At toxic levels, CsA also has the ability to cause renal damage and histological changes that can affect the function of a transplanted kidney. Some of the typical physiological effects of CsA include reduced glomerular filtration and changes in intrarenal hemodynamic function, which can start to occur one week after drug administration. In the early stages of CsA administration kidney damage can occur, which causes alterations in intrarenal hemodynamics related to afferent arteriolar vasoconstriction, causing a decrease in glomerular filtration rate, renal plasma flow, loss of proximal tubular cells brush border, proximal tubule dilatation, swelling, necrosis, and infiltration of white blood cells in the kidney cortex. Other complications associated with CsA administration include hepatic involvement and an increase in serum bilirubin. Renal tubular toxicity induced by CsA can be acute with the appearance of oligoanuria, presence of atrophic tubules, and edema. The purpose of this study was to evaluate delivery of TQ conventionally in CsA challenged RMKEC. Cell Count Results: After 24 hours of incubation the following groups decreased cell proliferation in the following order: CsA [50microM] +TQ [50microM] (63%) > CsA [10microM] +TQ [50microM] (55%) > CsA 50microM (24%) > TQ 50microM (7%). Glutathione Results: At 24 hours, CsA [50microM] +TQ [50microM] decreased glutathione levels by approximately 63% and CsA [10microM] +TQ [50microM] decreased glutathione levels by approximately 59%.
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