ABSTRACT
Es indispensable conservar la función renal de los pacientes con cirrosis hepática, ya que la insuficiencia renal se asocia con una alta morbimortalidad en dichos países. La vasoconstricción sistémica, la disminución del flujo sanguíneo renal y la disminución de metabolitos urinarios de prostaglandinas son importantes en la patogénesis de esta nefropatía. El misoprostol, prostaglandina sintética, puede modificar favorablemente algunos de los cambios en la hemodinamia renal de la cirrosis. Objetivo: Evaluar los cambios de la función renal en el paciente cirrótico con el uso de misoprostol. Metodología: se estudiaron 15 pacientes con cirrosis hepática que había desarrollado ascitis, con creatinina sérica menor a 1.5 mg/dL. Se determinaron: depuración de creatinina, volumen urinario, excreción de sodio urinario y la fracción excretada del mismo en 24 h., el filtrado glomerular y el flujo sanguíneo renal bilateral antes y después de la administración vía oral e misoprostol. Se aceptó un valor significativo a p < 0.05. resultados: Se encontró mejoría significativa únicamante en el flujo sanguíneo renal (p= 0.02), después de la administración de misoprostol. Sin embargo, al separar a los pacientes en dos grupos: los que usan diuréticos y aquellos que no los usan, se obtiene una diferencia significativa en el filtrado glomerular (p < 0.001), el flujo sanguíneo renal (p < 0.01) y la diurésis (p < 0.001). No hubo diferencias significativas en otros parámetros. Conclusiones: El uso de misoprostol en los pacientes cirróticos que utilizan diuréticos para el tratamiento de asitis y retención hídrica, mejora los parámetros de la función renal, al incrementar el flujo sanguíneo renal, el filtrado glomerular y la diuresis, actuando como vasodilatador en las arterias renales
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Liver Cirrhosis/complications , Liver Cirrhosis/urine , Liver Cirrhosis/therapy , Misoprostol/therapeutic use , Prostaglandins E/therapeutic use , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , Diuresis/drug effectsABSTRACT
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...
Subject(s)
Humans , Liver Cirrhosis/complications , Liver Cirrhosis/physiopathology , Liver Cirrhosis/urine , Kidney Diseases/etiology , Hepatorenal Syndrome/complications , Hepatorenal Syndrome/diagnosis , Hepatorenal Syndrome/epidemiology , Hepatorenal Syndrome/etiology , Hepatorenal Syndrome/physiopathology , Hepatorenal Syndrome/mortality , Hepatorenal Syndrome/drug therapy , Hepatorenal Syndrome/therapyABSTRACT
Foi investigado o fenótipo acetilador de isoniazida em 23 pacientes caucasóides com cirrose hepática, por intermédio da avaliaçäo do percentual de acetilisoniazida na urina. A proporçäo de acetiladores lentos entre cirróticos foi bem menor que aquela verificada em um grupo controle de caucasóides. Ao se separar os pacientes quanto ao grau de insuficiência hepática, os dados mostraram que a acetilaçäo da isoniazida é tanto mais lenta quanto maior é a insuficiência hepática. Concluiu-se que a cirrose afeta a capacidade hepática de acetilaçäo da isoniazida, alterando o fenótipo acetilador desse medicamento
Subject(s)
Humans , Isoniazid/metabolism , Liver Cirrhosis/metabolism , Phenotype , Isoniazid/urine , Acetylation , Liver Cirrhosis/urine , Liver/metabolismABSTRACT
This study was carried out on 50 male patients with schistosomal bepatic fibrosis, 30 with resistant ascites, 10 with reversible ascites and 10 non-ascitic patients. The schistosomal nature of the disease was ascertained by proper history, clinical picture, stool and urine analysis and rectal mucosal scraping with sigmoidoscopic examination. Thirty-two patients had schistosoma mansoni while the remaining eighteen had combined schistosoma mansoni and haematobium infestation. All the studied patients were subjected to full history taking, thorough clinical examination, routine laboratory tests and renal function studies. Marked degree of water retention was apparent in patients with resistant ascites. Dilution study revealed diminished water elimination in cases without or with reversible ascites. Renal tubular concentration studies appeared to be normal in patients without or with reversible ascites. On the other hand schistosomal patients with resistant ascites showed variable degrees of impaired renal tubular concentrating capacity. The data of sodium clearance studies indicated that all patients with schistosomal hepatic fibrosis retained sodium avidly, especially those with resistant ascites. The glomerular filtration rate as assessed by endogenous creatinine clearance was markedly reduced in schistosomal patients with resistant ascites. The glomerular filtration rate was normal in non-ascitic patients and moderately reduced in patients with reversible ascites. Renal plasma and renal blood flow were markedly reduced in patients with resistant ascites, while mild decrease was observed in patients with reversible ascites and normal levels were obtained it non-ascitic patients