title: Acute renal failure induced by carbon tetrachloride in rats with hepatic cirrhosis.
abstract: Relationship between cirrhosis and renal dysfunction is not yet fully understood. A model of cirrhosis with acute hepatic and renal damage (RF), produced by CCl4 in rats, with hemodynamic and renal functional alterations, similar to those observed in decompensated cirrhosis (DC) in man, was used to study chemical nephrotoxicity in animals. We performed in male Wistar rats hepatic and renal functional and hemodynamic studies in control, cirrhotic and decompensated cirrhotic (DC) groups. Cirrhosis was induced with carbon tetrachloride by chronic administration. Association between liver and renal functional alterations was detected in rats with decompensated cirrhosis, showing fall in mean arterial pressure and reduction of glomerular filtration rate and filtration fraction. Renal hemodynamics did not change in cirrhotic rats, similarly to what occurs in compensated cirrhotic patients. However, DC rats exhibited increased sodium, glucose and phosphate urinary excretions and decreased ATP in renal cortex. DC animals had severe hypoglycemia. There was an extensive liver fibrosis. Glomeruli had hypercellularity and tubules showed extensive vacuolization in cirrhotic and DC rats. The present study suggests that in this model, damage typical of acute tubular necrosis ensues in cirrhotic rats. We describe functional and morphological damage in liver and kidney in a model of cirrhosis that might predispose to the development of acute renal failure when an individual with hepatic damage is exposed in acute way to chemical toxicants.
authors.affiliation: Universidad Autónoma de Aguascalientes, Aguascalientes, México.
authors.forename: Fernando
authors.initials: F
authors.lastname: Jaramillo-Juárez
authors.forename: María Luisa
authors.initials: ML
authors.lastname: Rodríguez-Vázquez
authors.forename: Ana Rosa
authors.initials: AR
authors.lastname: Rincón-Sánchez
authors.forename: María
authors.initials: M
authors.lastname: Consolación Martínez
authors.forename: Genaro G
authors.initials: GG
authors.lastname: Ortiz
authors.forename: Javier
authors.initials: J
authors.lastname: Llamas
authors.forename: Francisco
authors.initials: F
authors.lastname: Anibal Posadas
authors.forename: José L
authors.initials: JL
authors.lastname: Reyes
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology*; D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D002251:Carbon Tetrachloride / Q000633:toxicity*; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology; D005919:Glomerular Filtration Rate; D006801:Humans; D007668:Kidney / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D007683:Kidney Tubular Necrosis, Acute / Q000209:etiology / Q000503:physiopathology; D007684:Kidney Tubules / Q000473:pathology / Q000503:physiopathology; D008099:Liver / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008106:Liver Cirrhosis, Experimental / Q000150:complications / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation
chemical_list: D000255:Adenosine Triphosphate; D002251:Carbon Tetrachloride