Simultaneous Liver-Kidney Transplantation in Sensitized Patient

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In patients undergoing simultaneous liver-kidney transplantation, the liver allograft can exert an immune-protective effect from antibody-mediated injury on the kidney allograft when anti-HLA donor-specific antibodies (DSA) are present at levels high enough to generate a positive crossmatch.^1,2 This protective effect is thought to be due to anti-HLA antibody absorption by the liver allograft, especially class 1 antibodies.³

A 51-year-old male with decompensated cirrhosis from non-alcoholic steatohepatitis and dialysis-dependent kidney failure of 6 months underwent 3 HLA antigen mismatch deceased donor orthotopic liver transplantation, followed by kidney transplantation from the same donor 6 hours later. The patient was highly sensitized with a pre-transplant calculated panel reactive antibody titer of 99% with positive preformed DSA to HLA B51 at 6700 MFI and to DQ7 at 10,000 MFI. Both T- and B-cell complement-dependent cytotoxic crossmatches were positive. The patient received perioperative induction with pulse methyl prednisolone and maintenance immunosuppression with tacrolimus, mycophenolic acid, and prednisone along with standard infection prophylaxis. There was prompt liver allograft function, but delayed graft function (DGF) in the kidney allograft. Repeat T- and B-cell crossmatches returned negative 3 days later with a decrease in DSA to 2700 MFI against B51 and 1700 MFI against DQ7. Kidney allograft biopsy performed 2 weeks later only showed mild tubular injury without rejection. Urine output improved subsequently with a decline in serum creatinine, and the patient came off dialysis. Serum creatinine was 1.5 mg/dL at the 3-month follow-up. Longitudinal serum creatinine and DSA have been shown in Figure 1.

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Figure 1:

(a) Longitudinal serum creatinine and (b) anti-HLA antibody titer trends. Blue line in 1a indicates serum creatinine level.

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Liver allograft appears to protect the kidney transplant from the same donor against antibody-mediated injury. Absorption of lymphocytotoxic antibodies and complement factors by non-parenchymal donor hepatic cells is the proposed mechanism. However, the liver may have a threshold for absorbing antibodies in extremely elevated antibody titers.⁴