Hyperkalemia Workup

  • Author: Eleanor Lederer, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Dec 16, 2011
 

Laboratory Studies

  • Assess renal function.
    • Check serum BUN and creatinine levels to determine whether renal insufficiency is present.
    • 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 (140 – age)(weight in kg)/(72)(serum creatinine). For women, the answer is multiplied by 0.8.
    • Estimate the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) formula, as follows: (GFR (mL/min/1.73 m2) = 186 x (serum creatinine) - 1.154 x (age) - 0.203 x (0.742 if female) x (1.210 if African American) (conventional units).[26]
  • Measure urine potassium and sodium concentrations and urine osmolality.
    • These tests are 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 greater than 40 mEq/L suggests intact renal excretory mechanisms, implying that high intake or failure of cell uptake is the major mechanism for hyperkalemia. However, an isolated urine potassium level often is misleading, because the concentration of potassium in the urine is influenced not only by secretion by the cortical collecting tubule but also by the degree of urinary concentration. If the urine osmolality is high (>700 mOsm/kg), then the absolute value of urine potassium concentration can be misleading and suggest that the kidneys are disposing of potassium appropriately.
      • For example, suppose serum potassium is 6 mEq/L and urine potassium 60 mEq/L. The high urine potassium level suggests appropriate renal potassium excretion. However, the final concentration of potassium in the urine not only is dependent on how much potassium is secreted in response to sodium reabsorption, but it also is dependent on how concentrated the urine is. In the above example, if urine osmolality is 300 mOsm/kg, that is, not concentrated relative to serum, then a measured urine potassium level of 60 mEq/L indeed suggests renal potassium loss. However, if the urine osmolality is 1200 mOsm/kg, that is, concentrated 4-fold relative to the serum, then the potassium concentration in the urine, in the absence of urinary concentration due to water reabsorption, is 15 mEq/L, which is very low.
      • The conclusion would then be that the kidneys are not appropriately excreting potassium. This adjustment in the evaluation of urinary potassium concentration for the degree of urinary concentration is called calculation of the transtubular potassium gradient (TTKG).
    • TTKG = (urine K x serum osmolarity)/(serum K x urine osmolarity)
      • A TTKG of less than 3 suggests a lack of aldosterone effect on 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.
      • These examples demonstrate that calculation of the TTKG is superior to using the urine potassium alone to assess contribution of decreased renal excretion to hyperkalemia. As useful as this test is, it is important to recognize that it is valid 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.
    • A 24-hour urine potassium measurement rarely is needed to assess renal potassium excretory ability.
  • Measure complete blood count.
    • A low hemoglobin and hematocrit (H/H) or abnormal red cell morphology may suggest hemolysis.
    • Severe leukocytosis or thrombocytosis raises the possibility of pseudohyperkalemia. When in doubt, measure the plasma potassium concentration. Plasma potassium is about the same as serum potassium.
  • Measure complete metabolic profile.
    • Low bicarbonate may suggest hyperkalemia due to metabolic acidosis.
    • Hyperglycemia suggests diabetes mellitus.
    • Elevated lactic dehydrogenase (LDH), uric acid, phosphate, and alanine aminotransferase (ALT) may suggest tissue breakdown, as occurs in hemolysis, rhabdomyolysis, or tumor lysis.
    • A creatine kinase (CK) elevation suggests rhabdomyolysis.
  • Depending on the results of the above laboratory work, the following may be indicated:
    • Serum cortisol (reference range 8 am 5-25 µg/mL, 4 pm 3-12 µg/mL) - Decrease may suggest adrenal insufficiency.
    • Serum renin and aldosterone (normal supine renin activity 3.2 ± 1 ng/mL/h; normal suppressed aldosterone 5-20 ng/mL) - Decrease may suggest adrenal insufficiency.
    • Fasting blood sugar (reference range 75-115 mg/dL), glycosylated hemoglobin (normal 6.5%), or glucose tolerance test (normal 2 h postprandial value < 140 mg/dL) - Increase suggests underlying diabetes mellitus.
    • Assays of 11-beta hydroxylase or 21-hydroxylase - Deficiencies of these enzymes produce syndromes of virilization and generally are recognized in the neonatal period. 11-beta hydroxylase deficiency is diagnosed by measurement of elevated plasma 11-deoxycortisol levels or increased urinary tetrahydro-ll-deoxycortisol levels. To detect mild cases, adrenocorticotropic hormone (ACTH) stimulation also may be performed to enhance synthesis of these products. 21-hydroxylase deficiency is detected by the measurement of elevated 17-hydroxyprogesterone levels in blood, generally 90-1200 nmol/L.
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Other Tests

  • Electrocardiogram (ECG) - This test is vital to assess the physiologic significance of the hyperkalemia. However, ECG changes often do not correlate with the degree of hyperkalemia. ECG changes suggestive of an effect of hyperkalemia on cardiac conduction include the following (in order of appearance)[27] :
    • Peaked T waves[28] (as seen in the image below.) Peaked T waves on an electrocardiogram, as seen inPeaked T waves on an electrocardiogram, as seen in hyperkalemia.
    • Prolongation of the PR interval
    • Widening of the QRS (as seen in the image below)Widened QRS complexes in a patient whose serum potWidened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
    • Loss of the P wave
    • Sine wave pattern
    • Sinus arrest
  • In patients with organic heart disease and abnormal baseline ECG, bradycardia may be the only new ECG abnormality.
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Contributor Information and Disclosures
Author

Eleanor Lederer, MD  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 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, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Coauthor(s)

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.

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

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

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.

Specialty Editor Board

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.

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 Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology

Disclosure: Nothing to disclose.

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Peaked T waves on an electrocardiogram, as seen in hyperkalemia.
Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
 
 
 
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