Hyperkalemia in CKD

Core IM

Join the hosts as they offer guidance on the diagnostic evaluation and initial management of hyperkalemia in CKD including guidelines for outpatient referrals in urgent management. In this episode of Core IM, the team will discuss this scenario and pearls that will lead to clinical practice improvement for a better understanding of Hyperkalemia in CKD.

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1. Referral for urgent management of hyperkalemia

  • Current guidelines suggest that the following outpatients should be referred for urgent management
    • K+ > 6.0 mEq/L with OR without ECG changes 
    • Anyone with hyperkalemia and documented EKG changes 
  • However, there is no consensus on these recommendations and many clinicians manage hyperkalemia in the outpatient setting differently (especially with hyperkalemia < 6.0 mEq/L)

2. Hyperkalemia and ECG changes

  • A retrospective chart review of about 90 patients admitted with severe hyperkalemia (K+ > 6 mEq/L (most patients had K+ < 7.2 mEq/L), who also received an ECG. 
    • Only 52% had ECG changes.  
    • Study authors could not identify a threshold at which you would see an EKG change.  
  • Recent retrospective study from 2019 compared ECG findings of 3 cohorts - K+ < 5.1 mEq/L (normokalemia), K+ between 6 and 7 mEq/L (moderate hyperkalemia), and K+ > 7.0 mEq/L (severe hyperkalemia)
    • No significant difference in the frequency of ECG changes were found between the normokalemia and moderate hyperkalemia group
    • More than half of all the hyperkalemic patients, including severe hyperkalemia, did NOT have any ECG changes.  

Take-home point: ECGs are not sensitive at all in the detection of hyperkalemia.  The absence OR presence of EKG changes does not predict the presence of hyperkalemia.

  • Case report from Japan presents a patient with an initial K+ of 8.5 mEq/L and a normal ECG
    • Returned <1 week later with recurrent K+ to 8.6 mEq/L. 
    • ECG now shows a sine wave pattern
  • No consensus or solid data on what “chronic” hyperkalemia means, with respect to how high or how long a patient needs to have it

Take-home point: The abrupt change from normokalemia to severe hyperkalemia, not necessarily the K+ level itself, is most worrisome and needs to be treated.

3. Pseudo-hyperkalemia

  • Conditions that lead to pseudo-hyperkalemia, the in vitro release of intracellular K+
    • Excessive tourniquet use
    • Fist clenching
    • Vein trauma from multiple phlebotomy attempts 
    • PICC/central line draws
    • Use of serum separator tube (clot activators) - commonly used to measure the “basic metabolic panel” 
  • Sending a whole blood sample, sent to the lab in an anticoagulated tube, is the most reliable way to get an accurate potassium reading

4. K+ restricted diets

  • Taking a detailed dietary history helps guide management
    • Common high K+ foods (“restriction” = < 2 g per day)
      • Fruits - oranges, mangoes, avocadoes, melon, prunes, raisins, dates
      • All types of potatoes, including yuca and yams   
      • Common side dishes, sauces, and snacks - tomatoes and tomato sauce, spinach, beans, lentils
      • Salt substitutes often contain potassium chloride (KCl)
    • Pro-tips for avoid complete K+ elimination from the diet include:
      • Focus on moderation and portion size rather complete elimination
      • Leach K+ from potatoes
      • Drain liquids from cooked fruits, vegetables, and meats
  • High K+ diets have been linked to better blood pressure control and improved cardiovascular mortality in patients with hypertension
    • K+-rich diets also have high amounts of alkali, which counteract the metabolic acidosis of CKD

Low K+ diet results in increased Na+ reabsorption, and worsening blood pressure control 

Take-home point: Complete elimination of K+ from the diet is not advisable.  High K+ foods should be consumed in moderation, as they provide significant cardiovascular health benefits, especially for those with CKD.

5. Key medications that can cause hyperkalemia

  • RAASi improve mortality, but are often the first medications to be discontinued when hyperkalemia is detected
  • Difficult to predict how much the K+ will improve with stopping a RAASi
    • Opposing driving forces for each individual’s potassium balance
      • Diabetes and lower baseline estimated GFR have higher propensity for high K+
        • Lack of insulin OR increased insulin resistance lead to a less robust insulin surge with meals (and less intracellular potassium shift)
        • Common etiology of hyporeninemic hypoaldosteronism  

NSAIDS and antibiotics are common medication offenders in hyperkalemia

  • NSAIDs (and beta blockers) decrease renin release (and less RAAS activation), with decreased K+ excretion
  • Antibiotics - the TMP component of TMP-SMX blocks potassium excretion in the collecting duct of the nephron

6. Treating outpatient hyperkalemia

  • Sodium polystyrene sulfonate (SPS, a.k.a Kayexalate)
    • Most of the data on SPS is retrospective, without any RCTs
    • Retrospective cohort study of 1.8 million patients over age 66 
    • SPS users had 2x higher rates of GI events vs. controls
      • GI events = intestinal ischemia, thrombosis, ulceration, perforation, resection, or ostomy creation
    • Adverse effects more common with pre-existing or active GI conditions
    • Most patients find SPS difficult to drink, as it tastes disgusting
  • Patiromer 
    • Gemstone trials - AMETHYST, OPAL-HK, and AMBER
      • Patiromer is effective at lowering K to more manageable levels 
      • High proportions of patients were able to stay on their RAASi 
      • Main side effects were hypomagnesemia and constipation, both reversible and manageable
  • Sodium zirconium cyclosilicate, SZC
    • Influential trials include HARMONIZE and ENERGIZE
    • The NEJM study in 2015 showed that 1 dose of SZC has a rapid onset, with normokalemia achieved in an average time of 2.2 hours 
    • Main side effect = occasional edema (from the sodium load), without any increase in blood pressure
    • Patient tolerability is much better - easy to take and tasteless

 

Contributors

Shreya Trivedi, MD - Editor, Host

Martin Fried, MD - Editor, Host

Larissa Kruger Gomes, MD - Editor, Host

Jeffery William, MD - Guest Expert

Shivam Joshi, MD - Guest Expert

Reviewers

Rachel Hilburg, MD

Swapnil Hiremath, MD, MPH

Those named above unless otherwise indicated have relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

*Dr. Joshi reports receiving honoraria from NKF and Vita Pharma, and is a Consultant for Insyght Interactive.

These relationships have been mitigated.

Release Date:  November 17, 2021

Expiration Date: November 17, 2024

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