Circulatory function and hepatorenal syndrome in cirrhosis†

Abstract

The pathogenic mechanism of hepatorenal syndrome is not well established. We investigated the circulatory function in cirrhosis before and after the development of hepatorenal syndrome. Systemic and hepatic hemodynamics and the activity of endogenous vasoactive systems were measured in 66 patients who had cirrhosis with tense ascites and normal serum creatinine levels; measurements were repeated at follow-up in 27 cases in whom hepatorenal syndrome had developed. At baseline, mean arterial pressure and cardiac output were significantly higher, and hepatic venous pressure gradient, plasma renin activity, and norepinephrine concentration were significantly lower in patients who did not develop hepatorenal syndrome compared with those presenting with this complication. Peripheral vascular resistance was decreased to the same extent in the two groups. Plasma renin activity and cardiac output were the only independent predictors of hepatorenal syndrome. Hepatorenal syndrome occurred in the setting of a significant reduction in mean arterial pressure (83 ؎ 9 to 75 ؎ 7 mmHg; P < .001), cardiac output (6.0 ؎ 1.2 to 5.4 ؎ 1.5 L/min; P < .01), and wegded pulmonary pressure (9.2 ؎ 2.6 to 7.5 ؎ 2.6 mmHg; P < .001) and an increase in plasma renin activity (9.9 ؎ 5.2 to 17.5 ؎ 11.4 ng/mL ⅐ hr; P < .001), norepinephrine concentration (571 ؎ 241 to 965 ؎ 502 pg/mL; P < .001), and hepatic venous pressure gradient. No changes were observed in peripheral vascular resistance. In conclusion, these data indicate that hepatorenal syndrome is the result of a decrease in cardiac output in the setting of a severe arterial vasodilation. (HEPATOLOGY 2005;42:439-447.)

Study on Assessment of Renal Function in Chronic Liver Disease

“…In the present study there was no statistically significant change in renal parameters in different aetiologies of liver disease but the result was different in other studies [18][19][20] like prevalence rate of AKI in cirrhosis was 68% in a study conducted by Fernandez-Seara J [18] but in our study only 10% patients had AKI. In the same study prevalence of hepatorenal syndrome was 25% [18].…”

“…In the same study prevalence of hepatorenal syndrome was 25% [18]. Another study showed that among patients with ascites, HRS developed in about 20% and 40% of the patients, at 1 and 5 years, respectively [19]. Ruiz-del-Arbol L et al, [20] in a study done on 23 cirrhotic patients with spontaneous Bacterial peritonitis of which 8 patients developed type-I Hepatorenal syndrome.…”

Hepatorenal Syndrome

“…The same group studied the systemic and hepatic hemodynamics of 66 patients with cirrhosis and tense ascites and normal serum creatinine at baseline with repeat measurement in 27 patients who subsequently developed HRS. At baseline, arterial BP and CO was significantly lower whereas RAAS and SNS activity were significantly higher in the group that developed HRS with further reduction in CO at the onset of renal dysfunction (43). The findings of these two studies suggest that a decrease in CO identifies a group of patients who are at risk for HRS and implicate decreased CO or its cause in HRS occurrence.…”

Cirrhotic cardiomyopathy

“…Indeed, in cirrhotic patients with spontaneous bacterial peritonitis, patients who went on to develop hepatorenal syndrome (HRS) had a reduced cardiac output at infection diagnosis, which decreased further at infection resolution [79], suggesting that the inability to mount a sufficient cardiac output in the presence of bacterial infection has contributed to a reduced renal perfusion pressure, thereby contributing to the development of HRS. In fact, the same authors reported that those cirrhotic patients destined to develop HRS had lower cardiac output even prior to the onset of HRS [80], with lower mean arterial pressure and higher neurohormonal levels, suggesting that an inadequate cardiac output in the presence of systemic arterial vasodilatation predisposes these cirrhotic patients to further complications. In the case of bacterial infections, the presence of negative inotropic cytokines such as TNF-a and interleukin-1b further lowers cardiac systolic function, thereby further reducing cardiac output, leading to the development of HRS.…”