Velez JCQ, Wickman TJ, Tayebi K, Mohamed MMB, Yousuf A, Kanduri SR, Lukitsch I, Vonderhaar D, Kovvuru K, Wentowski C
Abstract
Introduction: Diuretics are commonly discontinued in patients with cirrhosis with acute kidney injury because they are presumed to trigger hepatorenal syndrome type 1 (HRS-1). We hypothesized that 1 is adequately treated with a vasoconstrictor (mean arterial pressure [MAP] effectively increased), diuretics are safe and effective. Methods: Records of hospitalized patients with cirrhosis who received i.v. furosemide while receiving norepinephrine as a vasoconstrictor to treat HRS-1 were examined. We assessed change in urine (UOP), trajectory of serum creatinine (sCr), and impact of portopulmonary hypertension (PoPHTN) therapeutic response. Results: Twenty-six patients with HRS-1 received i.v. furosemide (median: 2 days, 160 mg boluses 6-24 hours) added to i.v. norepinephrine. Median age was 51 years; 91% were of White race, women, and median model for end-stage liver disease score was 32. The median initial sCr was Before treatment, median UOP was 358 ml/d. Norepinephrine alone led to a median increase in UOP ml/d. Addition of furosemide to norepinephrine induced a subsequent increase in median UOP to d (P < 0.0001), which was not observed in a control group (n = 22) who did not receive furosemide. Nineteen patients (73%) treated with norepinephrine plus furosemide (median MAP increase, 16 either maintained or improved their sCr trajectory. The magnitude of norepinephrine-induced MAP correlated with the norepinephrine plus furosemide-induced UOP (r = 0.67, P = 0.0002), correlation coefficient was numerically stronger among those with PoPHTN. Conclusion: In patients with HRS-1 who are adequately treated with norepinephrine and achieved optimal MAP increment, addition of i.v. furosemide enhances diuresis without negatively affecting recovery.
