Clinical diagnosis and management of the renal transplant recipient with cyclosporine nephrotoxicity.
The definition of CsA-induced nephrotoxicity is defined as impairment of renal function after transplantation exclusive of allograft rejection, vascular obstruction, and ureteral obstruction. This imprecise definition is one of exclusion and requires a careful clinical assessment of the patient, using information from the renal biopsy in appropriate circumstances in conjunction with the monitoring of CsA drug levels. The clinical effects of nephrotoxicity can be reported in four categories: delayed allograft function, acute nephrotoxicity, acute vasculopathy, and chronic nephropathy. The best method to avoid delayed allograft function in the cadaveric kidney is to make every effort to obtain a prompt diuresis. This can be accomplished in most patients, recognizing that in most centers 15% to 25% of cadaveric recipients will require one or more dialysis treatments. As renal function improves, the dosage of CsA can be increased. Acute nephrotoxicity must be differentiated from acute rejection, and if a reduction in CsA dosage is not accomplished by a prompt improvement in renal function, acute rejection must be considered with possible confirmation by a renal biopsy. Chronic nephrotoxicity rarely leads to chronic renal failure, but may be associated with a gradual increase in serum creatinine to a point where conversion from CsA to azathioprine should be considered. This conversion should be carried out slowly over a several month period.
D000208:Acute Disease; D001706:Biopsy; D002908:Chronic Disease; D003524:Cyclosporins / Q000008:administration & dosage / Q000009:adverse effects* / Q000097:blood; D006084:Graft Rejection; D006801:Humans; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced; D016030:Kidney Transplantation; D014184:Transplantation, Homologous; D014652:Vascular Diseases / Q000139:chemically induced
D003524:Cyclosporins