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© 1989 Oxford University Press

research-article

Increased Kidney Glucose Utilization Induced by Cyclosporine:Lack of Relation to Magnesium Excretion

J. L. BOROWITZ*, P. R. MAYER{dagger}, C. A. RODRIGUEZ{dagger} and M. ANTOUN{ddagger}

*Department of Pharmacology and Toxicology School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette Indiana 47907 {dagger}Department of Industrial and Physical Pharmacy School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette Indiana 47907 {ddagger}Department of Medicinal Chemistry School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette Indiana 47907

Received April 4, 1988; accepted June 6, 1988

Increased Kidney Glucose Utilization Induced by Cyclospone: Lack of Relation to Magnesium Excretion. BOROWITZ, J. L, MAYER, P. R., RODRIGUEZ, C A., AND ANTOUN, M. (1989).Fundam. Appl Toxicol 12, 158–162. Cyclosporine enhances D-[5-3H]glucose utilization in homogenates of rat kidney medulla but not kidney cortex or liver. This is true whether cyclosporine is added to fresh tissue homogenates or is given to rats prior to sacrifice. Through the use of isolated perfused rat kidneys, an attempt was made to relate increased glucose utilization by cyclosporine to a possible consequence of cyclosponne nephrotoxicity, viz., loss of magnesium in urine. Although an enhanced rate of glucose utilization by cyclosporine was evident in isolated kidneys, glucose consumption was not related to urinary magnesium loss. In fact, kidneys from cyclosporine-treated rats actually showed a normal or even diminished urinary magnesium loss. The data suggest that cyclosporine-induced magnesium imbalance may be extrarenal in origin and that the kidney medulla may be a primary site of the nephrotoxic action of cyclosporine since the drug increases glucose utilization at this site.


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