A 55 year old male with type II diabetes mellitus for 15 years having microvascular complications of diabetes like diabetic retinopathy and diabetic neuropathy, was diagnosed with chronic liver disease in 2011. The etiology of chronic liver disease was nonalcoholic steatohepatitis, presumed secondary to diabetes mellitus for which he had undergone liver transplant in 2013 (donor-wife, ABO compatible transplant ).
The patient was subsequently diagnosed with chronic kidney disease (CKD) in 2015 when he developed renal dysfunction (kidney biopsy-diabetic kidney disease). His renal function subsequently deteriorated over the next few years and he was started on maintenance hemodialysis from May,2020. Subsequently, transplant work up was started with wife as the donor.
Initial investigations were normal, however, Immunological work up revealed:
- HLA mismatch- 8/12 MISMATCH
- Flowcytometry crossmatch- B cell positive (MCS-208)
- Donor Specific Antibody (MFI)- DQB1*03 and DQB1*01 (>19,000 MFI)
- CDC crossmatch-T cell negative, B cell positive
Generally, kidney transplantation performed in such cases without desensitization generally results in hyper-acute or accelerated antibody-mediated rejection and rapid allograft loss. However, our patient had stable liver function which made us think that the body could have developed tolerance to high level of antibodies against the donor. Subsequently multidisciplinary meetings were held and allograft liver biopsy was planned to rule out evidence of rejection which generally should have occurred in presence of such high titres of DSAs. However, allograft liver biopsy showed histologically unremarkable portal tracts and parenchyma with no evidence of rejection.
This made us believe that the body could have developed tolerance to high level of antibodies against the donor. Subsequently he underwent renal transplant in September 2022 with methylprednisolone and anti-thymocyte globulin induction without administration of any desensitization therapy. In the post operative period, the patient had brisk diuresis and serum creatinine decreased and he was discharged with a serum creatinine of 0.9 mg/dl with no evidence of rejection. He is doing well on follow up outpatient visits with good urine output and normal renal function.
Kidney transplantation performed in the presence of high-titre of DSA generally results in hyper-acute or accelerated antibody-mediated rejection and rapid allograft loss. We report a very rare case of highly sensitized liver transplant patient who had a sustained depletion of all DSAs with no requirement of desensitization therapy after undergoing renal transplant from the same donor. If the recipients immune system is exposed to defined alloantigen previously, the immune response to the antigen will be modulated and subsequent unresponsiveness can occur as seen in our patient. Our case, thus, highlights the immunoregulatory role of the liver in protecting the kidney allograft.