Pseudohyperkalemia (In Vitro Release of Potassium From Cells)

  • Familial Pseudohyperkalemia
    • Genetics
      • Autosomal Dominant Inheritance (Maps to the 16q23–ter Locus)
    • Mechanism
      • Abnormally Increased Potassium Permeability of the Red Blood Cell Membrane, Resulting in a Temperature-Dependent Loss of Potassium from Red Blood Cells When Stored at Room Temperature
    • Clinical
      • Characterized by Hyperkalemia in Whole Blood Stored At or Below Room Temperature, Without Additional Hematologic Abnormalities
  • “Leaky” Cell Membranes
    • Mechanism
      • These Patients Appear to Be Prone to Hemolysis During Phlebotomy
  • Phlebotomy-Related Cell Lysis
    • Mechanisms
      • Delay in Processing of Blood Sample
        • May Result in Red Blood Cell Lysis
      • Excessive Vacuum with Very Small Gauge Needle During Phlebotomy
        • May Result in Red Blood Cell Lysis
      • Prolonged Tourniquet Time or Fist-Clenching During Phlebotomy
        • May Result in Efflux of Potassium from Myocytes (Fist-Clenching During Phlebotomy May Increase Potassium by as Much as 1–2 mmol/L)
      • Transportation of Blood Samples in Pneumatic Tube System
        • May Result in Mechanical Red Blood Cell Lysis
  • Severe Leukocytosis (>70k)
    • Mechanism
      • Due to Potassium Release from White Blood Cells in Sample
    • Clinical
      • Plasma, Rather than Serum, Potassium Should Be Measured (Plasma Potassium Will Be Normal in These Cases)
  • Severe Polycythemia (Hct >55%)
    • Mechanism
      • Due to Potassium Release from Red Blood Cells in Sample
    • Clinical
      • Plasma, Rather than Serum, Potassium Should Be Measured (Plasma Potassium Will Be Normal in These Cases)
  • Severe Thrombocytosis (>500k)
    • Mechanism
      • Due to Potassium Release from Platelets in Sample
        • For Every 100 x 10(9)/L of Platelets, Potassium Increases Approximately 0.07 to 0.15 mmol/L [MEDLINE]
    • Clinical
      • Plasma, Rather than Serum, Potassium Should Be Measured (Plasma Potassium Will Be Normal in These Cases)

Excessive Potassium Intake

  • Excessive Oral/Intravenous Potassium Chloride Intake or Administration
    • Epidemiology
      • Associated with Oral/Intravenous Potassium Chloride Administration (see Potassium Chloride)
      • Associated with Excessive Oral Salt Substitute Intake
        • Usually Causes Hyperkalemia Only in the Setting of Impaired Renal Function
      • Associated with Intravenous Total Parenteral Nutriton (TPN) Administration (see Total Parenteral Nutriton)
    • Mechanism
      • Excessive Potassium Content (Relative to the Patient’s Renal Function)
      • May Be Patient-Related (in the Outpatient Setting) or Iatrogenic (in the Inpatient Setting)
  • Lethal Injection
    • Mechanism
      • Capital Punishment Technique Uses Lethal Injection of Potassium Chloride

Intracellular to Extracellular Potassium Shift

Impaired Renal Potassium Excretion

Decreased Distal Potassium Delivery

Renal Disease

  • Acute Kidney Injury (AKI) (see Acute Kidney Injury)
  • Chronic Kidney Disease (CKD) (see Chronic Kidney Disease)
  • A nomogram to identify hyperkalemia risk in patients with advanced chronic kidney disease. Kidney360 September 2022. doi:10.34067/KID.0004752022 [MEDLINE]

Hypoaldosteronism (see Hypoaldosteronism)

Decreased Aldosterone Synthesis
  • Inherited Disorders
    • Congenital Isolated Hypoaldosteronism
      • 21 Hydroxylase Deficiency
      • Other Defects
    • Pseudohypoaldosteronism Type 2 (Gordon’s Syndrome)
      • Physiology
        • Defects in WKNK1 or WNK4 Kinases
      • Clinical
        • Familial Hypertension (see Hypertension)
        • Hyperkalemia (see Hyperkalemia)
        • Low or Low-Normal Plasma Renin Activity and Aldosterone Level
        • Metabolic Acidosis
        • Normal Renal Function
  • Hyporeninemic Hypoaldosteronism
    • General Comments
      • Hyporeninemic Hypoaldosteronism is Characterized by a Combination of Decreased Renin Release and an Intra-Adrenal Defect, Resulting in Decreased Systemic and Intra-Adrenal Angiotensin II Synthesis, Culminating in Decreased Aldosterone Secretion
        • The Intra-Adrenal Defect May Be Related to the Local Renin-Angiotensin System (This is Supported by the Fact that Angiotensin II Produced Locally Within the Adrenal Gland May Stimulate the Release of Aldosterone)
        • Many of These Patients May Also Have Decreased Aldosterone Responsiveness, Since They Require a Higher Mineralocorticoid Dose for Physiologic Replacement
    • Advanced Age
    • Drug-Induced Hyporeninemic Hypoaldosteronism
      • β-Blockers (see β-Adrenergic Receptor Antagonists)
      • Calcineurin Inhibitors (see Calcineurin Inhibitors)
        • Pharmacology
        • Due to Decreased Secretion of Aldosterone and decreased responsiveness to aldosterone (likely due to decreased mineralocorticoid receptor expression)
        • Cyclosporine A (see Cyclosporine A)
        • Tacrolimus (see Tacrolimus)
      • Nonsteroidal Anti-Inflammatory Drugs (NSAID’s) (see Nonsteroidal Anti-Inflammatory Drug)
        • Pharmacology
        • Dose-Dependent COX-Inhibition, Resulting in Decreased Renal Prostaglandin Synthesis (Since PGI2 Stimulates the Juxtaglomerular Cells in the Kidney to Release Renin, This Results in Decreased Renal Renin Secretion)
        • Additionally, Impaired Angiotensin II-Induced Release of Aldosterone May Occur
        • NSAID-Induced Decrease in Glomerular Filtration Rate May Also Contribute to the Development of Hyperkalemia
    • Intrinsic Renal Disease
      • Acute Glomerulonephritis with Volume Expansion (see Acute Glomerulonephritis)
        • Treatment: responds to mineralocorticoid replacement
        • Prognosis: recovery of renal function (typically within 1-2 wks) leads to resolution of hyperkalemia
      • Chronic Kidney Disease (CKD) (see Chronic Kidney Disease): with chronic interstitial nephritis
      • Diabetic Nephropathy (see Diabetes Mellitus): accounts for 50% of cases of hyporeninemic hypoaldosteronism
  • Drugs
    • Angiotensin Converting Enzyme (ACE) Inhibitors (see Angiotensin Converting Enzyme Inhibitors)
      • Pharmacology
        • Angiotensin Converting Enzyme Inhibitors Decrease the Conversion of Angiotensin I to Angiotensin II Systemically (and Possibly Within the Adrenal Zona Glomerulosa)
        • Since the Normal Stimulatory Effect of Hyperkalemia on Aldosterone Release May Be Mediated in Part by the Adrenal Generation of Angiotensin II, ACE Inhibitors Can Decrease Both Angiotensin II-Mediated and Potassium-Mediated Aldosterone Release
        • In Contrast to ARB’s and Renin Inhibitors, ACE Inhibitors Increase Renin Levels
      • Examples
    • Angiotensin II Receptor Blockers (ARB’s) (see Angiotensin II Receptor Blockers)
      • Pharmacology
        • Angiotensin II Receptor Blockers Inhibit Angiotensin II Activity at its Receptor
      • Examples
    • Heparins
      • Pharmacology
        • Heparins Have a Direct Toxic Effect on the Adrenal Zona Glomerulosa Cells (This May Be Mediated by a Decrease in the Number and Affinity of Adrenal Angiotensin II Receptors)
        • May Occur Even with the Low Doses of Heparin Used for Deep Venous Thrombosis Prophylaxis
      • Examples
    • Renin Inhibitors
      • Pharmacology
        • Renin Inhibitors Directly Inhibit Renin Activity
      • Examples
        • Aliskiren (Tekturna, Rasilez) (see Aliskiren): renin inhibitor (may cause hyperkalemia when used in combination with ACE inhibitors or ARB’s)
  • Other
    • Severe Illness
      • Physiology
        • Decreased Adrenal Aldosterone Synthesis (Perhaps Complicated by Volume Expansion)
        • Additionally, Stress-Induced ACTH Hypersecretion May Decrease Aldosterone Synthesis by Diverting Substrate to the Synthesis of Cortisol
    • Primary Adrenal Insufficiency (see Adrenal Insufficiency)
      • Physiology
        • Decreased Cortisol and Aldosterone
        • In Contrast, Pituitary Disease Does Not Result in Hypoaldosteronism, Since Corticotropin (ACTH) Does Not Play a Major Role in the Regulation of Aldosterone Release
Aldosterone Resistance
  • Inherited Disorders
    • Pseudohypoaldosteronism Type 1
      • Subtypes
        • Autosomal Recessive Pseudohypoaldosteronism Type 1
        • Autosomal Dominant/Sporadic Pseudohypoaldosteronism Type 1
      • Physiology
        • Resistance to Action of Aldosterone
  • Drugs
    • Aldosterone Antagonists (see Mineralocorticoid Receptor Antagonists)
      • Pharmacology
        • Aldosterone Antagonists Antagonize the Activity of Aldosterone on the Collecting Tubule Cells by Competition for the Aldosterone Receptor
      • Examples
        • Apararenone
        • Canrenone (Contaren, Luvion, Phanurane, Spiroletan) (see Canrenone)
        • Drospirenone (Yasmin, Yasminelle, Yaz, Beyaz, Ocella, Zarah, Angeliq) (see Drospirenone)
        • Synthetic Hormone Used in Oral Contraceptives
        • Eplerenone (Inspra, Epnone, Dosterep) (see Eplerenone)
        • Esaxerenone (Minnebro) (see Esaxerenone)
        • Finerenone (Kerendia) (see Finerenone)
        • Spironolactone (Aldactone) (see Spironolactone)
    • Epithelial Sodium Channel (ENaC) Antagonists (see Epithelial Sodium Channel Antagonists)
      • Pharmacology
        • Epithelial Sodium Channel (ENaC) Antagonists Act to Close Sodium Channels on the Luminal Membrane of Collecting Tubule Cells (Collecting Tubule is the Site of Action of Aldosterone)
      • Examples
  • Tubulointerstitial Renal Disease


Transtubular Potassium Gradient

  • Transtubular K Gradient= (Urine K/Plasm K)/(Urine Osm/Plasma Osm)
    • TTKG>8: normal aldosterone effect
    • TTKG<2: hypoaldo/aldosterone resistance of tubule
    • TTKG Assumes urine Na >20 and Urine Osm >300

Urine Potassium/Sodium Ratio

  • Urine K/Na Ratio = Urine K/Urine Na
    • Ratio <1: impaired aldosterone effect
    • Ratio >1: normal aldosterone effect

Clinical Manifestations

Cardiovascular Manifestations

Atrioventricular Heart Blocks

Sinus Bradycardia (see Sinus Bradycardia)

  • Epidemiology
    • May Occur in Some Cases

Cardiac Arrest (see Cardiac Arrest)

  • Epidemiology
    • May Occur in the Setting of Acute/Severe Hyperkalemia

Electrocardiographic (EKG) Changes

  • Clinical
    • Tall, Peaked T-Waves with Shortened QTc Interval (see xxxx): initial change which is usually noted
    • Widened PR Interval and Widened QRS Duration: seen later
    • Disappearance of P-Wave: may occur
    • QRS Widened to a Sine Wave Pattern: typically a late EKG finding
    • Ventricular Standstill (with Complete Absence of Electrical Activity)/Asystole: latest change

Gastrointestinal Manifestations

Hypoactive Bowel Sounds/Ileus (see Ileus)

  • Epidemiology
    • XXXX

Neurologic Manifestations

Depression (see Depression)

  • Epidemiology
    • XXXX

Fatigue (see Fatigue)

  • Epidemiology
    • XXXX

Hyporeflexia (see Hyporeflexia)

  • Epidemiology
    • XXXX

Muscle Weakness/Flaccid Paralysis (J Neurol Neurosurg Psychiatry, 1998) [MEDLINE]

  • Clinical
    • May Be Severe Enough to Mimic the Symptoms of Guillain-Barré Syndrome
    • Cranial Nerve Function and Sphincter Tone Function are Generally Intact
    • Respiratory Muscle Weakness is Rare

Pulmonary Manifestations

Acute/Chronic Hypoxemic/Hypercapnic Respiratory Failure (see Respiratory Failure)

  • Epidemiology
    • Respiratory Muscle Weakness is Rare (Br J Anaesth, 1993) [MEDLINE]
  • Physiology
    • Due to Respiratory Muscle Weakness

Renal Manifestations

Metabolic Acidosis (in the Setting of Type 4 Renal Tubular Acidosis) (see Metabolic Acidosis-Normal Anion Gap)

  • Epidemiology
    • In Type 4 Renal Tubular Acidosis in Animal Models, Hyperkalemia Decreases Proximal Tubule Ammonia Generation and Collecting Duct Ammonia Transport, Leading to Impaired Ammonia Excretion Which Causes Metabolic Acidosis (J Am Soc Nephrol, 2018) [MEDLINE]


Insulin (see Insulin)

  • Administration
    • UIntravenous: 5-10 U regular insulin + 1 ampule D50
  • Mechanism
    • Drives Potassium into Cells
  • Onset
    • Decreases Potassium by 1-2 within 30-60 min
  • Duration: hours
  • Adverse Effects
    • Hypoglycemia (see Hypoglycemia)
      • Weight-Based Intravenous Insulin Dosing (0.1 U/kg up to maximum of 10 U) for Hyperkalemia Decreases the Risk of Hypoglycemia (J Hosp Med, 2016) [MEDLINE]


  • Agents
  • Indication
    • Fastest Treatment for Cardiac Toxicity (Although it Has No Effect on the Serum Potassium Level)
  • Administration
    • Intravenous: 1 ampule calcium gluconate
  • Mechanism
    • Calcium Counteracts Potassium Effect on Neuromuscular Membranes
  • Onset: immediate
  • Duration: transient

Sodium Bicarbonate (see Sodium Bicarbonate)

  • Indication
    • Useful Even in Absence of Acidosis
  • Administration
    • Intravenous: 1 ampule sodium bicarb
  • Mechanism
    • Drives Potassium into Cells
  • Onset: 1 hr
  • Duration: hours
  • Adverse Effects
    • Possible Increase in Intracellular Calcium, Increasing the Risk of Arrhythmias

Hypertonic (3%) Saline (see Hypertonic Saline)

  • Indication
    • Useful for Cardiac Toxicity in Cases with Coexistent Hyponatremia (Due to Dilution of Plasma Potassium and Antagonism of Neuromuscular Toxicity)
  • Adverse Effects

Kayexelate (Sodium Polystyrene) (see Kayexelate)

  • Pharmacology
    • Sodium Polystyrene Sulfonate Cation Exchange Resin
      • Sodium Ions are Partially Released from the Resin and are Replaced by Potassium Ions
      • This Occurs Mostly in the Colon, Which Excretes Potassium Ions to a Greater Degree than Does the Small Intestine
  • Administration
    • Oral
    • Retention Enema
  • Mechanism
    • Binds Intestinal Potassium, Resulting in Enhanced GI Potassium Excretion
  • Onset: 50 g enema decreases K by 0.5-2.0 mEq within 1 hr
  • Adverse Effects
    • Hypokalemia (see Hypokalemia)
    • Metabolic Alkalosis (see Metabolic Alkalosis): reported when kayexelate has been given in combination with non-absorbable cation-donating antacids and laxatives (such as magnesium hydroxide and aluminum carbonate)

Patiromer (Veltassa) (see Patiromer)

  • Indications
    • FDA-Approved for Hyperkalemia in the Setting of Renin-Angiotensin-Aldosterone System (RAAS) Inhibitors
  • Pharmacology
    • Non-Absorbable Potassium Binder
  • Onset: takes hours-days
  • Administration
    • Oral: XXXX

Sodium Zirconium Cyclosilicate (Lokelma) (see Sodium Zirconium Cyclosilicate)

  • Mechanism
    • xxx
  • Administration
    • xxx
  • Adverse Effects
    • xxx

Albuterol (see Albuterol)

  • Administration
    • Inhaler
    • Nebulizer
  • Mechanism
    • Drives Potassium into Cells
  • Adverse Effects

Management of Hyperkalemia in Cardiorenal Patients on Renin–Angiotensin–Aldosterone System Inhibitors

Recommendations of International Delphi Consensus for Management of Hyperkalemia in Patients with Cardiorenal Syndrome (Eur J Heart Fail, 2022) [MEDLINE]

  • Risk Factors and Risk Stratification for Managing Hyperkalemia in the Setting of Cardiorenal Syndrome
    • Optimizing Renin–Angiotensin–Aldosterone System Inhibitor Therapy Provides Better Patient Outcome
    • Patients with Chronic Kidney Disease, Heart Failure, or Diabetes Mellitus are at Increased Risk of Hyperkalemia
    • Renin–Angiotensin–Aldosterone System Inhibitor Use is a Risk Factor for Hyperkalemia
    • Hyperkalemia Can Be Effectively Managed to Optimize Disease-Modifying Therapies, Which Improve Morbidity, Mortality, and Outcomes
    • New Risk Prediction Tools are Required if Clinicians are to Fully Individualize Risk Assessment for Patients with Cardiorenal Syndrome
    • Managing the Risk of Hyperkalemia Should Be Part of the Individualized Care Plan Already in Place or Planned
    • There is a Need for Consistent Thresholds for Defining and Treating Hyperkalemia Among Sub-Specialties
    • Hyperkalemia is Associated with Down-Titration or Discontinuation of Renin–Angiotensin–Aldosterone System Inhibitor Therapy
    • When Managing mild-to-moderate Hyperkalemia in Cardiorenal Patients, Renin–Angiotensin–Aldosterone System Inhibitors Should Be Maintained Due to the Inherent Benefit in This Patient Population
    • Mild-Moderate Hyperkalemia Should Be Managed without De-Escalating or Discontinuing Renin–Angiotensin–Aldosterone System Inhibitors
    • Hyperkalemia is a Known and Manageable Side Effect of Renin–Angiotensin–Aldosterone System Inhibitor Treatment
    • Hyperkalemia Should Be Recognized as a Predictable, Treatable, and Manageable Side Effect of Optimal Heart Failure/Chronic Kidney Disease Therapy
  • Prevention of Hyperkalemia for At-Risk Cardiorenal Patients
    • For High-Risk Patients Who are Not Currently Hyperkalemic, Preventative Measures Should Be Considered (Removal of Salt Substitutes from the Diet, Considering Diuretics for Patients with Hypertension or Volume Expansion)
    • For Those Patients Who have a Known History of Hyperkalemia Preventing Optimization of Renin–Angiotensin–Aldosterone System Inhibitor Therapy, a Novel Potassium Binder Can Be Used to Enable a Trial of Renin–Angiotensin–Aldosterone System Inhibitor Optimization
    • For High-risk Patients Who are Not Currently Hyperkalemic, the Use of a Novel Potassium Binder Can Be Considered When Starting or Up-Titrating a Renin–Angiotensin–Aldosterone System Inhibitor
    • Non-Disease-Modifying Therapies Which Cause Hyperkalemia (NSAIDs, Amiloride, and Herbal Supplements) Should Be Avoided in Patients at High-Risk of Hyperkalemia
    • Low Potassium Diet is Often Advised to Help Manage Potassium Levels, with No or Little Evidence to Support, and is Counter to a Healthy Diet Which is Beneficial to Cardiorenal Patients
    • In Patients for Whom Dietary Restrictions May Not Be Appropriate or Desirable, the Use of Novel Potassium Binders May Enable a Balanced Diet
    • Patients at Risk for Hyperkalemia Should Be Monitored Closely with a Strategy in Place to Manage Potassium Levels Effectively
  • Correction of Hyperkalemia for At-Risk Cardiorenal Patients with Potassium Lowering Therapy
    • A Reduction in Emergency Department Visits and Unplanned Hospitalizations Due to Complications Associated with Hyperkalemia Should Be a Goal of Good Management
    • A Goal for the Management of High-Risk Cardiorenal Patients Should Be to Utilize the Maximum Recommended Dose of Renin–Angiotensin–Aldosterone System Inhibitor Therapy
    • Renin–Angiotensin–Aldosterone System Inhibitor-Induced Hyperkalemia Should Not Be Considered Intolerance Until Other Strategies to Decrease Potassium Have Been Exhausted
    • De-Escalation or Discontinuation of Renin–Angiotensin–Aldosterone System Inhibitor Therapy is Associated with Worse Cardiovascular and Renal Outcomes in Cardiorenal Patients
    • Permanent Discontinuation of Renin–Angiotensin–Aldosterone System Inhibitor Therapy Should Only Be Considered as a Last Resort Strategy for Chronic Hyperkalemia
    • Hyperkalemia Should No Longer Be Seen as a Barrier to Optimization of Guideline-Directed Therapy
    • Novel Potassium Binders Enable Guideline-Recommended Renin–Angiotensin–Aldosterone System Inhibitor Dosing and the Proven Clinical Benefits
    • Use of Novel Potassium Binders in Patients with Mild Hyperkalemia Can Enable Guideline-Recommended Doses of Renin–Angiotensin–Aldosterone System Inhibitor Therapy
    • Renin–Angiotensin–Aldosterone System Inhibitor Use Should Not Be De-Escalated or Discontinued Due to Hyperkalemia Unless Alternative Measures of Hyperkalemia Management Have Been Optimized (Including the Initiation of POtassium Binder Therapy)
    • Novel Potassium Binders can enable optimization of Renin–Angiotensin–Aldosterone System Inhibitor therapy in a similar way that antiemetics can enable optimization of chemotherapy
    • Novel Potassium Binders Should Not Need to Demonstrate a Mortality Benefit
      • They Enable Renin–Angiotensin–Aldosterone System Inhibitor Therapy, Which Have an Already Proven Mortality Benefit
    • The Use of Sodium Polystyrene Sulfonate Should Be Avoided Due to Concerns with Gastrointestinal Toxicity, Low Compliance Due to Poor Palatability, and is Only Indicated in Severely Oliguric or Anuric Patients
    • Sodium Polystyrene Sulfonate Should Not Be Used in the Medium or Long-Term as it May Cause Severe Gastrointestinal Side Effects (Including Bowel Necrosis)
  • Cross-Specialty Alignment of Cardiology and Nephrology
    • Patients with Cardiorenal Comorbidities Should Be Managed by a Multidisciplinary Team with an Shared Management Plan
    • Cross-Specialty Alignment Can Enable Optimal Doses of Renin–Angiotensin–Aldosterone System Inhibitors to Be Maintained
    • Cross-Specialty Management Improves Patient Satisfaction, Patient Outcomes, and Quality of Life
    • Cross-Specialty Management is a Good Use of Resources and Should Improve Patient Outcomes
    • Enhanced Communication Between Interdisciplinary Teams Could Improve Patient Outcomes
    • Cardiology and Nephrology Guidelines Should Contain Consistent Recommendations for the Management of Hyperkalemia
    • Collaborative Care and Evidence-Based Decision Making (Based on Guidelines and Expert Consensus) is an Example of Best Practice and Patient-Centered Care
  • Hyperkalemia Should Be Recognized as a Predictable, Treatable, and Manageable Side Effect of Optimal Heart Failure/Chronic Kidney Disease Therapy in People with a History or at High-Risk of Hyperkalemia
  • Renin–Angiotensin–Aldosterone System Inhibitors Use Should Not Be De-Escalated or Discontinued Due to Hyperkalemia Unless Alternative Measures of Hyperkalemia Management Have Been Optimized
  • Novel Potassium Binders Should Be the Preferred Agent to Manage Hyperkalemia, and Should Be Used to Enable and Maintain Optimized Renin–Angiotensin–Aldosterone System Inhibitors Therapy
  • For High-Risk Individuals Who are Currently Not Hyperkalemic, a Thorough History is Critical to Inform Preventative Measures
  • Closer Cross-Specialty Collaboration Would Help Optimize Outcomes for Individuals with Cardiorenal Disease
    • Clinical Teams Should Be Encouraged and Supported to Identify Suitable Methods to Achieve This within Their Care Setting
  • Consistent Treatment Approach Should Be the Goal of New and Updated Guidelines Which Support People with Cardiorenal Disease, and Cross-Specialty Support Should Be Sought for These to Ensure Aligned Clinical Practice
  • Methods to Manage Hyperkalemia
    • Loop and Thiazide Diuretics Can Be Used to Increase Potassium Excretion by Increasing the Delivery of Sodium to the Collecting Ducts
      • Diuretics are Recommended for Use in Treating Mild-Moderate Hyperkalemia in Individuals with Adequate Renal Function
      • Diuretics Also Have Utility in Those with Hyperkalemia and Concomitant Volume Overload or Hypertension
    • Oral Sodium Bicarbonate May Be Considered in Patients with Hyperkalemia and Metabolic Acidosis, Particularly in Those with a Serum Bicarbonate Level of <22 mmol/L, But it is Important to Consider Sodium Load, Particularly in Those at Risk of Fluid Overload
      • In Those at Risk of Fluid Overload, Concurrent Diuretic Use Should Be Considered
    • Two Novel Potassium Binders Have Recently Been Developed, Patiromer (Veltassa) and Sodium Zirconium Cyclosilicate (Lokelma)
      • Both Have Demonstrated Efficacy, and the European Society of Cardiology Heart Failure guidelines (2021) and the Kidney Disease: Improving Global Outcomes (KDIGO) Guidelines for Managing Diabetes in Chronic Kidney Disease (2020) and for Managing Blood Pressure in Chronic Kidney Disease (2021) Recommend Their Use for the Treatment of Renin–Angiotensin–Aldosterone System Inhibitor-Associated Hyperkalemia
  • Sodium Polystyrene Sulfonate Has Traditionally Been Used to Treat Hyperkalemia, But There are Questions Regarding the Safety and Efficacy of This Agent