Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal dysfunction secondary to GI disorders may be relatively common in horses. Persistent dehydration of 8-10% of body weight can lead to prerenal azotemia, which may result in renal ischemia and renal disease if uncorrected. Dehydrated azotemic horses with a urine specific gravity less than 1.018 may have renal disease. Urine specific gravity readings greater than 1.025 usually indicate normal kidney function. A urine Na level less than 20 mEq/L and a urine/plasma creatinine ratio greater than or equal to 20:1 indicate prerenal problems. Use of nephrotoxic drugs should be avoided in septicemic or dehydrated horses. Salmonellosis and proximal enteritis often lead to renal complications. Renal disease associated with DIC warrants a poor prognosis. Treatment of acute renal failure is aimed at eliminating the underlying cause and correcting metabolic abnormalities. Use of IV fluids, dopamine, prostaglandin inhibitors, fresh and electrolyte-spiked water ad libitum, water-soluble vitamins and high-P diets is beneficial. Success of therapy should be judged by laboratory results rather than clinical impressions.
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PMID:Renal disease associated with colic in horses. 673 2

Apparently healthy Wistar rats of body weight 250-300 g were chosen for the experiments. A group of 6 rats were assigned for each fraction. The dose of Russell's viper venom (RVV) fraction used for in vivo experiments was 0.75 microgram/g body weight. Of each batch of 6 rats 3 were sacrificed on the third day and the remaining 3 on the fifth day after the administration of test venom fractions. Daily urine output with proteinuria and serum creatinine were determined on the day they were sacrificed. Kidneys from the rats were also examined under light microscopy after hematoxylin and eosin staining. In the in vitro experiment, kidney slices (1 mm thickness) from normal rat was incubated with RVV fractions of 5 mg/ml concentration. The predominant renal lesions observed in both sets of animal experiments were tubular degeneration and necrosis. The changes were mostly confined to proximal tubules. Glomerular changes were mild. Similar tubulotoxic effects were produced by whole RVV as well as single fractions. Therefore, it is possible that RVV contains a common nephrotoxic (protein) component which is present in all fractions of the venom. The renal damage caused by RVV seemed to be due to both systemic effects (mainly DIC and renal ischemia) and direct tubulotoxic effects of the venom.
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PMID:Russell's viper venom fractions and nephrotoxicity. 956 25