Low‐dose vasopressin restores diuresis both in patients with hepatorenal syndrome and in anuric patients with end‐stage heart failure

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Abstract
Eisenman A, Armali Z, Enat R, Bankir L, Baruch Y (Rambam Medical Center and Technion‐Israel Institute of Technology, Haifa, Israel; and INSERM, Necker Hospital, Paris, France). Low‐dose vasopressin restores diuresis both in patients with hepatorenal syndrome and in anuric patients with end‐stage heart failure. J Intern Med 1999; 246: 183–190.Objectives. The purpose of this study was to confirm earlier reports that low‐dose vasopressin (LDVP) analogues promote urine output in patients with hepatorenal syndrome (HRS) and to check whether this mode of therapy could also be effective in renal shutdown due to nonhepatic conditions.Design. A prospective, open, interventional study.Setting. An intermediate‐level (step‐down) medical intensive care unit within a general medical ward of a large university‐affiliated hospital.Subjects. Eighteen successive hospitalized patients with HRS (mean age 65 ± 13 years) and 11 patients with end‐stage congestive heart failure (CHF) (mean age 81 ± 5 years) who failed to restore urine output with conventional treatment (fluids, dopamine, and diuretics) given for at least 24 h.Interventions. The patients received LDVP (1 IU h−1) continuously in addition to the conventional treatment.Main outcome measures. Urine output and creatinine clearance every 24 h.Results. In the HRS group, before treatment the urine output was 155 ± 9 mL 24 –1h (mean ± SD). After treatment with LDVP for 24, 48, and 72 h, urine output improved to 1067 ± 87, 1020 ± 501, and 1311 ± 988 mL 24 –1h, respectively (P < 0.0001 for all measures; two‐tailed paired t‐test). In the CHF group, before treatment the urine output was 99 ± 99 mL 24 –1h. After treatment with LDVP for 24, 48, and 72 h, this improved to 1125 ± 994 mL 24 –1h (P = 0.0028), 1821 ± 1300 mL 24 –1h (P = 0.004), and 2920 ± 2423 mL 24 –1h (P = 0.0012), respectively. The improvement in urine output was not accompanied by a parallel improvement in creatinine clearance. The overall outcome did not change, and all patients except two in each group succumbed to their end‐stage disease, due to nonrenal causes.Conclusions. LDVP is effective in restoring urine output both in HRS and in CHF. This suggests that LDVP affects mechanisms not specifically related to liver disease. LDVP may be useful in critical patients with renal shutdown whilst awaiting liver or heart transplantation.