Hypertonic Saline as Adjunct for Diuretic Resistance in Cardiorenal Syndrome

Introduction: Diuresis remains the cornerstone of management in cardiorenal syndrome, particularly for addressing fluid overload. When combined with sequential nephron blockade (SNB), it serves as the mainstay strategy for overcoming diuretic resistance. We present a case of refractory cardiorenal syndrome managed with the adjunctive use of hypertonic saline. Case Description: A 77-year-old female with a history of chronic heart failure with reduced ejection fraction, type 2 diabetes mellitus, and atrial fibrillation on rivaroxaban presented as a trauma alert after a mechanical fall. She sustained a cervical spine fracture, right distal radius fracture, and facial trauma, and was transitioned to the medical service after no surgical intervention was required. During hospitalization, she developed shock presumed to be cardiogenic in origin, accompanied by progressive acute kidney injury (AKI) consistent with cardiorenal syndrome. Imaging ruled out pulmonary embolism. Her weight increased from 104 kg to 111 kg, and she became oliguric with progression of AKI to stage 3. Intravenous furosemide and milrinone were initiated, and SNB was employed with the addition of acetazolamide and hydrochlorothiazide. Despite these measures, oliguria persisted, and the patient declined temporary renal replacement therapy. A trial of hypertonic saline (3% NaCl, 250 mL daily) was initiated. Within 24 hours, urine output improved. Hypertonic saline was continued for four days, resulting in progressive diuresis and renal recovery to her baseline weight with tapering of diuretic therapy. Discussion: This case illustrates the utility of hypertonic saline as an adjunct to loop diuretics and sequential nephron blockade in overcoming diuretic resistance in cardiorenal syndome, particularly in individuals who decline temporary renal replacement therapy. Hypertonic saline enhances diuresis by several mechanisms essentially by expanding intravascular volume and improving renal perfusion via increased plasma tonicity and by increasing distal sodium delivery to potentiate the effects of loop and thiazide diuretics. Another less known mechanism is contributing to the restoration of the medullary osmotic gradient, often disrupted in ATN, thereby promoting natriuresis and free water clearance. In conclusion, hypertonic saline represents a viable adjunctive strategy in the management of diuretic-resistant volume overload.