We are grateful to Dr. Lenz and coworkers for their interest in our study.1 They remark on the complexity of circulatory dysfunction leading to hepatorenal syndrome in patients with cirrhosis and spontaneous bacterial peritonitis (SBP). They suggest that hypovolemia is a major event, since patients with hepatorenal syndrome showed low right-atrial pressure and wedged capillary pulmonary pressure. We did not observe an increase in peripheral vascular resistance in these patients, as Lenz et al. pointed out in their letter. In fact, no significant changes in this parameter were observed in patients who did and did not develop hepatorenal syndrome after SBP. Nevertheless, we agree with their suggestion. As indicated in the discussion of the article, a reduction in cardiac output in the absence of a significant increase in cardiopulmonary pressure is consistent with a decreased venous return to the heart. Also, the lack of increase in peripheral vascular resistance in the setting of a decrease in cardiac output and a marked stimulation of the renin-angiotensin system is consistent with an increase in arterial vasodilation, probably in the splanchnic circulation, since it is well known that in cirrhosis the vascular resistance in the renal,2 cutaneous, muscular,3 and cerebral4 territories is directly related to the plasma levels of renin. Therefore, the mechanism of circulatory dysfunction associated with hepatorenal syndrome in patients with SBP is probably the result of the simultaneous occurrence of progression of the arterial vasodilation already present in nonazotemic patients with decompensated cirrhosis together with impairment in cardiac function. This contention is further supported by the high efficacy of the simultaneous treatment with plasma volume expansion and vasoconstrictors in reversing hepatorenal syndrome,5 an effect rarely observed when these measures are provided alone.
However, the suggestion by Lenz et al. that the decrease in cardiac function is mainly related to hypovolemia is, in our opinion, an oversimplification of the problem. The lack of increase in heart rate observed in our study in patients developing type-1 hepatorenal syndrome is striking, since there was an intense stimulation of the sympathetic nervous system. This indicates a profound deterioration of the chronotropic function of the heart. The effect of SBP on cardiac inotropic function has never been explored.
We have previously shown that at the time of diagnosis of SBP, plasma volume expansion with albumin reduces the incidence of hepatorenal syndrome and hospital mortality by approximately 60%.6 The next step is to assess whether this figure could be improved by the simultaneous administration of vasoconstrictors and albumin or by the multiple treatments proposed by Lenz et al. in their letter.