bis(tri-n-butyltin)oxide and Glycosuria

Painting of tributyl-tin oxide on the skin induced a secondary Fanconi syndrome in guinea pigs. In the urine of these animals, excretion of sodium, chloride, phosphate, glucose and many kinds of amino acids increased and reached a maximum between day 40 and 50. In sera, the concentrations of phosphate and certain amino acids were low due to excessive loss into urine. Histological examination of the kidney revealed damage to the tubular epithelium with no glomerular change. It was also found that cytochrome P-450 in the kidney and 1-25-dihydroxy vitamin D in serum were reduced in the tin-treated animals. It is most likely that tributyl-tin oxide caused a secondary Fanconi syndrome as defined by renal tubular disturbances represented by glucosuria, generalized amino aciduria, phosphaturia, and hypophosphatemia.

Topics: Administration, Topical; Amino Acids; Animals; Electrolytes; Fanconi Syndrome; Glycosuria; Guinea Pigs; Kidney Tubules; Male; Trialkyltin Compounds