RESUMO
BACKGROUND: Renal failure (RF) is reported to occur in 11-49% of the patients with decompensated end-stage liver disease (ESLD) and has been associated with increased mortality, particularly in the occurrence of hepatorenal syndrome (HRS) type 1. AIMS: To evaluate the frequency and outcome of RF in patients admitted to the hospital due to decompensated ESLD and to assess the impact of the underlying cause of RF on survival. MATERIAL AND METHODS: Four hundred and six patients (65% males, mean age 62 ± 12 years) with decompensated ESLD were evaluated for the occurrence of RF (defined as serum creatinine ³ 1.5 mg/mL). The underlying cause of RF was reckoned in each subject and compared to outcome. RESULTS: Renal failure was observed in 39% of the patients at admission and in 10% of the subjects during hospitalization. Mortality was significantly higher in subjects with RF (26 vs. 1%, p < 0.000001). Hypovolemia, bacterial infections, parenchymal kidney diseases and HRS were identified as causes of RF in, respectively, 40, 32, 15 and 12% of the cases. Mortality was significantly higher in those subjects with HRS type 1 and bacterial infections, when compared to other causes of RF. CONCLUSIONS: Renal failure occurs in nearly half of the patients with decompensated ESLD. It is most commonly caused by hypovolemia and bacterial infections. Occurrence of RF has an adverse impact in patient survival, particularly in those subjects with bacterial infections and HRS type 1, prone to develop progressive renal dysfunction despite intensive medical care.
Assuntos
Doença Hepática Terminal/epidemiologia , Doença Hepática Terminal/mortalidade , Mortalidade Hospitalar , Cirrose Hepática/epidemiologia , Cirrose Hepática/mortalidade , Insuficiência Renal/epidemiologia , Insuficiência Renal/etiologia , Fatores Etários , Idoso , Infecções Bacterianas/complicações , Comorbidade , Progressão da Doença , Feminino , Síndrome Hepatorrenal/complicações , Humanos , Hipovolemia/complicações , Nefropatias/complicações , Masculino , Pessoa de Meia-Idade , Prevalência , Estudos Retrospectivos , Taxa de SobrevidaAssuntos
Ascite/diagnóstico , Biomarcadores/sangue , Síndrome Hepatorrenal/diagnóstico , Hipertensão Portal/diagnóstico , Rim/patologia , Cirrose Hepática/diagnóstico , Fígado/patologia , Ascite/sangue , Ascite/complicações , Ascite/mortalidade , Ascite/patologia , Bilirrubina/sangue , Creatinina/sangue , Síndrome Hepatorrenal/sangue , Síndrome Hepatorrenal/complicações , Síndrome Hepatorrenal/mortalidade , Síndrome Hepatorrenal/patologia , Humanos , Hipertensão Portal/sangue , Hipertensão Portal/complicações , Hipertensão Portal/mortalidade , Hipertensão Portal/patologia , Rim/metabolismo , Rim/fisiopatologia , Fígado/metabolismo , Fígado/fisiopatologia , Cirrose Hepática/sangue , Cirrose Hepática/complicações , Cirrose Hepática/mortalidade , Cirrose Hepática/patologia , Testes de Função Hepática , Prognóstico , Renina/sangue , Fatores de Risco , Albumina Sérica/análise , Índice de Gravidade de Doença , Taxa de SobrevidaRESUMO
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.
Assuntos
Ascite/complicações , Fibrose/complicações , Insuficiência Renal/etiologia , Adulto , Idoso , Biomarcadores/sangue , Métodos Epidemiológicos , Feminino , Síndrome Hepatorrenal/complicações , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Insuficiência Renal/sangue , Insuficiência Renal/mortalidadeRESUMO
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.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Ascite/complicações , Fibrose/complicações , Insuficiência Renal/etiologia , Insuficiência Renal/sangue , Insuficiência Renal/mortalidade , Biomarcadores/sangue , Métodos Epidemiológicos , Prognóstico , Síndrome Hepatorrenal/complicaçõesRESUMO
The mechanism by which ascites develops in cirrhosis is multifactorial Severe sinusoidal portal hypertension and hepatic insufficiency are the initial factors. They lead to a circulatory dysfunction characterized by arterial vasodilation, arterial hypotension, high cardiac output and hypervolemia and to renal sodium and water retention. There are evidences that arterial vasodilation in cirrhosis occurs in the splanchnic circulation and is related to an increased synthesis of local vasodilators. Vascular resistance is normal or increased in the remaining major vascular territories (kidney, muscle and skin and brain). Splanchnic arterial vasodilation not only impairs systemic hemodynamics and renal function but also alters hemodynamics in the splanchnic microcirculation. The rapid and high inflow of arterial blood into the splanchnic microcirculation is the main factor increasing hydrostatic pressure in the splanchnic capillaries leading to an excessive production of splanchnic lymph over lymphatic return. Lymph leakage from the liver and other splanchnic organs is the mechanism of fluid accumulation in the abdominal cavity. Continuous renal sodium and water retention perpetuates ascites formation. Large volume paracentesis associated with albumin infusion is the treatment of choice of tense ascites because it is very effective and rapid and is associated with fewer complications that the traditional treatment (sodium restriction and diuretics). However, diuretic should be given after paracentesis to prevent reaccumulation of ascites. In patients with moderate ascites diuretics should be preferred as initial therapy. Patients with refractory ascites could be treated by paracentesis or percutaneous transjugular portacaval shunt (TIPS). TIPS is more effective in the long term control of ascites but may impair hepatic function and induce chronic hepatic encephalopathy.
Assuntos
Ascite , Cirrose Hepática/complicações , Transplante de Fígado , Paracentese , Derivação Peritoneovenosa , Circulação Esplâncnica/fisiologia , Ascite/diagnóstico , Ascite/etiologia , Ascite/fisiopatologia , Ascite/terapia , Diuréticos/uso terapêutico , Síndrome Hepatorrenal/complicações , Síndrome Hepatorrenal/diagnóstico , Síndrome Hepatorrenal/terapia , Humanos , Cirrose Hepática/diagnóstico , Cirrose Hepática/terapia , Testes de Função Hepática , Prognóstico , Espironolactona/uso terapêuticoRESUMO
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
Assuntos
Humanos , Síndrome Hepatorrenal/complicações , Cirrose Hepática/etiologia , Diagnóstico Diferencial , Necrose Tubular Aguda/diagnóstico , Insuficiência Renal/diagnósticoRESUMO
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...