Abstract
We present a case of severe diuretic resistance and edema from acute cardiorenal syndrome complicating heart failure with preserved ejection fraction (HFpEF) and mild alcoholic liver disease. High doses of intravenous (iv) furosemide plus iv doses of chlorothiazide failed to increase the daily urine output (UV) above 1,500 mL or the fractional excretion of sodium (FE<sub>Na</sub>) above 2%. The addition of a relatively low dose of hydralazine (10 mg thrice daily PO) during 5 days of constant iv infusion of furosemide plus iv bolus chlorothiazide doubled the UV and FE<sub>Na</sub> while reducing the serum creatinine concentration from 3.3 to 2.0 mg/dL. Hydralazine may have restored a response to the diuretics by increasing the renal blood flow and thereby the renal diuretic delivery, or by reducing the filtration fraction or reducing the renal congestion and thereby reducing the proximal reabsorption during blockade of distal reabsorption with diuretics. Further mechanistic studies of low-dose hydralazine for diuretic resistance are warranted.
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