Kidney Week

Abstract: FR-PO0892

Severe Gram-Negative Sepsis Presenting as Refractory Complete Heart Block in Advanced CKD: Beyond BRASH Syndrome

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid, Electrolytes, and Acid-Base Disorders

• 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Sharma, Pranav K., Lake Cumberland Regional Hospital, Somerset, Kentucky, United States

Pranav K. Sharma, MD, FASN

• Khan, Alina S., Liaquat National Hospital and Medical College, Karachi, Sindh, Pakistan

Alina S. Khan, MD, MBBS

• Ripley, Shannon L., Lake Cumberland Regional Hospital, Somerset, Kentucky, United States

Shannon L. Ripley, DO

• Hays, Ray, Lake Cumberland Regional Hospital, Somerset, Kentucky, United States

Ray Hays, DO

• Tripathi, Devendra, Nazareth Hospital, Philadelphia, Pennsylvania, United States

Devendra Tripathi, MD

• Gurjar, Hitesh, Banner - University Medical Center Tucson, Tucson, Arizona, United States

Hitesh Gurjar, MD, MBBS

Introduction

Complete heart block (CHB) in advanced chronic kidney disease (CKD) is attributed to hyperkalemia, AV nodal blockade, or conduction dysfunction. BRASH syndrome (Bradycardia, Renal failure, AV nodal blockade, Shock, Hyperkalemia) reflects renal hypoperfusion and severe bradyarrhythmia. Delayed recognition of an underlying septic trigger may bias the diagnosis, increasing risk of recurrent hemodynamic instability. We present a case of refractory CHB in advanced CKD where gram-negative septic shock simulated BRASH physiology.

Case Description

A 73-year-old male with coronary artery disease, congestive heart failure, type 2 diabetes mellitus, prior cerebrovascular accident, and stage 4 CKD presented unresponsive with profound hypotension and severe bradycardia requiring emergent intubation and ICU admission, on metoprolol and empagliflozin. Electrocardiogram demonstrated CHB with a ventricular escape rhythm. Labs revealed potassium 7.7 mEq/L, severe lactic acidosis and acute kidney injury. BRASH syndrome was suspected and treated with calcium gluconate, insulin and dextrose, albuterol, vasopressors, emergent hemodialysis, and transcutaneous pacing. Despite rapid potassium correction following dialysis, CHB persisted with recurrent bradycardia and developed pulseless electrical activity requiring cardiopulmonary resuscitation and transvenous pacing. Cultures grew Klebsiella pneumoniae and Escherichia coli, confirming Gram-negative sepsis with septic shock. Broad-spectrum antibiotics, renal replacement therapy, and temporary pacing resulted in hemodynamic stabilization, extubation, recovery to baseline renal function, and restoration of sinus rhythm.

Discussion

This case manifests as severe Gram-negative sepsis mimicking BRASH physiology in advanced CKD. Although hyperkalemia initiated the bradyarrhythmia, persistent CHB despite metabolic correction suggested sepsis-related conduction dysfunction rather than isolated electrolyte toxicity. In patients with limited renal reserve, inflammatory cytokine release, renal hypoperfusion, and acidosis may impair AV nodal conduction and precipitate refractory bradyarrhythmias. Early recognition is critical, particularly when conduction abnormalities persist despite dialysis and potassium correction. Early renal replacement therapy, infection control, temporary pacing, and ICU management are essential to prevent multiorgan dysfunction