Doping represents a critical threat to the integrity of competitive sports, with diuretics frequently misused as masking agents to facilitate the urinary excretion of other prohibited substances. Torsemide (TSD), a widely misused loop diuretic, requires a sensitive and selective method for its determination in biological matrices to support efficient doping control. Herein, a sustainable fluorescent nanosensor based on multi-self-doped carbon quantum dots was synthesized for the first time from golden berry (GBQDs) via a rapid, one-step microwave-assisted approach at 800 W in just 7 min without additional surface passivation agents. Notably, these innovative CDs outperform previous traditional methods, as their preparation relies on minimum energy consumption and green natural substrate. The fabricated GBQDs exhibited intense blue fluorescence at λex/λem 350/423 nm, a quantum yield of 28.9%, nano-sized CDs (7.67 ± 1.02 nm), and a chemical composition of C (51.12%), N (22.8%), O (25.6%), S (0.02%), K (0.38%), Cl (0.04%), P (0.02%), and Cu (0.02%). The GBQDs demonstrated excellent aqueous solubility, remarkable photostability (3% fluorescence decrease after 60 min), and storage stability (in refrigerator) for 8 weeks. TSD selectively quenches GBQDs fluorescence via a combined inner filter effect and static quenching mechanism, forming the basis of a "turn-off" fluorescent nanosensor. Under optimized conditions, the method showed linearity over 0.5-30 μg/mL (r[2] = 0.9999), LOD of 0.110 μg/mL, LOQ of 0.335 μg/mL, high accuracy (99.75 ± 1.02%), precision (RSD < 1%), selectivity, and robustness. The proposed nanosensor was successfully applied for TSD determination in pharmaceutical dosage forms, human urine, and plasma with recoveries ranging from 99.43 to 100.29%. Greenness and blueness assessments using Complex-GAPI, BAGI (80), AGREE-Prep (0.79), and NAT (91) confirmed superior environmental sustainability and feasibility for on-site detection in doping regulation laboratories. This strategy offers a rapid, cost-effective, sensitive, and eco-friendly platform for anti-doping surveillance and therapeutic monitoring of TSD in biological matrices, guaranteeing fair competition and safeguarding athletes' health in the sports world.

GIM/FP/GP: [Formula: see text] Cardiology: [Formula: see text].

BRASH (Bradycardia, Renal failure, Atrioventricular nodal blockade, Shock, and Hyperkalemia) syndrome is a life-threatening clinical syndrome characterized by a vicious cycle in which hyperkalemia and AV nodal blocking medications synergistically produce profound bradycardia and hemodynamic instability. A 71-year-old male with stage IIIB chronic kidney disease (CKD), heart failure with improved ejection fraction, and coronary artery disease status post coronary artery bypass grafting, on carvedilol, losartan, and torsemide, was brought to the emergency room from a rehabilitation facility for a syncopal event and unresponsiveness. He had been recently hospitalized for multifocal pneumonia and respiratory syncytial virus infection, with suspected volume depletion and ongoing AV nodal blockade contributing to the development of BRASH syndrome. He was in respiratory distress, profound shock, and bradycardia with a heart rate of 30 BPM. Labs revealed severe acute kidney injury (creatinine 6.2 mg/dL), hyperkalemia (6.9 mmol/L), and metabolic acidosis (pH 7.19). Chest radiograph demonstrated pulmonary edema. His condition rapidly progressed to airway compromise requiring intubation, cardiogenic shock requiring vasopressors, and refractory bradycardia necessitating transvenous pacing after failure of atropine, dopamine, and transcutaneous pacing. He was admitted to the intensive care unit and promptly initiated on continuous renal replacement therapy (CRRT), resulting in correction of electrolyte and acid-base abnormalities with subsequent resolution of severe bradycardia, allowing discontinuation of transvenous pacing. Infectious workup remained negative, and echocardiography demonstrated preserved left ventricular systolic function. Following stabilization, he was successfully extubated and weaned off CRRT. His subsequent hospital course was complicated by recurrent oliguric renal failure requiring initiation of intermittent hemodialysis. Upon discharge, he remained hemodynamically stable with improved mental status and was planned for long-term hemodialysis and inpatient rehabilitation. The synergistic interaction of hyperkalemia and AV nodal blockade is the central pathophysiologic mechanism underlying BRASH syndrome. Common triggers include hypovolemia and medications that promote AV nodal blockade or hyperkalemia in vulnerable patients with advanced age, CKD, and heart failure. The resulting profound bradycardia further reduces cardiac output, worsening renal perfusion and perpetuating hemodynamic instability. Prognosis depends largely on early recognition and prompt intervention. This case highlights a severe presentation of BRASH syndrome in which timely initiation of CRRT corrected the underlying metabolic derangements, and transvenous pacing provided temporary hemodynamic support, ultimately leading to clinical recovery.

Congestion drives symptoms and adverse outcomes in heart failure (HF), and loop diuretics remain the cornerstone of decongestion. Yet randomized trials of diuretic strategies and other acute decongestive approaches have not shown mortality benefit, while mechanistic studies demonstrate rapid neurohormonal activation after acute loop diuretic administration. In chronic HF, observational data consistently associate higher loop diuretic requirements-particularly above ∼40 mg/day furosemide equivalent or with dose escalation-with worse prognosis across HF phenotypes, though confounding by disease severity is likely. Decongestion needs vary across the HF trajectory: early guideline-directed therapy provides intrinsic decongestive effects, whereas advanced HF is marked by diuretic resistance and renal vulnerability. Preload-dependent states (notably cardiac amyloidosis and selected HFpEF phenotypes) require especially careful titration to avoid hypovolemia and low output, and robust protocol-level trial evidence is lacking. Contemporary randomized data do not demonstrate superiority of torsemide over furosemide. Small trials and systematic reviews suggest that in carefully selected, stable, non-congested patients, diuretic withdrawal or reduction can be feasible, with ∼25-35% requiring re-initiation within 1-3 months and consistent lowering of renin activity; however, clinical outcome benefit remains unproven. Overall, evidence supports maintaining euvolemia with the lowest effective diuretic dose and considering monitored deprescribing in appropriate low-risk patients.

Torsemide (TOR) is increasingly misused in weight-loss products and livestock practices, posing significant health risks to consumers and athletes. In this study, novel potentiometric sensor integrating molecularly imprinted polymer (MIP) with MIL-101 (Cr) metal-organic framework was developed for selective and sensitive detection of TOR. The fabricated TOR-MIL/MIP sensor exhibited near-Nernstian slope of 56.3 mV/decade over wide linear response range of 1.0 × 10-7-1.0 × 10-3 M with LOD of 6.3 × 10-8 M. High porosity of MIL-101(Cr) greatly enhanced charge-transfer efficiency at electrode interface, facilitating ion-to-electron transduction and improving potential stability. Selectivity of sensor against common pharmaceutical adulterants was tested, and the sensor was used to analyze TOR in several dietary supplement matrices. Additionally, raw milk sample was fortified with TOR to assess method's applicability in food safety monitoring. Results showed recoveries ranging from 97.91%-104.53% and RSDs below 1.7%. These findings affirm sensor's precision and suitability for routine screening of TOR adulteration in both dietary supplements and food matrices.

Warfarin is a widely used oral anticoagulant with a narrow therapeutic index and multiple drug-drug interactions that may significantly alter its anticoagulant effect. Torsemide, a loop diuretic commonly prescribed for heart failure and fluid overload, shares metabolic pathways with warfarin, raising the possibility of clinically significant interactions. However, the evidence regarding this interaction remains limited and inconsistent. A 66-year-old male with a history of type 2 diabetes mellitus, hypertension, chronic kidney disease, and prior aortic valve replacement on chronic warfarin therapy presented with extensive soft tissue necrosis of the left leg following minor trauma. During hospitalization, warfarin (3 mg once daily) and Torsemide (20 mg once daily) were initiated concurrently. Subsequently, the patient developed a progressive elevation in international normalized ratio (INR), necessitating repeated fresh frozen plasma transfusions due to increased bleeding risk. Despite supportive management, INR remained elevated. Torsemide was discontinued and replaced with furosemide, after which a gradual stabilization of INR levels was observed. The patient later required left above-knee amputation due to worsening necrosis but recovered following multidisciplinary management. Assessment using the Naranjo Adverse Drug Reaction Probability Scale suggested a possible interaction between warfarin and Torsemide. This case highlights a potential interaction between warfarin and Torsemide resulting in elevated INR and increased bleeding risk. Clinicians should exercise caution and ensure close INR monitoring when initiating Torsemide in patients receiving warfarin therapy.