Kidney Week 2025 Annual Meeting-Hyperkalemia in the Time of Zirconium and Patiromer

Video Transcription

Video Summary

The symposium opens with Dr. Biff Palmer discussing whether the transtubular potassium gradient (TTKG) should still be used. He reviews pitfalls of spot urine potassium (affected by urine concentration) and explains how TTKG and the urine potassium-to-creatinine ratio can help distinguish renal potassium wasting from extrarenal causes in hypokalemia. Using hypokalemic periodic paralysis versus renal K-wasting disorders as an example, he argues TTKG can still discriminate well when prerequisites are met (urine osmolality > plasma; urine sodium ≥25). He also highlights underappreciated physiology (e.g., why type 1 RTA can cause renal K loss via acidosis-related proximal salt handling changes). For hyperkalemia, Palmer emphasizes clinical context usually identifies etiology; TTKG may help in select cases (e.g., assessing mineralocorticoid deficiency vs resistance after fludrocortisone).<br /><br />Dr. Ali Mehdi then focuses on hyperkalemia as a key reason clinicians discontinue RAAS inhibitors in CKD and HFrEF despite strong outcome benefits. He presents observational and trial data showing RAAS discontinuation worsens mortality, cardiovascular events, and kidney outcomes, and that many patients are never restarted. He challenges blanket dietary potassium restriction, citing weak correlation between intake and serum K and potential harms of reducing healthy plant-based foods. He advocates individualized dietary counseling, addressing contributors (acidosis, constipation, medications), and using supportive therapies—diuretics, SGLT2 inhibitors, GLP-1 receptor agonists, and potassium binders—to maintain guideline-directed RAAS therapy.<br /><br />Dr. Eli Kalantar-Zadeh (speaker name in transcript: Eli Kalopouros) reviews potassium binders: SPS (limited evidence, significant GI risk, sodium load), patiromer (calcium exchange; hypomagnesemia/constipation), and sodium zirconium cyclosilicate (rapid effect but sodium/edema considerations). She stresses matching binder choice to patient comorbidities and shared decision-making, including palatability and cost.<br /><br />Dr. David Mount covers acute hyperkalemia treatment: ECG effects, “BRASH” physiology, and practical thresholds. He supports treating K ≥6.5 aggressively even without ECG changes (insulin/glucose; calcium), monitoring for hypoglycemia, limited role for bicarbonate unless acidemic, growing use of SZC as adjunct, and dialysis as definitive removal.

Asset Subtitle

Moderator(s): Melanie Hoenig, Megan Prochaska

Presentation(s):

No More Transtubular Potassium Gradient: What's a Nephrology Professional to Do? - Biff Palmer
Hyperkalemia, RAAS, and CKD/Congestive Heart Failure Benefits - Ali Mehdi
Novel Potassium Binders - Ellie Kelepouris
Acute Hyperkalemia Treatment: Separating Lore from Reality - David Mount

Meta Tag

Date 11/8/2025

Pathway 1 Fluid, Electrolyte, and Acid-Base Disorders

Pathway 2 Hypertension and Cardiorenal Disorders

Session ID 507078

Keywords

transtubular potassium gradient (TTKG)

spot urine potassium pitfalls

urine potassium-to-creatinine ratio

renal potassium wasting

extrarenal hypokalemia causes

hypokalemic periodic paralysis

TTKG prerequisites (urine osmolality > plasma, urine sodium ≥25)

type 1 renal tubular acidosis (RTA) and hypokalemia

hyperkalemia clinical context

mineralocorticoid deficiency vs resistance

RAAS inhibitor discontinuation

chronic kidney disease (CKD) hyperkalemia

heart failure with reduced ejection fraction (HFrEF)

potassium binders (SPS, patiromer, sodium zirconium cyclosilicate)

acute hyperkalemia management (ECG, insulin/glucose, calcium, dialysis)