Kidney Week Educational Symposia-Strategies to Control Chronic Hyperkalemia in Patients with CKD and ESRD

Video Transcription

Video Summary

The session reviews strategies to manage chronic hyperkalemia in patients with CKD and ESRD and why the issue is clinically important. Dr. Elvira Gasmanova introduces potassium physiology: 98% of total body potassium is intracellular, and small extracellular changes affect resting membrane potential, leading to impaired cardiac conduction, arrhythmias, and muscle weakness in hyperkalemia. She notes challenges defining hyperkalemia due to lab variability, serum vs plasma differences, pseudohyperkalemia, and circadian variation; clinically, >5.0 mmol/L is commonly used (graded mild/moderate/severe). Population prevalence is ~3.3% (>5.0) but rises sharply as eGFR declines and with diabetes and heart failure. Both high and low potassium show U-shaped associations with mortality. RAAS inhibitors (ACEi/ARBs), despite renal/cardiac benefits, increase hyperkalemia risk and are often discontinued; real-world data show recurrent episodes in advanced CKD, yet high RAASi exposure may associate with lower post-dialysis mortality—highlighting the need for better potassium control to maintain evidence-based therapy.<br /><br />Dr. David Goldfarb emphasizes uncertainty in who to treat and how aggressively, citing over-treatment risks (e.g., insulin-induced hypoglycemia). He reviews renal potassium handling (distal secretion via ROMK/MAXI-K, aldosterone/ENaC coupling) and notes limited evidence supporting strict dietary potassium restriction; plant-based potassium may not raise serum levels as expected and may confer alkali/fiber benefits.<br /><br />Dr. Matt Luther outlines management: reduce intake, correct acidosis, optimize insulin in diabetics, increase urinary excretion (loop/thiazide diuretics), avoid offending drugs (notably trimethoprim with ACEi/spironolactone), and use potassium binders when needed to continue RAAS therapy. He contrasts older SPS (limited long-term evidence; rare colonic necrosis) with newer agents patiromer (risk hypomagnesemia; less edema) and sodium zirconium cyclosilicate (rapid onset; edema risk). Trials show these agents lower potassium and help patients remain on RAAS blockade, but definitive outcome data (mortality/hospitalization) are still needed.

Asset Subtitle

Elvira Gosmanova, David Goldfarb, James Luther
Support is provided by an educational grant from Relypsa, Inc., A Vifor Pharma Group Company.

Keywords

chronic hyperkalemia

chronic kidney disease (CKD)

end-stage renal disease (ESRD)

RAAS inhibitors (ACEi/ARB) continuation

potassium physiology and membrane potential

pseudohyperkalemia and lab variability

U-shaped mortality association with potassium

dietary potassium restriction and plant-based diet

potassium binders (patiromer, sodium zirconium cyclosilicate, SPS)

hyperkalemia management strategies (diuretics, acidosis correction, drug avoidance)