Ascites, Hepatorenal Syndrome and Spontaneous Bacterial Peritonitis in Patients with Portal Hypertension / 대한소화기학회지

Ascites, hepatic encephalopathy and variceal hemorrhage are three major complications of portal hypertension. The diagnostic evaluation of ascites involves an assessment of its etiology by determining the serum-ascites albumin gradient and the exclusion of spontaneous bacterial peritonitis. Ascites is primarily related to an inability to excrete an adequate amount of sodium into urine, leading to a positive sodium balance. Sodium restriction and diuretic therapy are keys of ascites control. But, with the case of refractory ascites, large volume paracentesis and transjugular portosystemic shunts are required. In hepatorenal syndrome, splanchnic vasodilatation with reduction in effective arterial volume causes intense renal vasoconstriction. Splanchnic and/or peripheral vasoconstrictors with albumin infusion, and renal replacement therapy are only bridging therapy. Liver transplantation is the only definitive modality of improving the long term prognosis.

Insuficiencia renal en pacientes con cirrosis y ascitis: incidencia, etiología y factores predictivos / Renal failure in patients with cirrhosis and ascites: incidence, etiology and predictive factors

BACKGROUND: renal insufficiency (RI) is a frequent complication in patients with cirrhosis and ascites. OBJECTIVE: to assess the incidence, causes, predictive factors and prognosis of RI in cirrhotic patients with ascites. PATIENT AND METHODS: descriptive study of cases and controls. Clinical histories of 162 admissions in 103 patients during 3 years were reviewed. It was considered RI when there was an increase of creatininemia > 1.5 mg/dl. The predictive factors, clinical features, and mortality of the patients with and without RI were compared. RESULTS: a diagnosis of RI was made in 35 cases (21.6%). Hospital mortality rate was 18.5%: with RI 57.1%, controls 7.8% (p<0.01). Etiology: reversible prerrenal failure (54.3%), SHR 1 (14.2%) and 2 (5.7%), septic shock by spontaneous bacterial peritonitis (SBP) (11.4%), NTA (8.5%). The patients with and without RI had a Child-Pügh score average (+/-DS): 12.8 (1.8) and 11.4 (1.9) (p=0.0002) respectively. The patients with RI had higher values of total bilirubin, AST, ALT, white blood cells, time prothrombin, and minors values of serum sodium, Hto, Hb, protein, albumin and cholinesterase that controls (p<0.05). The clinical variables associated with RI included infections (OR 1.4), SBP (OR 4) and hepatic encephalopathy (OR 2.4). In the multivariate analysis, the independent predictive factors for RI were hyponatremia, bilirubinemia greater to 10 mg/dl and SPB. CONCLUSION: in cirrhotic patients RI have high mortality. The most frequent cause was reversible prerrenal failure. The risk of RI was increased significantly in patients with hyponatremia, marked hyperbilirubinemia and SPB.

Background: renal insufficiency (RI) is a frequent complication in patients with cirrhosis and ascites. Objective: to assess the incidence, causes, predictive factors and prognosis of RI in cirrhotic patients with ascites. Patient and methods: descriptive study of cases andcontrols. Clinical histories of 162 admissions in 103 patients during 3 years were reviewed. It was consideredRI when there was an increase of creatininemia > 1,5 mg/dl. The predictive factors, clinical features, andmortality of the patients with and without RI were compared. Results: a diagnosis of RI was made in 35 cases (21.6%). Hospital mortality rate was 18.5%: with RI 57.1%, controls 7.8% (p< 0.01). Etiology: reversible prerrenal failure (54.3%), SHR 1 (14.2%) and 2 (5.7%), septic shock by spontaneous bacterial peritonitis (SBP) (11.4%), NTA (8.5%). The patientswith and without RI had a Child-Pügh score average (± DS): 12.8 (1.8) and 11,4 (1.9) (p=0.0002) respectively.The patients with RI had higher values of total bilirubin, AST, ALT, white blood cells, time prothrombin, and minors values of serum sodium, Hto, Hb, protein,albumin and cholinesterase that controls (p<0.05). The clinical variables associated with RI included infections (OR 1.4), SBP (OR 4) and hepatic encephalopathy (OR 2.4). In the multivariate analysis, the independent predictive factors for RI were hyponatremia, bilirubinemia greater to 10 mg/dl and SPB. Conclusion: in cirrhotic patients RI have high mortality.The most frequent cause was reversible prerrenal failure. The risk of RI was increased significantly in patients with hyponatremia, marked yperbilirubinemiaand SPB.

Síndrome hepato-renal / Hepatic-renal syndrome

Junto a la hemorragia digestiva alta por ruptura de várices esofágicas, la encefalopatía portal, el síndrome ascítico y la peritonitis bacteriana espontánea, el síndrome hepato-renal es una de las complicaciones de la cirrosis hepática avanzada. Es una insuficiencia renal aguda funcional habitualmente irreversible y de curso fatal. Se debería a una vasoconstricción cortical renal con aumento de substancias vasoconstrictoras endógenas (angiotensina, epinefrina y endotelinas) y disminución de las vasodilatadoras (protaglandinas y kalicreínas). Se caracteriza por oliguria con sedimento urinario normal pero con excreción baja o nula de sodio em la orina, osmolaridad urinaria elevada, hiponatremia y retención nitrogenada con elevación de nitrógeno uréico y de creatinina. El pronóstico es malo y solo existen medidas terapéuticas preventivas

Problemas renales de la cirrosis

Cirrhosis of the liver is a common entity frequently seen by the clinician only after initiation of edema or ascitis. Renal problems have been described for many years associated to all types of cirrhosis, and are responsible for many abnormalities of water and electrolytes seen in these patients. One of the most remarkable renal abnormalities is sodium retention, with urinary excretion (Una V) of less than 10 mEq/1. This fact explains the common appearance of edema and ascitis even in the early states of cirrhosis. For many years two main theories have been postulated in order to explain this avid sodium retention: 1) The "underfill theory" states that the initial event is a state of peripheral vasodilatation that causes ineffective plasma volume and sodium retention by the kidney, meaning that the sodium retention is a secondary event. 2) the "overflow theory" in contrast, emphasizes that the primary event is sodium retention by the kidney, with secondary expansion of plasma volume and associated sequestration of fluid in the abdomen due to portal hypertension and a reduction of the colloid-osmotic pressure. Recent evidence is suggestive that both theories play a significant role in the avid sodium retention of cirrhosis. In order to explain the sodium retention by the kidney the following humoral factors have been postulated: increased secretion and decreased degradation of aldosterone, decreased production of prostaglandin E, increased secretion of catecholamines, decreased response to the natriuretic atrial factor and abnormalities of the kalikrein-kinin system. Although some studies have shown abnormalities in the handling of water by the kidney, most of the evidence suggest that it is due to the sodium retention...