Opportunistic infection from immunosuppression after kidney transplant
After a kidney transplant, immunosuppressive drugs lower immune activity, and the ongoing complication that follows most directly is opportunistic infection: disease from organisms that seldom trouble people with healthy immunity.
Remember
Early problems after a kidney transplant are mostly surgical, whereas long-term immunosuppression keeps the risk of opportunistic infection raised, because protecting the graft (the transplanted organ) also lowers defence against organisms.
After a kidney transplant, patients take immunosuppressive drugs such as tacrolimus and ciclosporin. Tacrolimus and ciclosporin block T cell activation, and T cells (T lymphocytes) are white blood cells that kill infected cells and coordinate other defences. The drugs are given to prevent rejection, in which the immune system attacks the graft (the transplanted organ).
The drugs lower immune activity throughout the body, not only against the graft. Defence against infection is turned down as well, and the result is opportunistic infection: infection by organisms that seldom trouble people with a healthy immune system.
Cytomegalovirus (a common virus that can reactivate) is the most common example. Pneumocystis jirovecii, a fungus that causes pneumonia, is another, and it can be life-threatening.
Because the drugs are continued for as long as the graft is needed, usually for life after a kidney transplant, the risk is ongoing and can appear at any time. Most opportunistic infections occur within about six months of the transplant, and later infections are mostly ordinary community infections.
Surgical problems are different. Bleeding, vascular thrombosis (a clot blocking a blood vessel) and leakage or obstruction of the ureter (the tube carrying urine from the kidney to the bladder) come from the operation, not from the tablets. Rejection is what the drugs aim to prevent, so they reduce it rather than cause it. Weakened immune surveillance, the immune system's routine patrolling for infected or abnormal cells, also raises the long-term risk of cancer.
Key facts
- Drug action
- tacrolimus and ciclosporin block T cell activation, which lowers immune activity throughout the body.
- Direct complication
- infection, especially opportunistic infection, is the ongoing risk that follows directly from long-term immunosuppression.
- Commonest example
- cytomegalovirus is the most common opportunistic infection after transplantation.
- Timing
- complications of immunosuppression can occur at any time after the transplant.
- Second cost
- reduced immune surveillance raises cancer risk, with kidney transplant recipients about 2 to 4 times more likely to develop some form of cancer than the general population.
- Surgical problems
- bleeding, vascular thrombosis and ureteric leakage or obstruction occur mainly early after the operation.
Exam traps
- Hyperacute rejection (rejection within minutes to hours, when the recipient already has antibodies against the donor kidney) is a donor and recipient matching problem (blood group and tissue compatibility), not a consequence of the immunosuppressive drugs.
- Diabetes appearing after a transplant is a recognised drug toxicity (tacrolimus, for example, impairs insulin secretion by the pancreas), and it does not result from reduced lymphocyte defence.
- A blood clot in a deep vein after major surgery is a post-operative complication that arises from the operation, not from taking immunosuppressive drugs.
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