- Design
- Single-cell and spatial transcriptomic laboratory study
- Population
- 20 living and 6 deceased donor kidneys; 8 paired deceased donor grafts with delayed graft function
- Primary outcome
- Donor- and recipient-derived immune cell programmes
- Effect
- Persistent donor macrophages and early interferon-stimulated recipient macrophages in delayed function
This single-cell RNA sequencing study compared the immune landscape of 20 living and six deceased donor kidneys before transplantation, and followed eight deceased donor grafts that developed delayed graft function with paired samples before and after transplant.
Deceased donor kidneys held donor-derived resident macrophages with altered gene expression that persisted after transplantation, fewer regulatory-type NK and CD8 T cells, and more pro-inflammatory CD8 T cells. After transplant, a distinct interferon-stimulated macrophage population derived from the recipient appeared, with a profile suited to recruiting recipient B and T cells.
This is mechanistic work in small numbers. It may eventually point to targets for reducing delayed graft function in deceased donor transplantation.
- Recognise that delayed graft function carries a higher risk of acute rejection; monitor closely.
- Minimise cold ischaemic time wherever the logistics can be changed.
- Treat these immune signatures as research-stage, not as a basis for changing immunosuppression.
- Follow emerging trials targeting ischaemia-reperfusion injury in deceased donor grafts.
Why it matters
It begins to explain at a cellular level why deceased donor kidneys start work later and reject more often.
Don't overread it
Small laboratory study with no clinical intervention tested.
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