American Journal of Respiratory and Critical Care Medicine · May 2026
B51-21 BRASH Syndrome: Triggered by Sodium-glucose Cotransporter-2 (SGLT2) Inhibitors
By Moras C, Dey D, Gupta I et al.
Abstract Introduction BRASH is a clinical syndrome characterized by Bradycardia, Renal failure, Atrioventricular nodal(AV) blockade, Shock, and Hyperkalemia. The underlying mechanism involves the interaction between AV nodal blockade and hyperkalemia. Any minor event, such as dehydration, can lead to reduced renal perfusion and a drop in glomerular filtration rate. This reduction allows renally excreted beta-blockers to accumulate, causing severe bradycardia and decreased cardiac output. Pathophysiologic insight drives targeted treatment. Case An elderly male with a past medical history of coronary artery disease, systolic heart failure, atrial fibrillation, type 2 Diabetes Mellitus, chronic kidney disease on metoprolol, Spironolactone, and Sacubitril/Valsartan, presented with lethargy, altered mental status, anorexia, vomiting and reduced urine output. He was recently admitted for CHF exacerbation and was discharged on oral lasix and started on Dapagliflozin. On admission he was hypotensive and bradycardic. Laboratory findings revealed hyponatremia, hyperkalemia and elevated creatinine from baseline. EKG showed bradycardia. He was intubated for airway protection and admitted to MICU, treated with IV calcium, IV insulin, dextrose, vasopressor support, and hemodialysis(HD). He was successfully extubated on Day 8 of admission, with good renal recovery, requiring no further HD. Discussion The patient’s hypovolemic state was precipitated by the recent initiation of dapagliflozin, an SGLT2 inhibitor that promotes urinary glucose excretion and induces osmotic diuresis, thereby reducing intravascular volume. This effect is particularly pronounced in elderly individuals, those with impaired renal function, or patients on loop diuretics, and can manifest as symptomatic hypotension or transient elevations in serum creatinine. In this case, severe hyperkalemia was likely the result of acute-on-chronic kidney injury, exacerbated by concomitant use of spironolactone. The bradycardia was attributed to increased AV nodal blockade, likely due to impaired renal clearance of metoprolol. Despite a stable metoprolol dose, dapagliflozin-triggered volume depletion, combined with other medications, precipitated renal failure, hyperkalemia, and bradycardia consistent with BRASH syndrome. This abstract is funded by: NA