Background and Aims: Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic liver disease, occasionally fulminant hepatitis, who have portal hypertension and ascites. Estimates indicate that at least 40% of patients with cirrhosis and ascites will develop HRS during the natural history of their disease. Relevant studies include those implicating the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the role of renal prostaglandins (PGs). Strong associations have been reported between spontaneous bacterial peritonitis (SBP) and HRS and the use of vasopressin analogues with volume expanders in the management and prevention of HRS. Despite some encouraging studies of new pharmacological therapies, the development of HRS in people with cirrhosis portends a dismal prognosis because renal failure is usually irreversible unless liver transplantation is performed. Patients with renal failure and active bacterial infections (without septic shock) are currently considered as having type-1 HRS according to the new diagnostic criteria reported in 2007. Methods: Twentyone patients with cirrhosis and serum creatinine >2.5 mg/dL diagnosed between 2009-2010 were included in the study. Patients were classified into 2 groups according to the precipitating factor for HRS found at diagnosis. Ten patients developed HRS induced by SBP (group 1) and 11 patients, neither had SBP at admission to the hospital nor developed SBP during development of HRS (group 2). Patients receive terlipressin (1-2 mg/4 h iv) and albumin (1 g/kg followed by 20-40 g/day). The end points of the study were improvement of renal function and survival at 3 months. Improvement of renal function was defined as a decrease in serum creatinine to a value <1.5 mg/dl (complete response). Results: Both groups were similar with respect to renal function at enrollment. However, the impairment in MELD score was more marked in group 2 vs group 1 (32±6 vs. 24±6 points; respectively, p < 0.004). Reversal of HRS occurred in 7/10 patients (70%) in group 1 compared to only 4/11 patients (36%) in group 2 (p= 0.012). Independent predictive factors of response to therapy were baseline serum bilirubin, and SBP precipitating factor for HRS. There were significant differences between group 1 and group 2 in terms overall survival at 60 days 54% vs. 23%, respectively; (p = 0.042). However, survival at 3 months was not significantly different between the two groups. Reversal of HRS was associated with a prolonged survival (median survival 147 days) vs. 13 days in patients with no improvement of renal function; < 0.001). Independent predictive factors of survival were baseline MELD score and response to therapy. There were no significant differences between the two groups with respect to the overall frequency of side effects. Conclusion: Nonselective V1 vasopressin agonist (Terlipressine) that has similar vasoconstrictor potency to ornipressin but a lower incidence of ischemic complications. Inactive by itself but is transformed into a biologically active form (lysine-vasopressin) by the action of tissue endopeptidases and exopeptidases. Due to its longer half-life (2-10 h) compared to ornipressin, may be administered as a bolus. Has lower incidence of adverse ischemic effects. The plasma volume expanders are indicated for the correction of abnormal hemodynamic parameters in HRS and Albumin useful for plasma volume expansion and maintenance of cardiac output. In our study Terlipressin and albumin was significantly more effective for HRS type-1 and spontaneous bacterial peritonitis than HRS type-1 without active bacterial infections.
THE COMPARATIVE STUDY OF TERLIPRESSIN AND ALBUMIN FOR TYPE-1 HEPATORENAL SYNDROME (HRS) IN PATIENTS WITH CIRRHOSIS AND SPONTANEOUS BACTERIAL PERITONITIS (SBP) VS CIRRHOSIS ALONE
BERTINO, Gaetano;BRUNO, Cosimo Marcello;CAMPAGNA D;NERI, Sergio
2010-01-01
Abstract
Background and Aims: Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic liver disease, occasionally fulminant hepatitis, who have portal hypertension and ascites. Estimates indicate that at least 40% of patients with cirrhosis and ascites will develop HRS during the natural history of their disease. Relevant studies include those implicating the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the role of renal prostaglandins (PGs). Strong associations have been reported between spontaneous bacterial peritonitis (SBP) and HRS and the use of vasopressin analogues with volume expanders in the management and prevention of HRS. Despite some encouraging studies of new pharmacological therapies, the development of HRS in people with cirrhosis portends a dismal prognosis because renal failure is usually irreversible unless liver transplantation is performed. Patients with renal failure and active bacterial infections (without septic shock) are currently considered as having type-1 HRS according to the new diagnostic criteria reported in 2007. Methods: Twentyone patients with cirrhosis and serum creatinine >2.5 mg/dL diagnosed between 2009-2010 were included in the study. Patients were classified into 2 groups according to the precipitating factor for HRS found at diagnosis. Ten patients developed HRS induced by SBP (group 1) and 11 patients, neither had SBP at admission to the hospital nor developed SBP during development of HRS (group 2). Patients receive terlipressin (1-2 mg/4 h iv) and albumin (1 g/kg followed by 20-40 g/day). The end points of the study were improvement of renal function and survival at 3 months. Improvement of renal function was defined as a decrease in serum creatinine to a value <1.5 mg/dl (complete response). Results: Both groups were similar with respect to renal function at enrollment. However, the impairment in MELD score was more marked in group 2 vs group 1 (32±6 vs. 24±6 points; respectively, p < 0.004). Reversal of HRS occurred in 7/10 patients (70%) in group 1 compared to only 4/11 patients (36%) in group 2 (p= 0.012). Independent predictive factors of response to therapy were baseline serum bilirubin, and SBP precipitating factor for HRS. There were significant differences between group 1 and group 2 in terms overall survival at 60 days 54% vs. 23%, respectively; (p = 0.042). However, survival at 3 months was not significantly different between the two groups. Reversal of HRS was associated with a prolonged survival (median survival 147 days) vs. 13 days in patients with no improvement of renal function; < 0.001). Independent predictive factors of survival were baseline MELD score and response to therapy. There were no significant differences between the two groups with respect to the overall frequency of side effects. Conclusion: Nonselective V1 vasopressin agonist (Terlipressine) that has similar vasoconstrictor potency to ornipressin but a lower incidence of ischemic complications. Inactive by itself but is transformed into a biologically active form (lysine-vasopressin) by the action of tissue endopeptidases and exopeptidases. Due to its longer half-life (2-10 h) compared to ornipressin, may be administered as a bolus. Has lower incidence of adverse ischemic effects. The plasma volume expanders are indicated for the correction of abnormal hemodynamic parameters in HRS and Albumin useful for plasma volume expansion and maintenance of cardiac output. In our study Terlipressin and albumin was significantly more effective for HRS type-1 and spontaneous bacterial peritonitis than HRS type-1 without active bacterial infections.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
