Jeremy B Levy

Many patients receiving renal allografts become identified simply as recipients of kidney transplantation. All subsequent events involving changes in renal function are attributed to the process and natural history of transplantation itself: acute and chronic rejection, immunosuppressive drug nephrotoxicity, graft vasculature thrombosis or stenosis, ischemia, infection, and lymphoproliferative disorders. However, it is important to remember the nature of the underlying disease that caused the initial renal failure, even if the disease occurred many years previously. Recurrence of the primary disease often causes pathologic changes within the allograft; clinical manifestations such as proteinuria and hematuria; and less commonly, renal failure. Thus, focal segmental glomerulosclerosis (FSGS) frequently causes recurrent proteinuria after transplantation, which may begin as early as minutes after the graft is vascularized [1]. All patients with diabetes develop recurrent basement membrane and mesangial pathology within their allografts [2], and recurrent oxalate deposition can cause rapid renal allograft failure in patients with oxalosis [3]. Identifying patients at particular risk of primary disease recurrence allows consideration of therapeutic maneuvers that may minimize the incidence of recurrence.

Living-related transplantation poses additional dilemmas. For many nephritides good evidence exists for an increased incidence of recurrent primary disease in related as opposed to cadaveric grafts. Data from the Eurotransplant Registry suggests a fourfold increased incidence of recurrence of glomerulonephritis, causing graft loss in grafts from living related donors (16.7% vs 4%) [4].

Finally, the recurrence of glomerulonephritis after transplantation, in particular, can cause specific diagnostic problems. It may be caused by recurrent disease, development of de novo glomerulonephritis in the transplanted organ, or transplanted glomerulonephritis from a donor with unrecognized disease. Glomerulonephritis after transplantation must be distinguished from chronic rejection causing glomerulopathy and cyclosporine-induced glomerulotoxicity. Each of the following diseases can present diagnostic dilemmas and cause graft failure:

recurrence of FSGS, mesangial immunoglobulin A disease, hemolytic uremic syndrome, mesangiocapillary glomerulonephritis, and anti-glomerular basement membrane disease.

Overall, three groups of diseases recur in patients with transplantations: metabolic disorders, especially primary hyperoxaluria and diabetes; systemic diseases, including systemic lupus erythematosus, sickle cell disease, systemic sclerosis, hepatitis C virus-associated nephropathies and systemic vasculitis; and a variety of glomerulonephritides. For immunemediated systemic diseases the standard transplantation immunosuppressive regimens often prevent recurrence of primary disease, which also may be true for the glomerulonephritides. Some evidence exists that in the glomerulonephritides there is a reduced incidence of recurrence with the use of cyclosporine. Confirmed recurrence of all the glomerulonephritides causes graft loss in 4% of adults and 7% of children receiving allografts [4,5]. Although few data exist on the treatment of most forms of recurrent nephritis, plasma exchange or immunoadsorption are proving beneficial at reducing nephrotic range proteinuria in recurrent FSGS [6,7], and recurrent renal oxalate deposition often can be abrogated after transplantation in patients with primary hyperoxaluria [8,9].

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