Kidney Week Educational Symposia-Update on the Management of Recurrent Hyperkalemia Associated with RAAS Inhibitors in Patients with CKD and ESRD

Video Transcription

Video Summary

This symposium reviews why renin–angiotensin–aldosterone system (RAAS) inhibitors are central in chronic kidney disease (CKD) and cardiovascular disease, and why hyperkalemia limits their use. Vivek Bahla summarizes evidence that ACE inhibitors/ARBs slow progression of diabetic CKD (macro- and microalbuminuria) and non-diabetic proteinuric CKD, with some benefit even at lower eGFR, though newer data in advanced CKD create debate about continuing therapy. RAAS blockade also improves heart failure outcomes and reduces cardiovascular events, and mineralocorticoid receptor antagonists (MRAs) help resistant hypertension (e.g., PATHWAY-2). The major adverse effects are hyperkalemia and AKI risk, with hyperkalemia rates rising sharply when eGFR <30.<br /><br />Chow-Long Wong reviews potassium physiology: most filtered K is reabsorbed proximally and in the thick ascending limb; net K excretion depends on distal secretion (ROMK/BK) regulated by aldosterone, flow, and DCT sodium handling (NCC via WNK signaling). Kidneys adapt strongly to partial renal failure via tubular changes, but acute hyperkalemia often reflects extracellular shifts (insulin, beta-adrenergic tone, acidosis). He also highlights gut “feedforward” signaling that promotes kaliuresis without raising plasma K.<br /><br />Charles Wingo reviews therapies for recurrent hyperkalemia while preserving RAAS benefits. MRAs reduce mortality (RALES, EPHESUS) but increase hyperkalemia in practice. Newer nonsteroidal MRAs (finerenone) improve diabetic CKD outcomes yet still raise K. New K binders (patiromer, sodium zirconium cyclosilicate) lower K and may enable continued RAAS therapy, though adherence and outcomes data are concerns. SGLT2 inhibitors reduce CKD progression and may lower hyperkalemia risk; early studies suggest additive proteinuria reduction with combined MRA+SGLT2 therapy. Diuretics and chronic alkalinization help; strict dietary K restriction is questioned.

Asset Subtitle

Moderators: Alan Pao, Vivek Bhalla

Introduction: Rationale Behind Using RAAS Inhibitors in Patients with CKD and CVD - Alan Pao, Vivek Bhalla
Advances in Therapies for Recurrent Hyperkalemia in Patients with CKD and ESRD - Charles Wingo
Update on Potassium Balance and the Molecular Mechanism Underlying Hyperkalemia - Chou-Long Huang

Support is provided by an educational grant from CSL Vifor.

Meta Tag

Date 11/4/2022

Pathway 1 Fluid, Electrolyte, and Acid-Base Disorders

Pathway 2 CKD Non-Dialysis

Session ID 439548

Session Type ES - Educational Symposium

Keywords

RAAS inhibitors

chronic kidney disease (CKD) progression

hyperkalemia management

ACE inhibitors and ARBs

mineralocorticoid receptor antagonists (MRAs)

potassium physiology and renal tubular handling

potassium binders (patiromer, sodium zirconium cyclosilicate)

SGLT2 inhibitors in CKD

heart failure and cardiovascular outcomes