Conditions associated with high potassium values include the following:
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Hyperkalemia
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Blood transfusion
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Hemolytic anemia (red cell destruction)
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Acute kidney injury
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Addison disease
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Hypoaldosteronism
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Pseudohypoaldosteronism
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Tissue injury
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Eating disorders - Anorexia, bulimia
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Infection
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Dehydration
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Excessive potassium intake - Dietary or intravenous [2]
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Medications - Renin-angiotensin-aldosterone system (RAAS) inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), beta blockers, calcineurin inhibitors, heparin
Hyperkalemia is defined as a serum potassium concentration greater than the upper limit of the normal range. The range in children and infants is age-dependent, whereas the range for adults is approximately 3.5-5.0 mEq/L. Because hyperkalemia can cause lethal cardiac arrhythmias, it is one of the most serious electrolyte disturbances.
When the etiology of hyperkalemia remains unclear, calculation of the transtubular potassium gradient (TTKG) using the following formula may be useful:
TTKG = (K+ urine × Osm plasma)/(K+ plasma × Osm urine)
The normal TTKG varies from 5-15. In the setting of hyperkalemia with normal renal excretion of potassium, the TTKG should be greater than 10. A TTKG of less than 8 in the setting of hyperkalemia implies inadequate potassium excretion, which usually results from aldosterone deficiency or unresponsiveness. Checking the serum aldosterone level may be helpful.
With severe dehydration, potassium levels may be elevated (eg, congenital adrenal hyperplasia, acute kidney injury) or low (eg, pyloric stenosis, alkalosis).
Conditions associated with low potassium values include the following:
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Hypokalemia
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Dehydration
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Use of diuretics
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Vomiting
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Diarrhea
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Hyperaldosteronism
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Deficient potassium intake
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Acetaminophen overdose
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Magnesium deficiency
A spot urine potassium measurement is the easiest and most commonly obtained test for hypokalemia. A low urine potassium level (< 20 mEq/L) suggests poor intake, a shift into the intracellular space, or gastrointestinal loss. A clinician should question the patient regarding (1) diarrhea symptoms and use of laxatives; (2) diet and total parenteral nutrition contents; and (3) the use of insulin, excessive bicarbonate supplements, and a history of episodic weakness.
A high urine potassium level (>40 mEq/L) suggests kidney loss. Be sure to examine the patient's medication list and question the patient regarding the use of diuretics.
Look at the acid-base balance; alkalosis suggests vomiting, Bartter syndrome, Gitelman syndrome, diuretic abuse, or mineralocorticoid excess. Acidosis suggests renal tubular acidosis types I or II, or Fanconi syndrome (as is observed with paraproteinemias, amphotericin use, gentamicin use, or glue sniffing [toluene abuse]).
Also measure the magnesium level; if low, correct it before attempting to correct the potassium level. A deficiency of magnesium results in the continual opening of the ROMK channel, allowing potassium to flow out of the tubular cells into the urine unchecked.
Measure the patient's blood pressure. An elevated blood pressure suggests primary hyperaldosteronism, Cushing syndrome, congenital adrenal hyperplasia, glucocorticoid-remediable hypertension, renal artery stenosis, or Liddle syndrome. Low blood pressure suggests diuretic abuse or a renal tubular disorder such as Bartter syndrome, Gitelman syndrome, or renal tubular acidosis.
If the urine potassium level is greater than 20 mEq/L but less than 40 mEq/L, calculate the TTKG. A value less than 3 suggests that the kidney is not wasting excessive potassium, while a value greater than 7 suggests a significant renal loss. This test cannot be applied when the urine osmolality is less than the serum osmolality.
The TTKG is most helpful in discerning whether a low value in a patient with hyperkalemia is due to low aldosterone levels or aldosterone resistance.
Historically, the utility of the TTKG has been investigated in patients with medication-induced hyperkalemia, eg, combination of medications that potentiate hyperkalemia, such as ACE inhibitors, with spironolactone and potassium supplementations; and cyclosporine in kidney transplant patients. It has also been used to guide spironolactone therapy in patients with cirrhosis and ascites.
While more cumbersome to obtain, a 24-hour urine measurement of potassium excretion yields more precise data on exactly how much potassium is being lost through kidney excretion. Because the kidneys are able to conserve potassium up to approximately 10-15 mEq/d, a value of less than 20 mEq/24-hour urine specimen suggests appropriate kidney conservation of potassium, while values above that indicate some degree of kidney wasting. To ensure that a full and accurate 24-hour urine sample has been collected, urine creatinine should be measured simultaneously.
A spot urine sodium and osmolality test obtained simultaneously with a spot urine potassium test can help refine the interpretation of the urine potassium level. A low urine sodium level (< 20 mEq/L) with a high urine potassium level suggests the presence of secondary hyperaldosteronism. If the urine osmolality is high (>700 mOsm/kg), then the absolute value of the urine potassium concentration can be misleading and can suggest that the kidneys are wasting potassium.
Testing for potassium levels may be performed for the following additional conditions:
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Acute adrenal crisis
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Acute bilateral urinary tract obstruction
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Acute nephritic syndrome
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Bulimia
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Chronic kidney disease
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Cushing syndrome
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Diabetic ketoacidosis
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Primary thrombocythemia
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Rhabdomyolysis
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Thyrotoxic periodic paralysis
