ARF within the first 1 to 12 weeks posttransplantation is most likely secondary to complications of the transplant surgery itself, usually due to obstruction of a renal artery, vein, or ureter.
Rejection is related to activation of T cells, which in turn stimulate specific antibody production against the graft. Varying clinical syndromes of rejection can be correlated with the length of time after transplantation.
Hyperacute rejection occurs immediately in the operating room, when the graft becomes mottled and cyanotic. Hyperacute rejection is secondary to unrecognized ABO compatibility or a positive T-cell crossmatch.
Acute rejection appears within the first 3 months posttransplant and affects about 30 percent of cadaveric and 27 percent of living-donor transplants. 17 Approximately
15 to 20 percent of transplant patients experience recurrent rejection episodes. Patients present with decreasing urine output, elevated blood pressure, a rising creatinine level, and mild leukocytosis. Fever, graft swelling, pain, and tenderness may be seen with severe rejection episodes. Rejection is secondary to prior sensitization to donor alloantigens (occult T-cell crossmatch) or a positive B-cell crossmatch. Diagnosis depends on graft biopsy.
Late acute rejection commonly occurs 6 months after transplantation and is highly correlated with withdrawal of immunosuppressive therapy.
Chronic rejection occurs 1 year after transplantation secondary to both cellular and humoral immunologic factors. Progressive loss of renal function occurs.
Nephrotoxicity from CYA and Tracolimus (FK506) is related to hemodynamic factors.1 l9 Acute toxicity (CYA levels greater than 300 ng/mL whole blood) causes vasoconstriction and renal ischemia, which can be reversed with decreasing the drug dosage. Chronic toxicity results in fixed vascular lesions and irreversible renal ischemia.
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