A QUANTUM LEAP IN RENAL SCIENCE: THE FIRST EVER ABH INCOMPATIBLE RENAL TRANSPLANT IN A RECIPIENT WITH BOMBAY BLOOD PHENOTYPE

Introduction:

Blood group antigens play a vital role in organ transplantation. They are assigned to blood group systems based on oligosaccharide epitopes, including the ABO, P, and Lewis antigens. The Bombay Blood group or 'hh' blood group is a very rare blood phenotype, first discovered in the city of Bombay (currently Mumbai) in 1952 by Dr Y.M. Bhende. It’s prevalence is about 0.0004% (one in 4 million) of the total human population and 1:1,000,000 in the European population compared to 1:10,000 in Mumbai, India.

Methods:

The most common blood groups are ABO. Their antigens are classified as A, B, or H depending on the sugar composition. First step in synthesis of blood group antigens is the addition of a fucose residue to a glycan chain to obtain the H antigen. Subsequently, the A and B antigens are synthesized from the H antigen by specific glycosyl transferases. The RBCs of patients with Bombay blood group lack even the presence of the very basic H antigenic structure. Hence,their serum has anti-A, anti-B, and anti-H antibodies capable of agglutinating RBCs of the A, B, AB, and even O groups. 

Hence, a recipient with Bombay blood group can undergo renal transplant if the donor also has Bombay blood phenotype or the only other viable alternative is an ABH incompatible transplant. Clinical challenges in such a scenario are: 1. Titration of the Anti H antibodies in the recipient (needs infrastructure), 2. Determination of a safe Anti-H antibody titre cut-off, 3. High risk of Hyper-acute rejection as Anti-H antibodies are more potent than Anti-A or Anti-B antibodies, 4. Accommodation of Anti-H antibodies by the graft - has not been tested before, 5. No published literature regarding a successful organ transplant in a recipient with Bombay blood phenotype.

A 30-year-old male with ESKD secondary to Ig A Nephropathy was worked up for kidney transplantation with his mother as donor. Evaluation revealed presence of Bombay blood group in the recipient. His mother’s blood group was ‘B’. Titration for both Anti-H and Anti-B antibodies using Gel card method revealed Ig G titres of 1:64 in Coombs phase. CDC, Flow cytometry and DSA were within acceptable range. Patient underwent de-sensitization protocol with Rituximab 200 mg,Tacrolimus, Mycophenolate mofetil, oral Methylprednisoloneand 3 sessions of therapeutic plasma exchange (TPE) accompanied with 5 g of IVIG. On the day of transplant, his Ig G Anti-H titre was 1:16 and Anti-B titre was 1:8. 

Results:

Patient underwent renal transplant with Basiliximab induction. He had good graft function with a nadir creatinine of 1.5 mg (Donor to Recipient body weight ratio 0.65). His post-operative period was uneventful. His Ig G Anti-H and Anti-B titres remained stable at 1:16 post-transplant. Two months post-transplant, he has stable graft function with a creatinine of 1.6 mg/dL.

Conclusions:

To the best of our knowledge, this is the first report of a successful ABH incompatible organ transplantation in a recipient with Bombay blood phenotype. This report is the proof of concept that Anti-H iso-agglutinins are amenable to removal by extra-corporeal therapy, they abide by the rules of accommodation and a Ig G Anti-H titre of 1:16 after TPE may be considered safe to proceed with renal transplantation.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.