Hepatorenal syndrome (HRS) is still one of the most important challenges of medicine in 21st century. In spite of many years of experimental and clinical studies, it failed to discover precise pathomechanisms leading from hepatic damage to functional renal failure. Among many kinds and currents, experimental studies still play great role. There are few reported animal models of HRS, among them a rat model induced by galactosamine (GalN). In this model acute renal failure develops typically after hepatic damage.
Aim of the study: We tried to test, whether in this model different breeds might develop typical HRS in the same way.
Material and methods: We used 24 male Wistar and 16 Sprague-Dawley rats to achieve HRS by intraperitoneal injection of Ga1N. RESULTS. Liver failure with significant increase in serum concentration of bilirubin, alanine transaminase (ALT) and ammonia, as well as huge microscopic necrosis of hepatocytes developed in both groups, but we did not achieved any evidence of acute renal failure in Wistar rats group. Nevertheless, we found typical biochemical evidence of renal failure in Sprague-Dawley group.
Conclusion: We conclude, that opposite to Sprague-Dawley model, the Wistar rat model does not develop functional renal failure typical for HRS, probably because of some congenital, genetic predispositions.