin J Am Soc Nephrol. 2017 Feb 7. 12 (2):245-252. [Medline].

Braden GL, O’Shea MH, Mulhern JG, et al. Acute renal failure and hyperkalaemia associated with cyclooxygenase-2 inhibitors. Nephrol Dial Transplant. 2004 May. 19(5):1149-53. [Medline]. [Full Text].

Schepkens H, Vanholder R, Billiouw JM, Lameire N. Life-threatening hyperkalemia during combined therapy with angiotensin-converting enzyme inhibitors and spironolactone: an analysis of 25 cases. Am J Med. 2001 Apr 15. 110(6):438-41. [Medline].

Zietse R, Zoutendijk R, Hoorn EJ. Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol. 2009 Apr. 5(4):193-202. [Medline].

Kamel KS, Halperin ML. Intrarenal urea recycling leads to a higher rate of renal excretion of potassium: an hypothesis with clinical implications. Curr Opin Nephrol Hypertens. 2011 Sep. 20(5):547-54. [Medline].

Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med. 1999 Mar 16. 130(6):461-70. [Medline].

Watson M, Abbott KC, Yuan CM. Damned if you do, damned if you don’t: potassium binding resins in hyperkalemia. Clin J Am Soc Nephrol. 2010 Oct. 5(10):1723-6. [Medline].

[Guideline] Alfonzo A, Soar J, MacTier R, et al. Treatment of Acute Hyperkalaemia in Adults. The Renal Association. Available at http://www.renal.org/guidelines/joint-guidelines/treatment-of-acute-hyperkalaemia-in-adults#sthash.vXcD0IG3.QqdB4c5G.dpbs. March 1, 2014; Accessed: October 6, 2015.

Elliott MJ, Ronksley PE, Clase CM, Ahmed SB, Hemmelgarn BR. Management of patients with acute hyperkalemia. CMAJ. 2010 Oct 19. 182 (15):1631-5. [Medline]. [Full Text].

Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective?. J Am Soc Nephrol. 2010 May. 21(5):733-5. [Medline].

Pierce DA, Russell G, Pirkle JL Jr. The Incidence of Hypoglycemia in Patients With Low eGFR Treated With Insulin and Dextrose for Hyperkalemia. Ann Pharmacother. 2015 Sep 28. [Medline].

Dick TB, Raines AA, Stinson JB, Collingridge DS, Harmston GE. Fludrocortisone is effective in the management of tacrolimus-induced hyperkalemia in liver transplant recipients. Transplant Proc. 2011 Sep. 43(7):2664-8. [Medline].

Rogers FB, Li SC. Acute colonic necrosis associated with sodium polystyrene sulfonate (Kayexalate) enemas in a critically ill patient: case report and review of the literature. J Trauma. 2001 Aug. 51(2):395-7. [Medline].

McGowan CE, Saha S, Chu G, Resnick MB, Moss SF. Intestinal necrosis due to sodium polystyrene sulfonate (Kayexalate) in sorbitol. South Med J. 2009 May. 102(5):493-7. [Medline]. [Full Text].

US Food and Drug Administration. Safety: Kayexalate (sodium polystyrene sulfonate) powder. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/ucm186845.htm. Accessed: October 5, 2015.

Harel Z, Harel S, Shah PS, Wald R, Perl J, Bell CM. Gastrointestinal adverse events with sodium polystyrene sulfonate (Kayexalate) use: a systematic review. Am J Med. 2013 Mar. 126(3):264.e9-24. [Medline].

Bakris GL, Pitt B, Weir MR, Freeman MW, Mayo MR, Garza D, et al. Effect of Patiromer on Serum Potassium Level in Patients With Hyperkalemia and Diabetic Kidney Disease: The AMETHYST-DN Randomized Clinical Trial. JAMA. 2015 Jul 14. 314 (2):151-61. [Medline].

Pitt B, Bakris GL, Bushinsky DA, Garza D, Mayo MR, Stasiv Y, et al. Effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on RAAS inhibitors. Eur J Heart Fail. 2015 Oct. 17 (10):1057-65. [Medline].

Kosiborod M, Rasmussen HS, Lavin P, Qunibi WY, Spinowitz B, Packham D, et al. Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among outpatients with hyperkalemia: the HARMONIZE randomized clinical trial. JAMA. 2014 Dec 3. 312 (21):2223-33. [Medline]. [Full Text].

Anker SD, Kosiborod M, Zannad F, Piña IL, McCullough PA, Filippatos G, et al. Maintenance of serum potassium with sodium zirconium cyclosilicate (ZS-9) in heart failure patients: results from a phase 3 randomized, double-blind, placebo-controlled trial. Eur J Heart Fail. 2015 Oct. 17 (10):1050-6. [Medline]. [Full Text].

Khedr E, Abdelwhab S, El-Sharkay M, et al. Prevalence of hyperkalemia among hemodialysis patients in Egypt. Ren Fail. 2009. 31(10):891-8. [Medline].

Bercovitz RS, Greffe BS, Hunger SP. Acute tumor lysis syndrome in a 7-month-old with hepatoblastoma. Curr Opin Pediatr. 2010 Feb. 22(1):113-6. [Medline].

Schafers S, Naunheim R, Vijayan R. Incidence of hypoglycemia following insulin-based acute stabilization of hyperkalemia treatment. J Hospit Med. 15 Nov 2011. Early online:

An JN, Lee JP, Jeon HJ, Kim DH, Oh YK, Kim YS, et al. Severe hyperkalemia requiring hospitalization: predictors of mortality. Crit Care. 2012 Nov 21. 16(6):R225. [Medline].

Cheng CJ, Lin CS, Chang LW, et al. Perplexing hyperkalaemia. Nephrol Dial Transplant. 2006 Nov. 21(11):3320-3. [Medline]. [Full Text].

Fordjour KN, Walton T, Doran JJ. Management of Hyperkalemia in Hospitalized Patients. Am J Med Sci. 2012 Dec 18. [Medline].

Factor

Effect on Plasma K⁺

Mechanism

Aldosterone

Decrease

Increases sodium resorption, and increases K⁺ excretion

Insulin

Decrease

Stimulates K⁺ entry into cells by increasing sodium efflux (energy-dependent process)

Beta-adrenergic agents

Decrease

Increases skeletal muscle uptake of K⁺

Alpha-adrenergic agents

Increase

Impairs cellular K⁺ uptake

Acidosis (decreased pH)

Increase

Impairs cellular K⁺ uptake

Alkalosis (increased pH)

Decrease

Enhances cellular K⁺ uptake

Cell damage

Increase

Intracellular K⁺ release

Succinylcholine

Increase

Cell membrane depolarization

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc<br/>Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Zygimantas C Alsauskas, MD Assistant Professor of Medicine, Division of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

Zygimantas C Alsauskas, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Lina Mackelaite, MD Assistant Professor of Medicine, University of Louisville School of Medicine

Lina Mackelaite, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Transplantation, National Kidney Foundation

Disclosure: Nothing to disclose.

Vibha Nayak, MD Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville School of Medicine

Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Son Dinh, MD Nephrologist, Southland Renal Medical Group, Inc

Son Dinh, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation

Disclosure: Nothing to disclose.

Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Rosemary Ouseph, MD Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

Hyperkalemia

Research & References of Hyperkalemia|A&C Accounting And Tax Services
Source

Share on Facebook

Tweet

Follow us