# Xenotransplantation in Nephrology: A Narrative Review

**Authors:** Alice O’Regan, Johnny Thornton, Elisha Clark, Sam Kant

PMC · DOI: 10.3390/jpm16030161 · Journal of Personalized Medicine · 2026-03-14

## TL;DR

Xenotransplantation using genetically modified pig kidneys could address the shortage of human organs for kidney transplants.

## Contribution

This paper reviews recent scientific and clinical advancements in xenotransplantation for kidney disease.

## Key findings

- Genetic engineering and immunosuppression have made xenotransplantation a feasible solution for ESKD.
- Clinical trials are beginning, but long-term outcomes and societal impact remain uncertain.
- Challenges include cross-species infections and ethical concerns about scaling porcine organ donation.

## Abstract

End-stage kidney disease (ESKD) is a global health challenge, with kidney transplant demand outstripping supply. Allotransplantation remains the gold standard for treatment but organ scarcity leads to prolonged waiting times and high mortality. Xenotransplantation, using genetically modified porcine kidneys, offers a novel and potentially sustainable solution. Genetic engineering and immunosuppression advances have enabled xenotransplantation to transition from a theoretical possibility to feasible solution. This review explores the evolution of xenotransplantation, the scientific advancements in overcoming immunological barriers, and emerging clinical data. Furthermore, we discuss emerging approaches such as central immune tolerance induction, the ongoing risks of cross-species infection, and the ethical and environmental considerations inherent to scaling up porcine organ donation. With the commencement of the first formal clinical trials, progress in the field could transform kidney transplantation, though questions remain regarding long-term outcomes and societal impact.

## Linked entities

- **Diseases:** End-stage kidney disease (MONDO:0004375)

## Full-text entities

- **Genes:** CD40 (CD40 molecule) [NCBI Gene 958] {aka Bp50, CDW40, TNFRSF5, p50}, CD55 (CD55 molecule (Cromer blood group)) [NCBI Gene 1604] {aka CHAPLE, CR, CROM, DAF, TC}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CD59 (CD59 molecule (CD59 blood group)) [NCBI Gene 966] {aka 16.3A5, 1F5, EJ16, EJ30, EL32, G344}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, CD46 (CD46 molecule) [NCBI Gene 4179] {aka AHUS2, MCP, MIC10, TLX, TRA2.10}, CD47 (CD47 molecule) [NCBI Gene 961] {aka IAP, MER6, OA3}, SLA (Src like adaptor) [NCBI Gene 6503] {aka SLA1, SLAP}, SIRPA (signal regulatory protein alpha) [NCBI Gene 140885] {aka BIT, CD172A, MFR, MYD-1, MYD1, P84}, HLA-C (major histocompatibility complex, class I, C) [NCBI Gene 3107] {aka D6S204, HLA-JY3, HLAC, HLC-C, MHC, PSORS1}, CD40LG (CD40 ligand) [NCBI Gene 959] {aka CD154, CD40L, HIGM1, IGM, IMD3, T-BAM}
- **Diseases:** vascular injury (MESH:D057772), ABMR (MESH:D020274), death (MESH:D003643), cardiac (MESH:D006331), TMA (MESH:D000743), infection (MESH:D007239), anuria (MESH:D001002), TCMR (MESH:D016399), injury to (MESH:D014947), sudden cardiac death (MESH:D016757), organ failure (MESH:D009102), tubular injury (MESH:D000230), ESKD (MESH:D007676), thrombosis (MESH:D013927), inflammation (MESH:D007249), cardiac arrhythmia (MESH:D001145), kidney failure (MESH:D051437), chronic kidney disease (MESH:D051436), ischaemic cardiomyopathy (MESH:D009202), cranial defect (MESH:D003389), hypernatremia (MESH:D006955), gastrointestinal toxicity (MESH:D005767), TB (MESH:D014390), latent infections (MESH:D000085343), hypertension (MESH:D006973), dying (MESH:D064806), hypokalemia (MESH:D007008), Electrolyte abnormalities (MESH:D014883), arginine vasopressin deficiency (MESH:D020790), Infectious Disease (MESH:D003141), cardiac and renal failure (MESH:D006333), pain (MESH:D010146), cytotoxicity (MESH:D064420)
- **Chemicals:** methylprednisolone (MESH:D008775), creatinine (MESH:D003404), tocilizumab (MESH:C502936), C3b (-), mycophenolic acid (MESH:D009173), tacrolimus (MESH:D016559), prednisolone (MESH:D011239), ravulizumab (MESH:C000629409), Gal (MESH:C055075), rituximab (MESH:D000069283), carbohydrate (MESH:D002241), Pegcetacoplan (MESH:C000716074), eculizumab (MESH:C481642)
- **Species:** Canis lupus familiaris (dog, subspecies) [taxon 9615], Suid betaherpesvirus 2 (no rank) [taxon 1608255], Pan troglodytes (chimpanzee, species) [taxon 9598], Porcine endogenous retrovirus (no rank) [taxon 61673], Sus scrofa (pig, species) [taxon 9823], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13028289/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13028289/full.md

## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC13028289/full.md

---
Source: https://tomesphere.com/paper/PMC13028289