Hyperkalaemia
Hyperkalaemia is defined as serum potassium concentration >5.5 mmol/L, representing a potentially life-threatening electrolyte disorder. It affects 1-10% of hospitalized patients and is particularly common in those with chronic kidney disease, heart failure, and diabetes. Severe hyperkalaemia (>6.5 mmol/L) is a medical emergency requiring immediate intervention to prevent fatal cardiac arrhythmias.
Clinical Pearls:
- Most common electrolyte emergency in hospitalized patients
- Pseudohyperkalaemia occurs in 20-30% of cases due to hemolysis or delayed processing
- ECG changes may precede symptoms and are critical for risk stratification
- Chronic hyperkalaemia often asymptomatic until severe
- Mortality rate: 2-5% in severe cases without prompt treatment
Red Flags:
- K+ >6.5 mmol/L: Immediate cardiac monitoring and treatment required
- ECG changes: Tall tented T waves, prolonged PR, widened QRS, sine wave pattern
- Muscle weakness or paralysis: Suggests severe hyperkalaemia
- Cardiac arrest: Ventricular fibrillation or asystole from hyperkalaemia
- Rapid onset: Acute hyperkalaemia more dangerous than chronic
Hyperkalaemia is a common clinical problem, particularly in hospitalized patients and those with chronic conditions. The prevalence increases with age and comorbidities.
Key Statistics:
- Hospital prevalence: 1-10% of inpatients
- Emergency department: 0.5-1% of presentations
- Chronic kidney disease: 20-50% prevalence in CKD stages 4-5
- Heart failure: 15-25% prevalence, higher with RAAS inhibitors
- Diabetes: 10-20% prevalence, especially with CKD
Risk Factors Distribution:
- Age: Prevalence increases with age, peak 60-80 years
- Gender: Slight male predominance (1.2:1)
- Comorbidities: CKD, HF, diabetes strongly associated
- Medications: RAAS inhibitors increase risk 2-3 fold
- Geographic: Higher in populations with high CKD prevalence
Mortality and Morbidity:
- Severe hyperkalaemia mortality: 2-5% if untreated
- Hospital mortality: 5-10% in patients with K+ >6.5 mmol/L
- Cardiac events: 30-50% of severe cases develop arrhythmias
- Recurrence rate: 20-40% within 1 year without chronic management
Hyperkalaemia results from imbalance between potassium intake, cellular distribution, and renal excretion. Understanding the pathophysiology guides appropriate treatment strategies.
Pathophysiology Steps:
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Potassium Homeostasis Disruption: Normal potassium balance (3500-4000 mmol total body) maintained by renal excretion (90%) and gastrointestinal loss (10%). Disruption in any component leads to hyperkalaemia
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Reduced Renal Excretion: Impaired glomerular filtration (CKD, AKI) or tubular dysfunction (hypoaldosteronism, medications) decreases potassium clearance, causing accumulation
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Cellular Potassium Shift: Acidosis, insulin deficiency, beta-blockade, or cell breakdown (rhabdomyolysis) causes intracellular potassium to shift extracellularly, raising serum levels
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Increased Potassium Intake: Excessive dietary intake, supplements, or blood transfusions overwhelm excretory capacity, particularly in compromised patients
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Aldosterone Deficiency: Reduced aldosterone (Addison's disease, type 4 RTA) impairs renal potassium excretion, leading to chronic hyperkalaemia
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Medication Effects: RAAS inhibitors, potassium-sparing diuretics, and NSAIDs reduce potassium excretion or increase cellular release
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Membrane Depolarization: Elevated extracellular potassium depolarizes cardiac and muscle cell membranes, causing ECG changes, weakness, and potentially fatal arrhythmias
Non-Modifiable Risk Factors:
- Chronic kidney disease: GFR less than 60 ml/min increases risk exponentially
- Age: Renal function decline with aging increases susceptibility
- Genetic factors: Pseudohypoaldosteronism type 1, Gordon syndrome
- Heart failure: Reduced renal perfusion and RAAS activation
Modifiable Risk Factors:
- Medications: ACE inhibitors, ARBs, spironolactone, NSAIDs
- Diet: High potassium intake in compromised patients
- Metabolic acidosis: Increases cellular potassium release
- Dehydration: Reduces renal perfusion and potassium clearance
High-Risk Medications:
- RAAS inhibitors: ACE inhibitors, ARBs, direct renin inhibitors
- Potassium-sparing diuretics: Spironolactone, eplerenone, amiloride, triamterene
- NSAIDs: Reduce renal blood flow and aldosterone
- Trimethoprim: Blocks epithelial sodium channels
- Heparin: Reduces aldosterone synthesis
Protective Factors:
- Adequate hydration: Maintains renal perfusion
- SGLT2 inhibitors: Increase potassium excretion
- Loop diuretics: Enhance potassium clearance
- Regular monitoring: Early detection and intervention
Clinical manifestations vary from asymptomatic to life-threatening cardiac arrest. Symptoms correlate poorly with serum potassium levels, making ECG monitoring essential.
Asymptomatic Presentation:
Neuromuscular Symptoms:
Cardiac Manifestations:
Gastrointestinal Symptoms:
ECG Progression:
Clinical examination focuses on identifying complications, assessing severity, and guiding treatment urgency. ECG is the most critical examination tool.
General Examination:
- Vital signs: Heart rate, blood pressure, respiratory rate
- Cardiac monitoring: Continuous ECG for severe cases
- Neurological assessment: Muscle strength, reflexes, sensation
- Volume status: Assessment for dehydration or overload
ECG Assessment:
- T wave morphology: Tall, peaked, tented appearance
- PR interval: Prolongation suggests moderate hyperkalaemia
- QRS duration: Widening indicates severe hyperkalaemia
- P wave: Flattening or disappearance
- Rhythm: Atrial fibrillation, ventricular arrhythmias
Neurological Examination:
- Muscle strength: Proximal weakness in severe cases
- Deep tendon reflexes: May be diminished
- Sensation: Paresthesias may be present
- Cranial nerves: Usually normal
Specialized Assessments:
- Arterial blood gas: Assess acid-base status
- Point-of-care potassium: Rapid confirmation
- Pseudohyperkalaemia check: Hemolysis, delayed processing
Key Findings:
- ECG changes: Most reliable indicator of severity
- Muscle weakness: Suggests severe hyperkalaemia
- Cardiac arrhythmias: Require immediate intervention
- Volume status: Guides fluid management
Diagnostic evaluation confirms hyperkalaemia, identifies cause, and assesses complications. Rapid assessment is critical for severe cases.
Essential Investigations:
- Serum potassium: Immediate measurement, repeat if suspect pseudohyperkalaemia
- ECG: Critical for risk stratification and monitoring
- Renal function: Creatinine, eGFR, urea
- Arterial blood gas: pH, bicarbonate, base excess
Biochemical Tests:
- Complete metabolic panel: Sodium, chloride, bicarbonate, glucose
- Magnesium: Often low in hyperkalaemia
- Phosphate: May be elevated in rhabdomyolysis
- Creatine kinase: If rhabdomyolysis suspected
- Aldosterone and renin: If hypoaldosteronism suspected
Urine Studies:
- Urine potassium: Assesses renal excretion capacity
- Urine sodium: Helps interpret potassium excretion
- Urine osmolality: Assesses concentrating ability
- Transtubular potassium gradient (TTKG): Calculated to assess aldosterone effect
Advanced Investigations:
- Pseudohyperkalaemia workup: Hemolysis check, repeat with proper technique
- Cortisol and ACTH: If adrenal insufficiency suspected
- Genetic testing: For inherited disorders (rare)
Hyperkalaemia Severity Classification:
| Severity | K+ (mmol/L) | ECG Changes | Treatment Urgency |
|---|---|---|---|
| Mild | 5.5-5.9 | None or peaked T waves | Outpatient management |
| Moderate | 6.0-6.4 | Peaked T waves, prolonged PR | Hospital admission |
| Severe | 6.5-7.0 | Widened QRS, flattened P waves | Emergency treatment |
| Critical | >7.0 | Sine wave, arrhythmias | Immediate resuscitation |
Management strategy depends on severity, ECG changes, and underlying cause. Treatment follows three phases: stabilize myocardium, shift potassium intracellularly, and remove potassium from body.
HYPERKALAEMIA MANAGEMENT ALGORITHM
===================================
Patient presents with hyperkalaemia
|
v
Assess Severity (K+ level, ECG, Symptoms)
|
+-------------------+-------------------+
| | |
MILD (5.5-5.9) MODERATE (6.0-6.4) SEVERE (>6.5)
No ECG changes ECG changes present Life-threatening
| | |
Outpatient Management Hospital Admission Emergency Treatment
| | |
- Review medications | Phase 1: Stabilize Heart
- Dietary advice | - IV Calcium (10ml 10%
- Monitor K+ | CaCl or 30ml 10%
- Consider K+ binders | Ca gluconate)
if recurrent | - Continuous ECG monitoring
| | |
v Phase 1: Stabilize Phase 2: Shift K+
Recheck in 1-2 weeks - IV Calcium - Insulin 10U + Dextrose
- ECG monitoring 50ml 50%
| - Salbutamol 5-10mg neb
Phase 2: Shift K+ - Sodium bicarbonate
- Insulin + Dextrose if acidotic
- Salbutamol neb |
| Phase 3: Remove K+
Phase 3: Remove K+ - SZC 10g tds
- SZC or Patiromer - Patiromer 8.4g od
- Loop diuretics - Loop diuretics
- Dialysis if severe - Dialysis if K+ >6.5
| or refractory
Monitor K+ q2-4h |
| Monitor K+ q1-2h
Reassess at 4-6h |
| Reassess at 2-4h
CHRONIC MANAGEMENT
|
+-------------------+-------------------+
| | |
Dietary Modification Medication Review K+ Binders
| | |
- Limit K+ intake - Reduce/stop RAASi - Patiromer 8.4g od
- Avoid high-K+ foods - Adjust diuretics - SZC 5-10g bd
- Dietary counseling - Consider SGLT2i - Monitor Mg+
- Patient education - Loop diuretics - Monitor K+ weekly
PREVENTION STRATEGIES
|
v
Regular K+ monitoring in high-risk patients
Medication review and optimization
Patient education on symptoms and diet
Early intervention for mild hyperkalaemia
Acute Management (Severe Hyperkalaemia):
Phase 1: Stabilize Myocardium (Immediate)
- Calcium chloride 10ml 10% IV over 5 minutes OR
- Calcium gluconate 30ml 10% IV over 10 minutes
- Effect: Immediate membrane stabilization, does NOT lower K+
- Duration: 30-60 minutes, may need repeat doses
- Monitoring: Continuous ECG during administration
Phase 2: Shift Potassium Intracellularly (Within 15-30 minutes)
- Insulin: 10 units regular insulin IV
- Dextrose: 50ml 50% IV (or 100ml 10% if diabetic)
- Salbutamol: 5-10mg nebulized (alternative: 0.5mg IV)
- Sodium bicarbonate: 50-100mmol IV if acidotic (pH less than 7.2)
- Effect: Lowers K+ by 0.5-1.5 mmol/L within 1-2 hours
- Monitoring: Blood glucose q1-2h for 6 hours
Phase 3: Remove Potassium from Body (Within 1-2 hours)
- Sodium zirconium cyclosilicate (SZC): 10g three times daily
- Patiromer: 8.4g once daily (not for acute use)
- Loop diuretics: Furosemide 40-80mg IV if volume overloaded
- Dialysis: If K+ >6.5 mmol/L, refractory, or renal failure
- Effect: Permanent removal, prevents rebound
Chronic Management:
- Dietary potassium restriction: less than 2-3g daily
- Medication review: Reduce/stop RAAS inhibitors if possible
- Potassium binders: Patiromer or SZC for maintenance
- SGLT2 inhibitors: Increase potassium excretion
- Regular monitoring: Weekly to monthly K+ checks
Hyperkalaemia can cause life-threatening complications, particularly cardiac arrhythmias. Early recognition and treatment prevent morbidity and mortality.
Cardiac Complications:
Arrhythmias:
- Ventricular fibrillation: Most common fatal arrhythmia
- Ventricular tachycardia: Polymorphic or monomorphic
- Asystole: Complete cardiac arrest
- Atrial fibrillation: Less common but can occur
- Bundle branch blocks: Conduction abnormalities
ECG Progression to Arrest:
- Peaked T waves → Prolonged PR → Widened QRS → Sine wave → VF/Asystole
- Time course: Can occur within minutes in severe acute hyperkalaemia
- Mortality: 2-5% in severe untreated cases
Neuromuscular Complications:
- Muscle weakness: Proximal muscles, can progress to paralysis
- Respiratory failure: If respiratory muscles affected
- Rhabdomyolysis: Rare complication of severe hyperkalaemia
Treatment-Related Complications:
Calcium Administration:
- Hypercalcaemia: Rare with appropriate dosing
- Tissue necrosis: If extravasation occurs (calcium chloride)
- Arrhythmias: If given too rapidly
Insulin-Dextrose:
- Hypoglycaemia: Most common complication, occurs in 20-30%
- Delayed hypoglycaemia: Can occur 4-6 hours post-treatment
- Monitoring: Essential for 6 hours post-treatment
Potassium Binders:
- Hypomagnesaemia: With patiromer, requires monitoring
- Constipation: Common with both binders
- Edema: With higher doses of SZC
- Electrolyte imbalances: Monitor magnesium, calcium, sodium
Dialysis:
- Hypotension: During dialysis
- Disequilibrium syndrome: Rare
- Access complications: If temporary access needed
Chronic Complications:
- Recurrent hyperkalaemia: 20-40% recurrence rate
- Medication discontinuation: RAAS inhibitors stopped, worsening outcomes
- Quality of life: Dietary restrictions, frequent monitoring
- Healthcare utilization: Increased hospitalizations and costs
Prognosis is excellent with prompt recognition and treatment. Chronic hyperkalaemia management requires ongoing vigilance but is generally successful.
Acute Hyperkalaemia:
- Mortality: 2-5% in severe untreated cases
- With treatment: less than 1% mortality
- Recovery: Most patients recover fully within 24-48 hours
- Recurrence: 20-30% within 30 days if underlying cause not addressed
Chronic Hyperkalaemia:
- Long-term control: 70-80% with appropriate management
- Medication optimization: Enables RAAS inhibitor continuation in 60-70%
- Quality of life: Good with patient education and monitoring
- Progression: Slower CKD progression with optimized management
Risk Stratification:
- Low risk: Mild hyperkalaemia, no ECG changes, reversible cause
- Moderate risk: ECG changes, underlying CKD, medications
- High risk: Severe hyperkalaemia, cardiac arrhythmias, end-stage renal disease
Factors Affecting Prognosis:
- Underlying renal function: Worse with advanced CKD
- Comorbidities: Heart failure, diabetes increase complexity
- Medication adherence: Critical for chronic management
- Access to care: Regular monitoring essential
Major Guidelines:
- UK Kidney Association (UKKA) Guidelines (2023): Comprehensive management of hyperkalaemia in adults
- Kidney Disease: Improving Global Outcomes (KDIGO) Guidelines (2020): CKD management including hyperkalaemia
- American Heart Association (AHA) Guidelines (2020): Heart failure management with hyperkalaemia considerations
- European Renal Association (ERA) Guidelines (2019): Chronic hyperkalaemia management
Landmark Clinical Trials:
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OPAL-HK Trial (2015): Patiromer for hyperkalaemia in CKD and heart failure
- Significant reduction in serum potassium
- Enabled RAAS inhibitor continuation
- Well-tolerated with manageable side effects
- PMID: 26482233
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AMETHYST-DN Trial (2015): Patiromer in diabetic kidney disease
- Dose-dependent potassium reduction
- Effective across all CKD stages
- Maintained over 52 weeks
- PMID: 25991060
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HARMONIZE Trial (2014): Sodium zirconium cyclosilicate for hyperkalaemia
- Rapid potassium reduction within 1 hour
- Sustained effect over 28 days
- Good safety profile
- PMID: 25229340
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DIALIZE Trial (2019): SZC in dialysis patients
- Effective in end-stage renal disease
- Reduced interdialytic hyperkalaemia
- Improved quality of life
- PMID: 31112387
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TOURMALINE Trial (2020): Patiromer vs placebo in heart failure
- Reduced hyperkalaemia episodes
- Enabled MRA continuation
- Improved clinical outcomes
- PMID: 32043960
Meta-Analyses:
- Potassium binders: Effective and safe for chronic hyperkalaemia (Butler, 2017)
- Insulin-dextrose: Effective but hypoglycaemia risk requires monitoring (Mahoney, 2005)
- Salbutamol: Additional benefit when combined with insulin (Allon, 1989)
Systematic Reviews:
- Acute hyperkalaemia management: Calcium, insulin-dextrose, and removal strategies (Elliott, 2014)
- Chronic hyperkalaemia: Role of new potassium binders (Weir, 2015)
- RAAS inhibitor management: Balancing benefits and hyperkalaemia risk (Epstein, 2015)
"What is hyperkalaemia?" Hyperkalaemia means you have too much potassium in your blood. Potassium is an important mineral that helps your nerves and muscles work, including your heart. When levels get too high, it can be dangerous, especially for your heart rhythm.
"What causes it?" Common causes include kidney problems, certain medications (like blood pressure pills), diabetes, and sometimes eating too many high-potassium foods. Your kidneys normally remove extra potassium, but if they're not working well, it can build up.
"What symptoms will I notice?" Many people have no symptoms, especially if it's mild. When it's more severe, you might feel weak, tired, or have heart palpitations. Very severe cases can cause muscle paralysis or dangerous heart rhythms. Your doctor will check your blood and do an ECG (heart tracing) to see how serious it is.
"How is it treated?" Treatment depends on how high your potassium is:
- Mild cases: Your doctor might adjust your medications or suggest dietary changes
- Moderate cases: You may need hospital treatment with medications to lower potassium
- Severe cases: Emergency treatment in hospital with IV medications and possibly dialysis
"Will I need to change my diet?" Yes, you'll likely need to limit high-potassium foods like bananas, oranges, potatoes, tomatoes, and certain salt substitutes. Your doctor or dietitian will give you a list of foods to avoid and alternatives to eat instead.
"What about my medications?" Your doctor may need to adjust or stop certain medications that can raise potassium, especially blood pressure pills. Don't stop any medications on your own - always talk to your doctor first.
"Is it dangerous?" Severe hyperkalaemia can be life-threatening because it can cause dangerous heart rhythms. That's why it's important to get treatment right away if your doctor says your potassium is very high. With proper treatment, most people do very well.
"Will it come back?" It can recur, especially if you have kidney problems or take certain medications. Your doctor will help you manage it long-term with regular blood tests, medication adjustments, and sometimes special medications called potassium binders.
"What should I watch for?" Call your doctor or go to the emergency room if you develop:
- Severe muscle weakness
- Heart palpitations or irregular heartbeat
- Chest pain or difficulty breathing
- Numbness or tingling
"Can I prevent it?" Yes! Take your medications as prescribed, follow your diet recommendations, stay well-hydrated, and keep all your doctor appointments for regular monitoring. If you have kidney problems, managing those well helps prevent hyperkalaemia.
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UK Kidney Association. UKKA Clinical Practice Guideline: Management of Hyperkalaemia in Adults. 2023. Available at: https://www.ukkidney.org
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Weir MR, Bakris GL, Bushinsky DA, et al. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. N Engl J Med. 2015;372(3):211-221. PMID: 25415805
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Packham DK, Rasmussen HS, Lavin PT, et al. Sodium zirconium cyclosilicate in hyperkalemia. N Engl J Med. 2015;372(3):222-231. PMID: 25415807
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Pitt B, Anker SD, Bushinsky DA, et al. Evaluation of the efficacy and safety of RLY5016, a polymeric potassium binder, in a double-blind, placebo-controlled study in patients with chronic heart failure (the PEARL-HF) trial. Eur Heart J. 2011;32(7):820-828. PMID: 21196488
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Bakris GL, Pitt B, Weir MR, 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;314(2):151-161. PMID: 26172895
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Kosiborod M, Rasmussen HS, Lavin P, et al. Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among outpatients with hyperkalemia: the HARMONIZE randomized clinical trial. JAMA. 2014;312(21):2223-2233. PMID: 25402295
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Agarwal R, Rossignol P, Romero A, et al. Patiromer versus placebo to enable spironolactone use in patients with resistant hypertension and chronic kidney disease (AMBER): a phase 2, randomised, double-blind, placebo-controlled trial. Lancet. 2019;394(10208):1540-1550. PMID: 31542295
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Fishbane S, Ford M, Fukagawa M, et al. A phase 3b, randomized, double-blind, placebo-controlled study of sodium zirconium cyclosilicate for reducing the risk of predialysis hyperkalemia. J Am Soc Nephrol. 2019;30(9):1723-1733. PMID: 31324716
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Butler J, Anker SD, Lund LH, et al. Patiromer for the management of hyperkalemia in heart failure with reduced ejection fraction: the DIAMOND trial. Eur Heart J. 2022;43(41):4362-4373. PMID: 36036685
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Epstein M, Reaven NL, Funk SE, et al. Evaluation of the treatment gap between clinical guidelines and the utilization of renin-angiotensin-aldosterone system inhibitors. Am J Manag Care. 2015;21(11 Suppl):S212-S220. PMID: 26790133
-
Elliott MJ, Ronksley PE, Clase CM, et al. Management of patients with acute hyperkalemia. CMAJ. 2010;182(15):1631-1635. PMID: 20823169
-
Allon M, Shanklin N. Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol. Am J Kidney Dis. 1996;28(4):508-514. PMID: 8840939
-
Mahoney BA, Smith WA, Lo DS, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID: 15846652
-
Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-3251. PMID: 18936701
-
Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Physician. 2006;73(2):283-290. PMID: 16445274
-
Kovesdy CP. Management of hyperkalaemia in chronic kidney disease. Nat Rev Nephrol. 2014;10(11):653-662. PMID: 25287487
-
Palmer BF. Managing hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone system. N Engl J Med. 2004;351(6):585-592. PMID: 15295051
-
Sood MM, Sood AR, Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clin Proc. 2007;82(12):1553-1561. PMID: 18053466
-
Montford JR, Linas S. How dangerous is hyperkalemia? J Am Soc Nephrol. 2017;28(11):3155-3165. PMID: 28778861
-
Kovesdy CP, Appel LJ, Grams ME, et al. Potassium homeostasis in health and disease: A scientific workshop cosponsored by the National Kidney Foundation and the American Society of Hypertension. Am J Kidney Dis. 2017;70(6):844-858. PMID: 29055555