Renal effects of long term administration of triamcinolone acetonide in normal dogs.
Triamcinolone acetonide was administered in excessive dosage to dogs to study the renal mechanism responsible for polyuria which is a clinically undesirable side effect of long term glucocorticoid therapy.Polyuria occurred coincident with a significant increase in urinary solute output. Although continuous administration of triamcinolone acetonide at 0.1 or 0.2 mg/lb/day caused a small but significant increase in creatinine output, the primary mechanism for the polyuria was increased solute excretion. Associated with the polyuria was pronounced hyperphagia and polydipsia. The cause of the hyperphagia was not established. The increase in electrolyte excretion caused by this synthetic steroid was probably compensated for by the hyperphagia. Because all the dogs showed muscle weakness and loss of body condition, it is likely that alteration in protein and amino acid metabolism was responsible for the hyperphagia.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003404:Creatinine / Q000652:urine; D004231:Diuresis / Q000187:drug effects; D004283:Dog Diseases / Q000139:chemically induced; D004285:Dogs / Q000187:drug effects*; D001068:Feeding and Eating Disorders / Q000139:chemically induced / Q000662:veterinary; D006801:Humans; D007668:Kidney / Q000187:drug effects*; D007677:Kidney Function Tests; D009135:Muscular Diseases / Q000139:chemically induced; D011141:Polyuria / Q000139:chemically induced / Q000150:complications / Q000662:veterinary; D011188:Potassium / Q000097:blood / Q000652:urine; D012964:Sodium / Q000097:blood / Q000652:urine; D013894:Thirst; D013997:Time Factors; D014222:Triamcinolone Acetonide / Q000008:administration & dosage / Q000633:toxicity*; D014667:Vasopressins / Q000494:pharmacology
D001786:Blood Glucose; D014667:Vasopressins; D012964:Sodium; D003404:Creatinine; D014222:Triamcinolone Acetonide; D011188:Potassium