Renal Tubular Epithelial Necrosis Research Articles

Histopathologic and ultrastructural findings in oak (Quercus spp.) toxicity on 2 beef cattle farms in Colorado.

Natural oak toxicity, a phenomenon sporadically reported in the United States, is due to consumption of any part of most oak trees (Quercus spp.). Ruminants, mainly cattle, are disproportionately susceptible to oak toxicity. Toxicity is attributed to degradation of the oak plant hydrolysable tannins by rumen microbes and enzymes into absorbable low-molecular-weight metabolites, which are postulated to bind and damage endothelial cells by unknown mechanisms. The clinical manifestations of acute toxicosis are nonspecific or broadly suggestive of renal disease due to acute tubular injury. Here we document the clinical, gross, histopathologic, and novel ultrastructural features of natural acute oak nephrotoxicity in 3 beef calves on 2 farms in Colorado, USA. Gross postmortem findings included perirenal edema with renomegaly and hemorrhagic gastroenteritis. Histologically, renal tubular epithelial necrosis was severe, with hemorrhage and intratubular hyaline casts. Transmission electron microscopy revealed extensive involvement of proximal and distal convoluted tubules, with predominantly intact basement membranes, and glomerular and interstitial endothelial injury and necrosis. The ultrastructural details of toxic nephropathy and vasculopathy induced by oak metabolites in natural cases of bovine oak toxicosis have not been described previously, to our knowledge.

Mortality of Clarias gariepinus caused by Aeromonas caviae and nitrite toxicity in a fish farm

In Nigeria, farming of freshwater fish, mainly that of Clarias gariepinus has gained prominence as means of improved protein supply and livelihood. Many farmers suffer untold losses in their bid to make a living from commercial fish production. Among the major causes of infectious disease outbreaks in fish farms are pathogenic bacteria of the genus Aeromonas. This is a case report of outbreak of Aeromonas caviae infection complicated by nitrite toxicity in Clarias gariepinus. Carcasses of 17 African catfish juveniles and two water samples were presented to the poultry and fish clinic of the Veterinary Teaching Hospital, University of Jos for investigation. The fishes had been on medication (Fish cure antibiotic +®) for over 5 days with cumulative mortality of 230 out of 2,500 fishes (9.2 %). Necropsy was conducted and samples were taken for microbial analysis and histopathology while water samples were subjected to chemical analysis. Gross lesions were broken barbels, cutaneous depigmentation, branchial pallor, ascites, renal and splenic congestion. Histologically, there was dissociation of hepatic cords, necrosis of hepatocytes with vacuolation and mononuclear cellular infiltrations. Also, there was renal tubular epithelial necrosis with mononuclear and heterophilic infiltration while micro abscesses were observed in the brain. Marked Zenker’s necrosis and edema were seen in the skeletal muscles. Organism isolated from livers and kidneys was identified as Aeromonas caviae and was susceptible to enrofloxacin, furaltadone and florfenicol. Nitrite in fish pond water was 1mg/L. Bath medication with enrofloxacin at 33mg/litre of water for 6 hours treatment per day was done to reduce the mortality. The farmer was advised to change the source of water for the fish pond immediately. It is recommended that to avoid losses in fish farming, farmers should check the quality of water intended for use on fish farms and ensure early health check on fingerlings purchased for rearing.

Role of Olive leaves Zinc Oxide Nanoparticles in Alleviating The Molecular and Histological Changes of Kidney in Female Goats-Induced by Gentamicin (Part III)

This study aimed to investigate the protective influence of olive leave extract zinc oxide nanoparticles (OLEZnONPs) complex against gentamicin–induced kidney dysfunctions in goats. Twenty five adult female goats were randomly divided into five equal groups and treated as follows: control group (C) administered sterile distilled water (IM) for 10 days, group G administered 25 mg/kg BW gentamicin (IM) for 7 days, group Z administered 10 ìg/kg BW of OLEZnONPs (IP) for 3 days, group GTZ administered 25 mg/kg BW gentamicin (IM) for 7 days and then 10 ìg/kg BW of OLEZnONPs (IP) for 3 days, group GWZ administered 25 mg/kg BWs gentamicin (IM) and 10 ìg/kg BW of OLEZnONPs (IP) together for first 3 days and then followed by gentamicin only for 4 days. After seven days of the experiment, the gene expression of kidney injury molcule-1(KIM-1) and neutrophil gelatinase-association lipocalin (NGAL) gene expression of kidney tissue were measured. In addition, samples of kidney were obtained for histopathological examination. Gentamicin medication induced a marked elevation in kidney tissue KIM-1 and NGAL gene expression in G and GTZ groups compared to control and other groups. Intraperitoneal treatment of goats with OLEZnONPs did not significantly affect NGAL and KIM-1 gene expression in Z, GWZ, and control groups. Histologically, in contrast to control, gentamicin induced more extensive kidney damages such as necrotized glomeruli, atrophic glomeruli, and renal tubular epithelial necrosis, while it was found that these alterations in kidney tissues wereimproved in goats given OLEZnONPs with gentamicin compared to group G. In conclusion, our results demonstrate that OLEZnONPs reduce the deleterious effects of gentamicin with significantly decreasing of KIM-1 and NGAL gene expression and remodeling the histological changes of kidney in goats.