Clinicopathological Spectrum of Renal Allograft Dysfunction.

Peter Wright in his brainy quote, ‘I had been living with dialysis for three years or so, and the new kidney felt like a reprieve, a new gift of life. I felt alive again and I guess that has had an effect on my use of colour.’ Hence a small transplant makes a great difference for many of the young transplant recipients. The renal transplantation represents a major step in fighting against kidney disease. Although transplantation is by no means a cure for kidney failure, it is by far the best treatment method available to us at this time... By increasing the number of effective kidney transplants we help in extending the gift of life for many poor recipients. Studies have proved that renal transplantation is distinctly superior and is associated with reduced mortality and morbidity compared to hemodialysis or peritoneal dialysis. Due to shortage of organs and prolonged period to get deceased kidneys prevention of re transplant is gaining more importance. To improve the graft survival identifying the etiology and pathology of graft dysfunction or loss is most essential thereby effective measures can be taken to prevent the graft loss and prolong the survival of the recipient. Based on this study on clinicopathological study of renal allograft dysfunction the following findings were noted: Donor age has significant impact on long term graft survival; younger the donor better the outcome. With female donors the graft dysfunction is more, may be due to different in antigenicity and smaller renal mass. Live related renal transplantation had better outcomes than deceased donor transplants, reasons being better HLA match, reduced cold ischemic time and low incidence of delayed graft function. Delayed graft function occurred in 20% patients, which is a significant impact on long term graft function survival. 90% deceased donor recipients have delayed graft function. Prolonged Cold ischaemic time is an important cause delayed graft function. There is a significant p value of 0.002 between live and deceased donor transplant. [47 minutes versus 157 minutes]. Antibody mediated rejection occurred in 6% of patients. None of them had hyper acute rejection, which implies better method of cross match in our set up. Acute cellular rejection occurred in 30% patients which is relatively high when compared to western standards of 10-15%, where all patients undergo anti induction therapy to prevent early rejection. 50% acute cellular rejection occurred in less than 1 month of transplantation, hence there is a need for anti induction therapy to prevent early rejection. 75% of cellular rejections were of Banff type 1 A variant, which responded very well to treatment. 20% our patient had interstial fibrosis and tubular atrophy, which is a important cause of late allograft failure