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Kidney Week Educational Symposia
Hyperkalemia: Understanding and Applying Innovativ ...
Hyperkalemia: Understanding and Applying Innovative Approaches to the Management of CKD and ESKD
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Video Summary
The symposium, supported by an educational grant from AZ Pharmaceuticals, focused on contemporary issues in hyperkalemia. Dr. Mitch Rosner reviewed potassium physiology and emphasized that kidneys normally excrete ~90% of potassium, making clinically significant hyperkalemia uncommon without impaired kidney function or disrupted aldosterone activity. Acute potassium balance is protected by insulin-mediated cellular shifts, aldosterone, and gut–kidney signaling; chronic control relies mainly on aldosterone action in the distal nephron. Hyperkalemia risk rises with declining GFR (roughly doubling for each 15 mL/min drop), and is amplified by CKD, diabetes, heart failure, and renin–angiotensin–aldosterone system (RAAS) inhibitors. In dialysis patients, hyperkalemia is most frequent after the long interdialytic interval, and mortality risk increases particularly at potassium levels around ≥5.8–6.0 mmol/L. Importantly, discontinuing or reducing RAAS inhibitors in response to hyperkalemia is associated with worse outcomes, underscoring the need for active potassium management rather than stopping beneficial therapies.<br /><br />Dr. Biff Palmer discussed management strategies using a case of weakness after spironolactone initiation. First steps include medication review (NSAIDs, beta-blockers, ACEi/ARBs, MRAs, heparin, trimethoprim, etc.), nuanced dietary counseling (not all fruits/vegetables have equal bioavailable potassium and may be kidney/cardioprotective), optimizing diuretics, and correcting metabolic acidosis (bicarbonate or fruit/vegetable-based alkali). SGLT2 inhibitors may reduce hyperkalemia risk when combined with RAAS blockade. Newer potassium binders—patiromer and sodium zirconium cyclosilicate—are effective for chronic control and can help maintain RAAS therapy; zirconium may cause edema at higher doses, while patiromer can lower magnesium. Q&A highlighted increasing ER use of binders, special dietary offenders (e.g., cactus salsa), and individualized decisions in dialysis and hyporeninemic hypoaldosteronism.
Asset Subtitle
Moderators: Kim Zuber
Introduction: The Physiology of Hyperkalemia
- Kim Zuber
The Impact of Hyperkalemia in the Treatment of CKD
- Mitchell Rosner
Pharmacological and Nonpharmacological Approaches to the Management of Hyperkalemia
- Biff Palmer
Support is provided by an educational grant from AstraZeneca Pharmaceuticals.
Meta Tag
Date
11/5/2022
Pathway 1
Fluid, Electrolyte, and Acid-Base Disorders
Pathway 2
CKD Non-Dialysis
Session ID
438092
Session Type
ES - Educational Symposium
Keywords
hyperkalemia
potassium physiology
chronic kidney disease (CKD)
glomerular filtration rate (GFR) decline
RAAS inhibitors (ACEi/ARB) management
aldosterone and distal nephron regulation
dialysis interdialytic hyperkalemia
potassium binders (patiromer, sodium zirconium cyclosilicate)
dietary potassium counseling and bioavailability
SGLT2 inhibitors and hyperkalemia risk reduction
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