{"@context":"https://schema.org","@type":"Article","headline":"Circulatory function and hepatorenal syndrome in cirrhosis","description":"HepatologyVolume 42, Issue 2 p. 439-447 Liver Failure and Liver DiseaseFree Access Circulatory function and hepatorenal syndrome in cirrhosis† Luis Ruiz-del-Arbol, Corresponding Author Luis Ruiz-del-Arbol lruizarbol@meditex.es Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain fax: (34) 91-336-80-85Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, Ctra. de Colmenar Viejo Km 9.1, 28034 Madrid, Spain===Search for more papers by this authorAlberto Monescillo, Alberto Monescillo Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorCarlos Arocena, Carlos Arocena Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorPaz Valer, Paz Valer Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorPere Ginès, Pere Ginès Liver Unit, Institute of Digestive and Metabolic Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques, August Pi-Sunyer (IDIBAPS), University of Barcelona, Barcelona, SpainSearch for more papers by this authorVíctor Moreira, Víctor Moreira Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorJosé María Milicua, José María Milicua Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorWladimiro Jiménez, Wladimiro Jiménez Hormonal Laboratory, IDIBAPS, Hospital Clinic, University of Barcelona, Barcelona, SpainSearch for more papers by this authorVicente Arroyo, Vicente Arroyo Liver Unit, Institute of Digestive and Metabolic Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques, August Pi-Sunyer (IDIBAPS), University of Barcelona, Barcelona, SpainSearch for more papers by this author Luis Ruiz-del-Arbol, Corresponding Author Luis Ruiz-del-Arbol lruizarbol@meditex.es Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, Spain fax: (34) 91-336-80-85Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, Ctra. de Colmenar Viejo Km 9.1, 28034 Madrid, Spain===Search for more papers by this authorAlberto Monescillo, Alberto Monescillo Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorCarlos Arocena, Carlos Arocena Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorPaz Valer, Paz Valer Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorPere Ginès, Pere Ginès Liver Unit, Institute of Digestive and Metabolic Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques, August Pi-Sunyer (IDIBAPS), University of Barcelona, Barcelona, SpainSearch for more papers by this authorVíctor Moreira, Víctor Moreira Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorJosé María Milicua, José María Milicua Hepatic Hemodynamic Unit, Gastroenterology Department, Hospital Ramón y Cajal, University of Alcalá, Madrid, SpainSearch for more papers by this authorWladimiro Jiménez, Wladimiro Jiménez Hormonal Laboratory, IDIBAPS, Hospital Clinic, University of Barcelona, Barcelona, SpainSearch for more papers by this authorVicente Arroyo, Vicente Arroyo Liver Unit, Institute of Digestive and Metabolic Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques, August Pi-Sunyer (IDIBAPS), University of Barcelona, Barcelona, SpainSearch for more papers by this author First published: 23 June 2005 https://doi.org/10.1002/hep.20766Citations: 400 † Potential conflict of interest: Nothing to report. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat 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 · 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.) Hepatorenal syndrome is a functional renal failure due to intense renal vasoconstriction that frequently develops in patients with cirrhosis and ascites.1 Two types of hepatorenal syndrome have been identified.2 Type 1 is characterized by rapidly progressive renal failure. It frequently follows a precipitating event—usually an infection—and is associated with extremely short survival. Type 2 is characterized by moderate and steady renal failure that develops insidiously. It is usually detected in patients who respond poorly to diuretics and is associated with longer survival. Hepatorenal syndrome occurs in the setting of a circulatory dysfunction characterized by arterial hypotension and marked activation of the renin-angiotensin and sympathetic nervous systems.2 Because there is vasoconstriction in the kidneys3 and in other extrasplanchnic territories,4, 5 the suggestion has been raised that hepatorenal syndrome is caused by an accentuation of the splanchnic arterial vasodilation present in nonazotemic patients with cirrhosis and ascites.6 However, there is no study proving this contention. The potential differences in systemic hemodynamics between type 1 and type 2 hepatorenal syndrome have never been explored. This article reports a study assessing systemic and hepatic hemodynamics and the activity of the endogenous vasoactive systems in a large series of patients who had cirrhosis with ascites before and after the development of hepatorenal syndrome. Patients and Methods Study Design. Patients under 75 years of age without insulin-dependent diabetes mellitus, arterial hypertension, or any significant disease other than cirrhosis who were admitted to the hospital with tense ascites and normal serum creatinine concentration (<1.2 mg/dL) were considered for the study. Patients with tense ascites and infection or gastrointestinal hemorrhage were considered after 5 days of recovery from these complications; patients with encephalopathy were considered after 2 days of recovery provided they showed normal serum creatinine concentration at the time of resolution of these complications. Diagnosis of cirrhosis was based on histology or on clinical, laboratory, and ultrasonography findings. Complete history and physical examination, chest and abdominal X-rays, electrocardiography, abdominal ultrasonography, laboratory tests, and blood and ascitic fluid cultures were performed. Patients were excluded if they had proteinuria above 500 mg/dL, abnormal renal ultrasonography, or hepatocellular carcinoma. Patients gave written informed consent to participate in the study, which was approved by the Ethics Committee of the Hospital Ramón y Cajal and conducted according to the guidelines of Good Clinical Practice. A baseline study was performed after at least 4 days on a 50-70 mmol/d sodium diet and without diuretics or beta-blockers. At 8 A.M. of the fifth day, after overnight fasting and following 1 hour of bed rest, samples were obtained to measure liver and renal function tests, plasma renin activity, and plasma concentrations of aldosterone and norepinephrine. Urine was subsequently collected for 24 hours. Hemodynamic measurements were performed on the sixth day. Patients were then treated by total paracentesis plus intravenous albumin (8 g/L of ascitic fluid removed; Grifols International S.A., Barcelona, Spain), discharged from the hospital with diuretics, and followed up until the end of the study (1 year after the inclusion of the last patient), liver transplantation, or death. Diuretic dosage was adjusted to prevent ascites recurrence. Patients were advised to avoid nonsteroidal anti-inflammatory drugs. Patients who developed hepatorenal syndrome during follow-up were studied again using an identical protocol. Because of the high prevalence of prerenal azotemia in decompensated patients with cirrhosis who were treated with diuretics, and because of the complexity of the differential diagnosis of hepatorenal syndrome, which requires an acute expansion of the plasma volume, renal failure detected in otherwise uncomplicated patients during their regular follow-up visits to the outpatient clinic were considered to be diuretic-induced. Hepatorenal syndrome was therefore diagnosed in all patients during a hospital admission for the treatment of a complication: tense ascites refractory to diuretics in most patients with type 2 hepatorenal syndrome and in some with type 1 hepatorenal syndrome; encephalopathy; infection; or gastrointestinal hemorrhage. In 1 patient, hepatorenal syndrome was detected in the postoperative period of a partial hepatectomy to remove a hepatocellular carcinoma. The diagnostic criteria for hepatorenal syndrome were those proposed by the International Ascites Club.2 In patients with bacterial infections or gastrointestinal hemorrhage and in patients with hepatic encephalopathy, the protocol was repeated after 5 and 2 days, respectively, of recovery from these complications. Ascites was treated after completion of the protocol. No patient had more than one follow-up investigation. Hemodynamic and Neurohormonal Measurements. Under local anesthesia, a catheter introducer (USCI International, Galway, Ireland) was placed in the right jugular vein using the Seldinger technique. Under fluoroscopic guidance, a Swan-Ganz catheter (Edwards Laboratory, Los Angeles, CA) was advanced into the pulmonary artery for measurement of cardiopulmonary pressures and cardiac output via thermodilution. A 7 French balloon-tipped catheter (MediTech Cooper Scientific Corp., Watertown, MA) was advanced into the main right hepatic vein to measure wedged and free hepatic venous pressures and the hepatic venous pressure gradient. Measurements were performed in triplicate, and the average was taken.7 The external zero-pressure point was at the level of the right atrium (midaxillary line). The hepatic blood flow was measured during a continuous intravenous infusion of an indocyanine green solution (Serb; Laboratoires Pharmaceutiques, Paris, France) at a constant rate of 0.1 or 0.2 mg/min−1 (Child-Turcotte-Pugh class C and B patients, respectively) as previously described.8 A hepatic extraction of more than 10% and steady venous indocyanine green solution levels were required for the calculation of hepatic blood flow. Heart rate and arterial pressure were measured with an automatic sphyngomanometer (Dinamap-Critikion, Tampa, FL). Systemic vascular resistance was calculated as mean arterial pressure (mm Hg) − right atrial pressure (mm Hg)/cardiac output (L/min−1) × 80. Stroke work was calculated as (MAP-PWCP) × (stroke volume) × 0.0136 (gm-m). Left ventricular stroke work was calculated as systolic arterial pressure × systolic volume × 0.0136 (gm-m). Plasma renin activity and plasma concentration of aldosterone and norepinephrine were determined via radioimmunoassay (Clinical Assays, Cambridge, MA; Diagnostic and Products Corp., Los Angeles, CA; and CAIBL Laboratories, Hamburg, Germany, respectively).9, 10 Values in healthy subjects on a low sodium diet were: 1.35 ± 0.94 ng/mL · hr, 24.2 ± 11.3 ng/dL, and 253 ± 114 pg/mL, respectively. Statistical Analysis. Calculations were performed with SPSS version 10.0 software (SPSS, Chicago, IL). Comparisons between groups were performed with the chi-square test or Fisher exact test for categorical data and the Student t test and Mann-Whitney test for continuous data. Stepwise logistic regression was used to identify independent predictors for development of hepatorenal syndrome. Probability of survival curves was constructed using the Kaplan-Meier method and was compared with the log-rank test. Patients submitted to liver transplantation or who were lost from follow-up were considered censored. Results are expressed as the mean ± SD. All reported P values are two-tailed, with values less than .05 considered significant. Results Clinical Data. Eighty-two patients admitted between February 1995 and November 1999 who agreed to participate in the study were considered. Nine patients were excluded before baseline investigations because of hepatocellular carcinoma (n = 5) or renal, cardiac, or respiratory disease (n = 4). Seven additional patients were excluded after baseline investigations because they were lost from follow-up (n = 6) or refused to continue in the study (n = 1). The investigation thus included 66 patients. Forty-seven of the patients were male, and the mean age was 60 ± 9 years. The cause of cirrhosis was alcoholic in 35 patients, hepatitis C virus infection in 25, and alcohol plus hepatitis C in 6. Fifteen of the 41 patients with alcoholism were active drinkers at inclusion. Four of them stopped drinking during follow-up. On the other hand, 5 out the 26 abstainers at inclusion reassumed alcohol intake during the study period. Most of the patients were admitted to the hospital for the treatment of an episode of tense ascites alone (n = 54) or associated to hepatic encephalopathy (n = 6). The remaining 6 patients were admitted with ascites and severe infections (n = 4) or gastrointestinal hemorrhage (n = 2). In these 6 patients, arterial pressure, pulse rate, and renal function remained stable during the 5-day washout period between recovery from these complications and the initiation of the protocol. At inclusion, 34 patients were Child-Turcotte-Pugh grade C, and 32 were grade B. Five patients (2 with hepatorenal syndrome) underwent transplantation. The 7 patients excluded after baseline measurements did not differ from the 65 included into the study regarding the cause of cirrhosis (4 had alcoholic cirrhosis and 3 had cirrhosis associated with hepatitis C) and Child-Turcotte-Pugh grade (3 were grade B and 4 were grade C). There were also no differences between patients excluded after baseline measurements and those included into the study in age, sex, renal and hepatic function, systemic and hepatic hemodynamics, and degree of activity of the renin-angiotensin and sympathetic nervous systems (data not shown). Thirty-nine patients did not develop hepatorenal syndrome during the study period (group A). The remaining 27 patients developed hepatorenal syndrome (group B). The prevalence of hepatorenal syndrome was unrelated to the cause of cirrhosis. On the other hand, in patients with alcohol-associated cirrhosis, the prevalence of hepatorenal syndrome was similar in active drinkers (8 cases with hepatorenal syndrome from the 20 active drinkers at inclusion or during follow-up) and abstainers (7 cases with hepatorenal syndrome from the 21 patients who abstained throughout the study period). Hepatorenal syndrome was type 1 in 12 cases and type 2 in 15. Type 1 hepatorenal syndrome was chronologically related to severe bacterial infection in 6 cases and to surgical operation and variceal hemorrhage in 1 case. Type 1 hepatorenal syndrome was detected during a hospitalization for refractory ascites (n = 2) and hepatic encephalopathy (n = 3) in the 5 patients without a precipitating event. The time between baseline and follow-up studies in patients developing hepatorenal syndrome was 359 ± 212 days (275 ± 153 and 425 ± 233 in patients with type 1 and type 2 hepatorenal syndrome, respectively). The mean follow-up period in the group A patients was 639 ± 329 days. Differences Between Patients From Groups A and B at Baseline and Changes Associated With the Development of Hepatorenal Syndrome in Patients From Group B. At baseline, patients from group A showed significantly higher mean arterial pressure, cardiac output, stroke volume, stroke work, and urinary sodium excretion and significantly lower plasma renin activity, plasma concentrations of aldosterone and norepinephrine, wedged hepatic venous pressure, and hepatic venous pressure gradient compared with patients from group B (Table 1). Although baseline serum creatinine was within the normal limits in all cases, the mean value was significantly lower in group A. There were no differences in peripheral vascular resistance and heart rate. Of the 10 variables showing significant difference between groups, only plasma renin activity (RR: 31.3; 95% CI: 6.5-150.3; P < .0001) and cardiac output (RR: 5.8; 95% CI: 1.3-25.2; P < .05) were independently associated with the development of hepatorenal syndrome according to a multivariate analysis (Fig. 1). Table 1. Baseline Measurements in Patients Who Did Not Develop Hepatorenal Syndrome (Group A) and Baseline and Follow-up Measurements in Patients Who Presented With Hepatorenal Syndrome (Group B) Group A (n = 39) Group B (n = 27) Baseline Measurements Baseline Measurements Follow-up Measurements Serum bilirubin (mg/dL) 2.7 ± 1.9 3.8 ± 3.9 4.3 ± 3.9 Serum albumin (g/L) 24 ± 4 24 ± 5 24 ± 4 Prothrombin index (%) 64 ± 14 59 ± 14 51 ± 13††††††††, ††† P < .001 with respect to baseline values of group B. Child-Turcotte-Pugh score (points) 9.7 ± 1.3 9.9 ± 1.3 10.8 ± 2.1†† P < .05; MELD score (points) 13.7 ± 4.0 15.8 ± 4.6 25.7 ± 6.8††††††††, ††† P < .001 with respect to baseline values of group B. Serum creatinine (mg/dL) 0.85 ± 0.18 1.05 ± 0.26****** P < .005; 3.03 ± 1.49††††††††, ††† P < .001 with respect to baseline values of group B. Serum sodium (mmol/L) 134.5 ± 4.8 132.6 ± 4.6 127.0 ± 5.1††††††††, ††† P < .001 with respect to baseline values of group B. Urinary sodium (mmol/L) 17.4 ± 18.9 7.0 ± 6.1****** P < .005; 4.0 ± 4.5†† P < .05; MAP (mmHg) 88 ± 9 83 ± 9** P < .05; 75 ± 7††††††††, ††† P < .001 with respect to baseline values of group B. HR (bpm) 87 ± 15 85 ± 13 82 ± 14 RAP (mmHg) 6.7 ± 2.5 6.9 ± 2.6 5.7 ± 2.2†† P < .05; PAP (mmHg) 15.2 ± 3.8 14.3 ± 4.3 12.8 ± 2.8†††† P < .01; PCWP (mmHg) 9.2 ± 3.2 9.2 ± 2.6 7.5 ± 2.6††††††††, ††† P < .001 with respect to baseline values of group B. CO (L/min) 7.2 ± 1.8 6.0 ± 1.2**** P < .01; 5.4 ± 1.5†††††††, ††† P < .001 with respect to baseline values of group B. SVR (dyne · s/cm−5) 962.0 ± 256.4 1,058.6 ± 265.6 1,096.1 ± 327.6 Stroke volume (mL/beat) 85.2 ± 17.0 73.2 ± 18.9** P < .05; 65.3 ± 18.8†† P < .05; Stroke work (gm-m) 91.3 ± 17.9 75.3 ± 22.9**** P < .01; 62.7 ± 21.3††††††††, ††† P < .001 with respect to baseline values of group B. Left ventricular stroke work (gm-m) 140.0 ± 32.6 114.2 ± 43.5** P < .05; 88.5 ± 32.3††††††††, ††† P < .001 with respect to baseline values of group B. Plasma renin activity (ng/mL · hr) 3.1 ± 2.3 9.9 ± 5.2******** P < .001 with respect to baseline values of group A. 17.5 ± 11.4††††††††, ††† P < .001 with respect to baseline values of group B. Plasma aldosterone (ng/dL) 32.0 ± 30.7 130.5 ± 69.4****** P < .005; 202.5 ± 130.0††††††††, ††† P < .001 with respect to baseline values of group B. Plasma norepinephrine (pg/mL) 221.6 ± 68.2 571.1 ± 241.1******** P < .001 with respect to baseline values of group A. 965.0 ± 502.5††††††††, ††† P < .001 with respect to baseline values of group B. WHVP (mmHg) 28.0 ± 4.0 30.5 ± 4.0** P < .05; 29.5 ± 5.0 FHVP (mmHg) 11.5 ± 3.0 11.0 ± 4.0 8.5 ± 3.5†††† P < .01; HVPG (mmHg) 16.5 ± 3.0 19.5 ± 3.0****** P < .005; 21.0 ± 4.0†††† P < .01; HBF (mL/min)‡‡ A hepatic extraction greater than 10% was required for the calculation of hepatic blood flow in 15 patients of group A and 19 patients of group B. 1,123 ± 328.0 948 ± 221.1 713 ± 188.4††††††††, ††† P < .001 with respect to baseline values of group B. NOTE. Data are presented as mean ± SD. Abbreviations: MELD, Model for End-Stage Liver Disease; MAP, mean arterial pressure; HR, heart rate; RAP, right atrial pressure; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedged pressure; CO, cardiac output; SVR, systemic vascular resistance; WHVP, wedged hepatic venous pressure; FHVP, free hepatic venous pressure; HVPG, hepatic venous pressure gradient; HBF, hepatic blood flow. * P < .05; ** P < .01; *** P < .005; **** P < .001 with respect to baseline values of group A. † P < .05; †† P < .01; g P < .005; ††††, ††† P < .001 with respect to baseline values of group B. ‡ A hepatic extraction greater than 10% was required for the calculation of hepatic blood flow in 15 patients of group A and 19 patients of group B. Figure 1Open in figure viewerPowerPoint (A) Probability of developing hepatorenal syndrome during follow-up in patients with baseline plasma renin activity equal or lower and higher than 4 ng/mL · hr (upper value in healthy subjects on a 50-mEq sodium diet during 5 days). (B) Probability of developing hepatorenal syndrome during follow-up in patients with baseline cardiac output higher and lower than 6 L/min (median value in the entire series of patients). Development of hepatorenal syndrome in group B was associated with a significant decrease in prothrombin index; an increase in Child-Turcotte-Pugh score, Model for End-Stage Liver Disease score, and hepatic venous pressure gradient; a reduction in hepatic blood flow; dilutional hyponatremia; a significant decrease in mean arterial pressure, cardiac output, stroke volume, stroke work, and cardiopulmonary pressures (pulmonary capillary wedged pressure, pulmonary artery pressure, and right atrial pressure); and marked stimulation of the renin-angiotensin-aldosterone system and sympathetic nervous system (Table 1; Figs. 2, 3). No significant changes were observed in heart rate and peripheral vascular resistance (Table 1; Fig. 3). Figure 2Open in figure viewerPowerPoint Individual changes of mean arterial pressure, cardiac output, and pulmonary capillary wedged pressure associated with hepatorenal syndrome in patients from group B. BS-M, baseline measurements; HRS-M, measurements after development of hepatorenal syndrome. Figure 3Open in figure viewerPowerPoint Individual changes in systemic vascular resistance and plasma renin activity associated with hepatorenal syndrome in patients from group B. Systemic vascular resistance remained unchanged despite a marked increase in plasma renin activity, suggesting an accentuation of the arterial vasodilatation already present in nonazotemic cirrhosis with ascites compensated by a stimulation of the renin-angiotensin system and other endogenous vasoconstrictors. BS-M, baseline measurements; HRS-M, measurements after development of hepatorenal syndrome. Differences Between Patients With Type 1 and Type 2 Hepatorenal Syndrome. The only significant difference between patients who developed type 1 and type 2 hepatorenal syndrome at baseline was a higher plasma renin activity and higher aldosterone and norepinephrine concentration (P < .001) in the former group of patients (Tables 2, 3). Table 2. Baseline and Follow-up Measurements in Patients Who Developed Type 2 Hepatorenal Syndrome Baseline Measurements (n = 15) Follow-up Measurements (n = 15) P Value Serum bilirubin (mg/dL) 3.7 ± 4.6 3.2 ± 3.0 NS Serum albumin (g/L) 26 ± 5 26 ± 4 NS Prothrombin index (%) 59 ± 13 55 ± 14 NS Child-Turcotte-Pugh score (points) 9.8 ± 1.6 9.8 ± 1.9 NS MELD score (points) 15.6 ± 4.9 21.9 ± 5.7 <.001 Serum creatinine (mg/dL) 1.05 ± 0.2 2.11 ± 0.4 <.001 Serum sodium (mmol/L) 133.2 ± 4.7 129.6 ± 4.0 .01 Urinary sodium (mmol/L) 7.2 ± 6.2 5.6 ± 5.1 NS MAP (mmHg) 86 ± 10 79 ± 7 .005 HR (bpm) 84 ± 12 80 ± 14 NS RAP (mmHg) 6.8 ± 2.1 6.1 ± 1.8 NS PAP (mmHg) 14.0 ± 3.0 12.9 ± 2.1 NS PCWP (mmHg) 8.9 ± 1.6 8.3 ± 2.0 NS CO (L/min) 6.2 ± 1.4 5.8 ± 1.2 NS SVR (dyne · s/cm−5) 1,032.0 ± 251.3 1,014.3 ± 276.4 NS Stroke volume (mL/beat) 75.6 ± 19.8 71.7 ± 18.2 NS Stroke work (gm-m) 79.5 ± 28.1 73.9 ± 20.3 NS Left ventricular stroke work (gm-m) 120.8 ± 53.5 106.5 ± 29.9 NS Plasma renin activity (ng/mL · hr) 7.5 ± 3.7 11.9 ± 4.8 <.001 Plasma aldosterone (ng/dL) 86.8 ± 61.3 118.4 ± 80.1 .01 Plasma norepinephrine (pg/mL) 411.8 ± 155.4 628.8 ± 320.3 <.01 WHVP (mmHg) 29.5 ± 5.5 27.5 ± 5.5 <.005 FHVP (mmHg) 10.5 ± 4.0 8.0 ± 3.0 <.005 HVPG (mmHg) 19.0 ± 3.2 19.5 ± 2.0 NS HBF (mL/min)** A hepatic extraction greater than 10% was required for the calculation of hepatic blood flow in 10 patients. 1,064 ± 223 824 ± 180 <.005 NOTE. Data are presented as mean ± SD. Abbreviations: NS, not significant; MELD, Model for End-Stage Liver Disease; MAP, mean arterial pressure; HR, heart rate; RAP, right atrial pressure; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedged pressure; CO, cardiac output; SVR, systemic vascular resistance; WHVP, wedged hepatic venous pressure; FHVP, free hepatic venous pressure; HVPG, hepatic venous pressure gradient; HBF, hepatic blood flow. * A hepatic extraction greater than 10% was required for the calculation of hepatic blood flow in 10 patients. Table 3. Baseline and Follow-up Measurements in Patients Who Developed Type 1 Hepatorenal Syndrome Baseline Measurements (n = 12) Follow-up Measurements (n = 12) P Value Serum bilirubin (mg/dL) 3.8 ± 2.8 5.6 ± 4.5 <.05 Serum albumin (g/L) 23 ± 4 22 ± 4 NS Prothrombin index (%) 59 ± 15 46 ± 10 <.05 Child-Turcotte-Pugh score (points) 10.1 ± 0.9 12.0 ± 1.7**** P < .01; <.005 MELD score (points) 16.0 ± 4.5 30.4 ± 5.1******** P < .001 with respect to values (baseline and follow-up) of patients who developed type 2 hepatorenal syndrome shown in Table 2. <.001 Serum creatinine (mg/dL) 1.04 ± 0.3 4.26 ± 1.4******** P < .001 with respect to values (baseline and follow-up) of patients who developed type 2 hepatorenal syndrome shown in Table 2.","datePublished":"2024-10-05T20:33:59.148894Z","author":[{"@type":"Person","name":"Luís Ruíz-del-Árbol","url":"/author/4081700"},{"@type":"Person","name":"Alberto Monescillo","url":"/author/4397768"},{"@type":"Person","name":"Carlos Arocena","url":"/author/4411440"},{"@type":"Person","name":"Paz Valer","url":"/author/4411441"},{"@type":"Person","name":"Pere Ginès","url":"/author/2832661"},{"@type":"Person","name":"Víctor Moreira","url":"/author/4411442"},{"@type":"Person","name":"José Milicua","url":"/author/4411443"},{"@type":"Person","name":"Wladimiro Jiménez","url":"/author/1270084"},{"@type":"Person","name":"Vicente Arroyo","url":"/author/2830238"}],"publisher":{"@type":"Organization","name":"ResearchHub","logo":{"@type":"ImageObject","url":"https://researchhub.com/logo.png","width":512,"height":512},"url":"https://researchhub.com"},"inLanguage":"en-US"}

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