Nephrotoxicity glomerular atrophy

Acute renal toxicity may occur within days of initiating therapy. Serum creatinine concentration rises and creatinine clearance decreases. Hypertension, hyperkalemia, sodium avidity, and hypomagnesemia may occur. No urine sediment abnormalities are seen. Urinary enzyme excretions increase, but are not reliable indicators of toxicity. Renal biopsy reveals thickening of arterioles, mild focal glomerular sclerosis, proximal tubular epithelial cell vacuolization and atrophy, and interstitial fibrosis. Biopsy is useful to distinguish acute cyclosporine nephrotoxicity from renal allograft rejection, the latter being evidenced by cellular infiltration. ... 

The immunosuppressive drug cyclosporine A (CSA) has revolutionized transplant medicine. However, CSA induced-nephrotoxicity still represents a major therapeutic challenge. Chronic CSA nephropathy is characterized by a decrease in glomerular filtration rate (GFR), tubular atrophy, interstitial fibrosis and progressive renal dysfunction. It is difficult to delineate the mechanisms of CSA toxicity from clinical data since the majority of clinical experiences with CSA have been in renal transplant recipients. Animal models of CSA nephropathy have brought some insights, how-... 

---