M. A. (1991). Sex differences in the management of coronary artery disease.

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We analyzed clinical and pathologic data from 36 recipients of 38 renal allografts who developed nephrotic syndrome following transplantation. Three groups were identified on the basis of histologic changes in the graft, and each group had a distinct clinical course. Nine grafts (23.7%) had recurrent glomerulonephritis (GN) (5 membrano-proliferative, 4 focal glomerulosclerosis) and developed nephrotic syndrome at 5.1 months (mean) posttransplant. Renal function deteriorated rapidly, with a 2-year graft survival of 29.7%. Four grafts (10.5%) with de novo GN (3 epimembranous, 1 minimal change) developed nephrotic syndrome at 32 months posttransplant, and all functioned for more than 3 years. Twenty-five grafts (65.8%) had allograft glomerulopathy with the onset of nephrotic syndrome at 9.1 months posttransplant and a 2-year graft survival of 66.6%. The differences in duratin of graft function between grafts with allograft glomerulopathy and recurrent GN (P < 0.01) and in graft survival rates at 2 years among the three groups (P < 0.05) are statistically significant. This analysis indicates that allograft glomerulopathy is the most common cause of kidney transplant nephrotic syndrome. Membranoproliferative GN and focal glomerulosclerosis may recur soon after transplantation and rapidly progress to renal failure in marked contrast to grafts with either de novo epimembranous nephropathy or minimal glomerular change, lesions that are compatible with prolonged graft function.

We found a significant improvement in both short-term and long-term GSR of deceased-donor kidney transplants over the last four decades. These improvements are most likely related to the decreased incidence of acute rejection episodes. Minimizing acute rejection events and preventing DGF could result in further improvement in the GSR. Our experience in the judicious use of ECD kidneys suggests that this source of kidneys could be expanded further.

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