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Hyperkalemia Workup

  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jan 11, 2016
 

Approach Considerations

Ascertain whether the elevated potassium level is real or factitious (see DDx). 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 changes are present on electrocardiography (ECG).

Renal function testing is important. If the patient has renal failure, the serum calcium level should be checked because hypocalcemia can exacerbate cardiac rhythm disturbances. Other tests include the following:

Measurement of the trans-tubular potassium gradient (TTKG) remains widely used as a means of assessing whether decreased renal excretion of potassium is contributing to hyperkalemia. Despite its initial promise, however, recent research has called its accuracy into question,[54] and some experts now recommend that TTKG measurement be abandoned.

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
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Potassium Assay

The relationship between the serum potassium level and symptoms of hyperkalemia is not consistent. For example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients are. The rapidity of change in the potassium level influences the symptoms observed at various potassium levels.

In pediatric patients, capillary blood gas sampling should not routinely be used to evaluate for hyperkalemia, because of the significant risks of factitious hyperkalemia.

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Electrocardiography

ECG is vital for assessing the physiologic significance of 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.[2] Early changes of hyperkalemia include tall, peaked T waves with a narrow base, best seen in precordial leads[3] ; shortened QT interval; and ST-segment depression. These changes are typically seen at a serum potassium level of 5.5-6.5 mEq/L.

At a serum potassium level of 6.5-8.0 mEq/L, in addition to peaked T waves, the ECG shows the following:

  • Prolonged PR interval
  • Decreased or disappearing P wave
  • Widening of the QRS (see the images below)
  • Amplified R wave
    Widened QRS complexes in hyperkalemia. Widened QRS complexes in hyperkalemia.
    Widened QRS complexes in patient whose serum potas Widened QRS complexes in patient whose serum potassium level was 7.8 mEq/L.

At a serum potassium level higher than 8.0 mEq/L, the ECG shows absence of P wave, progressive QRS widening, and 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.

The ECG changes of hyperkalemia reverse with appropriate treatment (see the image below).

ECG of patient with pretreatment potassium level o ECG of patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Note narrowing of QRS complexes and reduction of T waves.
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Renal Function Determination

Check serum levels of blood urea nitrogen (BUN) and creatinine to determine whether renal insufficiency is present. If such insufficiency is confirmed, check 24-hour urine for creatinine clearance or estimate the creatinine clearance using the Cockroft-Gault equation to assess whether the degree of renal insufficiency alone explains the hyperkalemia. The Cockroft-Gault equation is as follows:

(140 – age [y]) ´ weight (kg)/72 ´ serum creatinine (mg/dL)

For women, the result is multiplied by 0.8.

It must be kept in mind that because the serum creatinine level is dependent on muscle mass, a seemingly normal creatinine level in a geriatric or cirrhotic patient will actually indicate impaired renal function. Tools such as the Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formulas are recommended for estimating glomerular filtration rate (GFR) in these patients.[1] The MDRD formula for estimating the GFR is as follows[55] :

186 ´ serum creatinine (mg/dL)−1.154 ´ age (y)−0.203 (´ 0.742 if female) (´ 1.210 if black)

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Urine Potassium, Sodium, and Osmolality

Measurement of urine potassium and sodium concentrations and urine osmolality is essential to determine whether impairment of renal excretion is contributing to the hyperkalemia. A urine potassium level below 20 mEq/L suggests impaired renal excretion. A urine potassium level above 40 mEq/L suggests intact renal excretory mechanisms, implying that high intake or failure of cell uptake is the major mechanism for hyperkalemia.

A spot urine potassium measurement is the easiest and most commonly obtained test; a 24-hour urine potassium measurement is rarely needed. However, an isolated urine potassium level often is misleading, because the urine potassium concentration is influenced not only by secretion by the cortical collecting tubule but also by the degree of urinary concentration. If urine osmolality is high (>700 mOsm/kg), the absolute value for urine potassium concentration can be misleading and suggest that the kidneys are disposing of potassium appropriately.

For example, if serum potassium is 6 mEq/L and urine potassium 60 mEq/L, the high urine potassium level may be taken as suggesting appropriate renal potassium excretion. However, the final concentration of potassium in the urine depends not only on how much potassium is secreted in response to sodium reabsorption but also on how concentrated the urine is.

In this example, if urine osmolality is 300 mOsm/kg—that is, not concentrated in relation to serum—then a measured urine potassium level of 60 mEq/L indeed suggests renal potassium loss. However, if urine osmolality is 1200 mOsm/kg—that is, concentrated 4-fold in relation to serum—then the urine potassium concentration, in the absence of urinary concentration due to water reabsorption, is 15 mEq/L, which is very low. In the latter case, the conclusion would be that the kidneys are not appropriately excreting potassium.

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Trans-Tubular Potassium Gradient

The trans-tubular potassium gradient (TTKG) was developed to account for the potentially confounding effect of urine concentration on the interpretation of the urine potassium concentration. In effect, the TTKG back-calculates what the serum-to–tubular fluid ratio of potassium would be at the level of the cortical collecting tubule, where potassium is secreted before urine concentration has occurred.

The TTKG is determined by the following equation:

TTKG = (urine K x serum osmolarity)

(serum K x urine osmolarity)

A TTKG of less than 3 suggests a lack of aldosterone effect on the collecting tubules (that is, the kidneys are not excreting potassium appropriately). A TTKG greater than 7 suggests an aldosterone effect, which would be appropriate in the setting of hyperkalemia. In pediatric patients with hyperkalemia, a TTKG greater than 10 is consistent with normal renal excretion of potassium; a TTKG of less than 8 implies inadequate potassium excretion, which is usually secondary to aldosterone deficiency or unresponsiveness. Checking a serum aldosterone level may be helpful.

Measurement of the TTKG was initially considered superior to measurement of urine potassium alone for assessing the contribution of decreased renal excretion to hyperkalemia. However, it is important to recognize that the TTKG is valid for this purpose only if (1) the urine osmolality is greater than the serum osmolality—that is, the urine is concentrated relative to the serum—and (2) the urine sodium is greater than 20 mEq/L—that is, distal delivery of sodium is adequate for potassium excretion.

Furthermore, recent evidence suggesting that urea recycling may influence potassium secretion has cast some doubt on the utility of the TTKG.[54] One assumption inherent in the calculation of the TTKG is that the absorption of osmoles distal to the cortical collecting duct is negligible. If further studies suggest that urea transport can influence potassium handling, this test may have to be abandoned.

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Contributor Information and Disclosures
Author

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, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: 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.

Coauthor(s)

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.

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.

Specialty Editor Board

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, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: 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.

Chief Editor

Vecihi Batuman, MD, FACP, 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, FACP, 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

Disclosure: Nothing to disclose.

Acknowledgements

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.

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Widened QRS complexes in patient whose serum potassium level was 7.8 mEq/L.
ECG of patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Note narrowing of QRS complexes and reduction of T waves.
Hyperkalemia diagnosis and treatment flow chart.
Widened QRS complexes in hyperkalemia.
Table. Selected Factors Affecting Plasma Potassium
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
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