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Acute glomerular rejection is a distinct pathologic subtype of rejection that is often refractory to standard therapy and is associated with significant risk of graft loss. Both cellular and humoral mechanisms have been shown to be involved in the pathophysiology of acute glomerular rejection. FK506, because of its ability to inhibit both cellular and humoral mechanisms of rejection, provides a theoretically attractive approach for treating acute glomerular rejection. This initial experience with FK 506 treatment of acute glomerular rejection occurred in a 58-yr-old woman who received a 0 AB, 2 DR-match cadaveric renal transplant. A renal allograft biopsy performed on post-transplant day 77 for renal dysfunction (serum creatine 1.3→1.8 mg/dl) revealed moderate cellular and vascular rejection. Corticosteroid therapy provided a transient improvement in renal function; however, a repeat biopsy 7 d later revealed acute glomerular rejection with immunohistologic evidence of antibody-mediated rejection (immunoglobulin and complement deposition in glomerular capillaries). FK 506 therapy was instituted and provided prompt reversal of the acute glomerular rejection as determined by serial renal allograft biopsies. One year later, recurrent rejection has not been observed, and good renal function is present. (Current serum creatine 1.7 mg/dl, creatine clearance 35 ml/min/m2, and 24 h urinary protein 230 mg.) Successful corticosteroid withdrawal has been achieved, and current immunosuppressive therapy consists only of FK 606 and azathioprine. This experience indicates that FK 506 can provide effective therapy for acute glomerular rejection, and that simultaneous treatment with plasmapheresis and an antilymphocyte antibody preparation may not be necessary. This experience also provides further evidence of the ability of FK 506 to inhibit antibody-mediated rejection processes.