ABSTRACT
La disfunción renal es una complicación común en pacientes con cirrosis avanzada y está asociadaa un incremento significativo en la mortalidad. Este deterioro de la función renal puede ser reversible en algunos casos, si se identifica y se trata su etiología. La lesión renal aguda (LRA) de origen prerrenal y la necrosis tubular aguda (NTA) son las entidades más frecuentes en pacientes con enfermedad hepática crónica y cirrosis, constituyendo un desafío en los escenarios clínicos actuales. La aparición de nuevos biomarcadores como la lipocalina asociada a la gelatinasa de neutrófilos (NGAL), puede ser un factor determinante para esclarecer el origen de estas dos entidades. En la actualidad, la clasificación de la enfermedad renal establece que un aumento en la creatinina sérica basal >0,3 mg/dL dentro de las primeras 48 horas, o un incremento mayor al 50% desde la línea de base, son suficientes para definir lesión renal aguda, por lo cual, cambios leves en la creatinina sérica en un periodo corto de tiempo, contribuyen a una identificación temprana y previenen desenlaces negativos. Esta revisión de tema abordará la lesión renal aguda en cirrosis desde la fisiopatología, la clasificación actual según guías internacionales, los avances en biomarcadores y las principales etiologías, finalizando con un abordaje general y estrategias de prevención.
Kidney dysfunction is a common complication in patients with advanced cirrhosis and is associated with a significant increase in mortality. This deterioration of kidney function may be reversible in some cases, if its etiology is identified and treated. Acute kidney injury (AKI) of prerenal origin and acute tubular necrosis (ATN) are the most frequent entities in patients with chronic liver disease and cirrhosis, constituting a challenge in current clinical scenarios. The emergence of new biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), may be a determining factor in clarifying the origin of these two entities. Currently, the classification of renal disease establishes that an increase in basal serum creatinine >0,3 mg/dL within the first 48 hours, or an increase higher than 50% from the baseline, are enough to define acute kidney injury, therefore slight changes in serum creatinine in a short period of time contribute to an early identification and prevent negative outcomes. This literature review will address acute kidney injury in cirrhosis from its pathophysiology, current classification according to international guidelines, advances in biomarkers and the main etiologies associated with it, ending with a general approach and prevention strategies.
Subject(s)
Humans , Hepatorenal Syndrome , Acute Kidney Injury , Liver Cirrhosis , Kidney Diseases , Liver DiseasesABSTRACT
Objective To investigate the role of N-acetylcysteine as a protective agent in rifampicin-induced hepatic injury of mice. Methods Thirth-two Kunming mice were randomly divided into four groups(n=8 each).The mice in each group were injected intraperitoneally with 0.9% sodium chloride solution (control), N-acetylcysteine (NAC), combination of rifampicin (R), or NAC and R (NAC+R) once every day.After 14 days, the liver index (LI), alanine aminotransferase (ALT) and aspartate aminotransferase ( AST) activity in serum, and the level of malondialdehyde( MDA) ,superoxide dismutase( SOD) activity in liver tissues were measured respectively.Hepatic tissue morphology was observed under light microscope. Results Macroscopic analysis revealed that rifampicin led to severe liver tissue injury,including a wide range of hepatocellular vascular congestion,fatty change and local necrosis, whereas the administrationof NAC produced a significant reduction of rifampicin-induced hepatotoxicity .LI,ALT and AST activities in R or NAC+R group were significantly elevated as compared with the control group(P<0.01) .LI, activities of ALT and AST in serum,and MDA levels in liver tissues in NAC+R group were significantly lower than those in R group ( P<0.01) ,but the SOD activity in NAC+R group was increased significantly in comparison with R group (P<0.01). Conclusion Rifampicin was able to cause severe hepatic injury.Pre-administration of NAC reduced the side-effect induced by the treatment with the rifampicin.
ABSTRACT
Objective To investigate the protective effect of total flavones of Artemisia capillaris Thunb.on acute hepat-ic injury in rats. Methods Rats were randomly divided into blank control group,model control group, Yinzhihuang group,and groups of total flavones of Artemisia capillaris Thunb.(low,medium and high dose) in terms of 7-day different treatments.All rats except those in the blank control group were administrated with D-galactosamine hydrochloride ( 500 mg?g-1 , ip ) once at the sixth day.Then,concentrations of ALT and AST were detected 48 h later,and the liver samples were collected from each group for pathological examination. Results The serum ALT and AST in high-dose group of total flavones of Artemisia capillaris Thunb. was [(189.2±112.9) and (231.7±149.9) U?L-1],respectively,significantly lower than those in model control group ALT [(391.9±181.3) U?L-1] and AST [(403.9±133.8) U?L-1].Fragmented necrosis,fatty degeneration,inflammatory cells infil-tration and acidophilic degeneration of hepatic cells were improved to varying degrees in groups of total flavones of Artemisia capil-laris Thunb.compared with model control group.Fragmented necrosis of liver cells and steatosis occurred in 20 and 19 rats,respec-tively,in the model control group,while those appeared in 1 and 2 rats,respectively,in high-dose group of total flavones of Artemi-sia capillaris Thunb.. Conclusion Total flavones of Artemisia capillaris Thunb. are effective in protecting D-galactosamine hydrochloride-induced acute hepatic injury in rats.
ABSTRACT
Our findings in this study show (a) that hepatic uptake can be substantially increased even after injury, by the additon of a strong binding substance, preferably in its purified form, to vitamin B12 upon parenteral administration, (b) hepatic uptake for vitamin B12 can be enhanced further by mixing increasing doses of the intrinsic factor to vitamin B12 upon administration, (c) vitamin B12 mixed with intrinsic factor does not readily diffuse to storage depots, but rather remains at the site of injection, when administered by the intramuscular route, (d) vitamin B12-intrinsic factor complex is held more tenaciously by the liver than vitamin B12 alone. (Summary and conclusion)