ABSTRACT. Rabbit hemorrhagic disease virus (RHDV) induced viral fulminant hepatitis in adult rabbits. We investigated the damage of renal function and electrolyte balance in experimentally infected rabbit by measuring the related serum parameters to elucidate the pathogenesis of RHDV as an index for medical treatment. Nineteen New Zealand White rabbits, ten females and nine males, were each intramuscularly inoculated with 0.5 ml 50% rabbit lethal dose (RLD 50 ) rabbit hemorrhagic disease virus. Blood samples were collected at 0 hr post inoculation (HPI) and every 6 hr from 18 HPI repeatedly through 66 HPI. After virus inoculation, serum blood urea nitrogen (BUN), creatinine (CREA) and sodium (Na + ) were elevated to a highly significant level (p<0.0001), whereas serum potassium (K + ) was moderately elevated to a significant level (p<0.05). Hypoglycemia developed highly significantly (p<0.0001). Serum chloride ion (Cl -) was the only parameter which did not change significantly (p=0.077). No significant sexual difference was observed among these parameters. Renal insufficiency progressed from 36 hr, as indicated by the increases in BUN and CREA; significant changes in electrolytes resulting in the increased osmolality of extracellular fluid that induced flow disturbance which consequently destroy the homeostasis in cells. Therefore, the later impairments in renal function and electrolyte balance might be an important threat for rabbits which might have survived from acute fulminant hepatitis in RHD. KEY WORDS: electrolyte balance, rabbit hemorrhagic disease virus, renal insufficiency, serum.J. Vet. Med. Sci. 70(9): 951-958, 2008 Rabbit hemorrhagic disease (RHD) was first reported in 1984 in the People's Republic of China [12] and widespread worldwide to Europe, Australia, Mexico, North Africa and New Zealand in the following years. In 1994, RHD was first recognized in Taiwan by Dr. Y. S. Lu through serological tests and was characterized by hemagglutination, electron microscopic examination, viral protein analysis and RT-PCR in 1998 [20]. The characteristic pathological signs for RHD were hemorrhages in the respiratory system, liver, spleen, cardiac muscle, and occasionally in the kidneys. Incubation period in rabbits is 2 to 3 days, morbidity approaches 100%, and mortality is sometimes over 90% in adults. The high morbidity and mortality rates have made RHD a big threat for rabbit industry and also a biological control tool for wild rabbit population. The causative virus, rabbit hemorrhagic disease virus (RHDV), was classified into the family Caliciviridae. This single-stranded nonenvelope RNA virus has a 7.5-kb genome and a 2.2 kb subgenome well packaged in a 27 to 35 nm (in diameter) icosahedral capsid with a major structural protein of about 60 kDa (VP60), and 10 peripheral cup-shaped depressions [12,20]. The ability to agglutinate human erythrocytes of group O, A, B and AB were reported [12,15,20].Detection by reverse transcriptase-polymerase chain reaction (RT-PCR) in a rabbit inoculation model showed t...