A Blood-Type-Free Kidney Just Worked Inside a Human for the First Time

Every day in the United States, 11 people die waiting for a kidney transplant. More than half of them share the same problem: they have type O blood, and there are not enough type O kidneys to go around. Type O patients can only receive type O organs, yet type O kidneys work in anyone, so they get distributed to patients with other blood types. The result is a cruel math problem where the people who can donate to everyone must wait the longest to receive. For decades, scientists have searched for a way around this bottleneck. Now, a team from the University of British Columbia and partner institutions in China has done something no one has done before. They chemically erased the blood type from a human kidney, transplanted it into a brain-dead recipient with a mismatched blood type, and watched it function without immediate immune destruction. It is not a finished solution. But it is the first proof that this approach works inside the human body.

Why Blood Type Makes Kidney Transplants So Difficult

Your blood type is determined by sugar molecules called antigens that coat the surface of your red blood cells and the blood vessels inside your organs. Type A blood has A-antigens. Type B has B-antigens. Type AB has both. Type O has neither.

Your immune system is trained to recognize foreign antigens. If a type O patient receives a type A kidney, their immune system detects the A-antigens on the organ’s blood vessels and launches an attack. In the worst case, this triggers hyperacute rejection, a rapid, violent immune response that can destroy the transplanted organ within minutes.

To get around this mismatch, doctors currently use a process called desensitization. Over several days, they strip antibodies from the recipient’s blood through plasmapheresis, then suppress the immune system with drugs. It works, but the approach is expensive, time-consuming, and risky. It increases the chance of bleeding and infection. And it requires a living donor, because the recipient needs days of preparation before the transplant can happen.

For deceased-donor kidneys, where timing is measured in hours rather than days, desensitization is not practical. That leaves type O patients stuck in line, waiting an average of two to four years longer than patients with other blood types. Many do not survive the wait. More than 13% of U.S. patients on the 2021 waiting list had been waiting over five years.

Molecular Scissors That Strip Away Blood Type

Rather than changing the patient to fit the organ, the UBC team asked a different question: what if you changed the organ to fit the patient?

In 2019, biochemist Stephen Withers and pathology professor Jayachandran Kizhakkedathu discovered two enzymes that can remove the sugar molecule (N-acetylgalactosamine) that defines type A blood. Applied to cells, these molecular scissors snip off the A-antigen, leaving behind the neutral surface structure that characterizes type O blood.

Withers compared it to removing red paint from a car to reveal the neutral primer underneath. Once the A-antigen is gone, the immune system no longer recognizes the organ as foreign.

What made these particular enzymes special was their efficiency. They work at very low concentrations, are highly selective, and operate fast. Kizhakkedathu noted that this level of performance was what made the whole concept feasible. Previous enzyme candidates could not remove enough antigen quickly enough to be practical for organ transplantation.

From Blood Cells to Lungs to Kidneys

The UBC team spent years scaling up their approach, moving from individual cells to whole organs. Early work focused on converting red blood cells, demonstrating that enzyme-treated type A blood could be safely transformed into type O. In 2022, a Toronto team showed that the same enzymes could convert human lungs. Parallel work with the University of Cambridge tested the approach on kidneys outside the body.

Each step confirmed that the enzymes could remove A-antigens from the complex vascular networks inside whole organs, not just isolated cells in a dish. But one question remained unanswered: could an enzyme-converted organ survive inside a living human immune system?

The First Human Test

In late 2023, collaborators in China put the technology to its ultimate test. They took a type A kidney, treated it with the UBC enzymes during hypothermic perfusion at 4 degrees Celsius (the standard temperature for organ preservation), and removed over 96% of A-antigens within two hours. After flushing the organ, they transplanted it into a 68-year-old brain-dead recipient with type O blood and high levels of anti-A antibodies.

The recipient received no desensitization treatment. No plasmapheresis. No antibody stripping. The converted kidney was transplanted directly into an immune system fully armed to attack type A tissue.

For two days, the kidney worked. It produced 1,300 milliliters of urine in the first 24 hours. Blood flow remained stable. No hyperacute rejection occurred. The immune system did not destroy the organ.

When Kizhakkedathu received the data during an overseas trip, he stayed up late to call Withers first thing in the morning, British Columbia time. He described it as a dream moment.

The recipient’s family had consented to the research. Because the patient was brain-dead and had been denied organ donation due to severe medical complications, the experiment allowed extended observation without putting a living patient at risk. Ethics committees at West China Hospital of Sichuan University and the Second Affiliated Hospital of Chongqing Medical University approved the study.

Day Three: The Antigens Came Back

By the third day, something researchers had anticipated began to happen. A-antigens started regenerating on the kidney’s surface. The organ’s own cells were producing new antigen molecules, gradually restoring the type A markers the enzymes had removed.

This regeneration triggered a mild immune response. By day four, antibody-mediated rejection was diagnosed. But the pattern of injury looked very different from what happens in a typical blood type mismatch.

Researchers compared their results to two clinical cases of hyperacute rejection. In those cases, the kidneys were removed within 24 hours and showed extensive blood vessel clotting, red blood cell congestion, and massive antibody deposits. The enzyme-converted kidney, even a full week after transplant, showed significantly less damage.

More encouraging, single-cell sequencing revealed that the recipient’s body was activating genes associated with a phenomenon called accommodation, a process where the immune system begins to tolerate a foreign organ rather than destroy it. Accommodation sometimes develops two to three weeks after blood-type incompatible transplants from living donors. Researchers saw early signs of it here within days.

Forty Biopsies and a Wealth of Data

Over seven days, the research team performed 40 biopsies on the transplanted kidney. That level of monitoring would be impossible in a living patient and impractical in animal models. The data they collected on antigen regeneration timing, immune response patterns, and gene expression is unlike anything previously available.

For the first time, scientists could observe exactly how fast blood type antigens regenerate inside a functioning human organ, how the immune system responds at each stage, and which molecular pathways activate during the transition from rejection to potential tolerance.

That information is now being used to design next-generation protocols. One proposed approach: infusing the enzymes as a drug starting around day two after transplant, keeping antigen levels low during the critical first weeks while accommodation develops naturally. Previous studies showed that injecting similar enzymes into baboons and transgenic mice effectively reduced blood-type antigens in kidneys, hearts, and lungs.

What Still Needs to Happen

The study has significant limitations, and the researchers were candid about them. Only one kidney was tested. The recipient was elderly, brain-dead, and in poor clinical condition, which complicated the interpretation of immune responses. The frequent biopsies themselves caused physical damage to the organ. Seven days of observation could not capture the full accommodation, which needs two to three weeks to develop.

Regulatory approval for clinical trials is the next major hurdle. Avivo Biomedical, a UBC spin-off company, will lead development of the enzymes for transplant applications and for creating universal donor blood for transfusion medicine.

Before human clinical trials can begin, researchers need to solve the antigen regeneration problem, either by improving enzyme durability, developing repeat-dosing protocols, or finding ways to slow the organ’s own antigen production during the critical tolerance window.

A Problem Worth Solving

The statistics behind this research are hard to ignore. Over 100,000 people are on the U.S. kidney transplant waiting list at any given time. Type O patients make up the majority. Globally, the shortage is even more severe.

If enzyme conversion proves safe and effective in clinical trials, it could reshape organ allocation worldwide. Kidneys from any deceased donor could go to any recipient, regardless of blood type. Wait times would drop. Fewer people would die in line. And the technology is not limited to the kidneys. The same approach could apply to hearts, lungs, livers, and other solid organs.

Withers captured the significance of reaching this milestone: seeing discoveries edge closer to real-world impact is what keeps the team pushing forward. For the thousands of patients waiting for a call that may never come, that progress cannot arrive soon enough.

My Personal RX on Supporting Kidney Health and Organ Wellness

Kidney disease often develops silently over the years before symptoms appear. Protecting your kidneys starts with daily habits that reduce inflammation, manage blood pressure, and support your body’s natural filtration systems. I tell my patients that prevention is always easier than treatment, and small daily choices add up to major protection over time. Here is what I recommend:

1. Prioritize Restorative Sleep Every Night: Your kidneys regulate fluid balance around the clock, and poor sleep disrupts that process. Sleep Max combines magnesium, GABA, 5-HTP, and taurine to calm your mind, support neurotransmitter balance, and promote deep REM sleep so your body can maintain healthy kidney function overnight.
   
2. Know Your Nutrient Gaps After 40: Declining nutrient absorption affects kidney health, immune function, and blood pressure regulation. Download my free guide, The 7 Supplements You Can’t Live Without, to learn which supplements support organ health, which “healthy” foods may be misleading you, and how to spot quality products.
   
3. Stay Well Hydrated: Your kidneys need adequate water to filter waste from your blood. Aim for at least eight glasses per day, and increase your intake during hot weather or exercise. Dehydration forces the kidneys to work harder and raises the risk of kidney stones.
   
4. Monitor Your Blood Pressure Regularly: High blood pressure is the second leading cause of kidney failure. Check your numbers at least twice a year, and work with your doctor to keep readings below 120/80 if possible.
   
5. Limit Sodium Intake: Excess salt raises blood pressure and forces the kidneys to retain more water. Cook at home using herbs and spices for flavor instead of relying on processed or restaurant meals that are loaded with hidden sodium.
   
6. Reduce Sugar and Processed Food Consumption: High-sugar diets promote insulin resistance and chronic inflammation, both of which damage kidney tissue over time. Replace sugary drinks and snacks with whole fruits, vegetables, and nuts.

Source: Zeng, J., Ma, M., Tao, Z., Rao, Z., Wu, C., Yin, S., Jiang, X., Chen, G., Wang, Z., Huang, D., Zhu, M., Liu, L., Huo, W., Yang, H., Guo, H., Chen, G., Li, F., Zheng, C., Huang, D., . . . Song, T. (2025). Enzyme-converted O kidneys allow ABO-incompatible transplantation without hyperacute rejection in a human decedent model. Nature Biomedical Engineering. https://doi.org/10.1038/s41551-025-01513-6