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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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TCMR remains a major cause of kidney allograft dysfunction despite immunosuppressive therapy. Achieving optimal tacrolimus trough levels early post-transplantation is crucial to prevent acute rejection episodes. Subtherapeutic tacrolimus concentrations increase immunological risk, especially with donor-specific antibodies (DSA) and high calculated panel reactive antibodies (cPRA).
Case : A 23-year-old male with ESRD underwent hemodialysis for 2 years before receiving a living donor kidney transplant from his mother. He had GERD with esophagitis grade D and received lansoprazole. Pre-transplant screening showed DSA against HLA DPA1 02:02, negative virtual T-cell crossmatch, and 99% cPRA. Induction therapy included basiliximab and methylprednisolone, and maintenance immunosuppression was tacrolimus and mycophenolate mofetil. Prophylactic antibiotics included cotrimoxazole and valacyclovir. Despite tacrolimus, therapeutic trough levels were not achieved. The patient developed progressive renal dysfunction and hyperkalemia. A kidney biopsy showed tubulitis and interstitial nephritis consistent with acute T-cell mediated rejection. Pulse-dose methylprednisolone and conversion to cyclosporine stabilized graft function.
Discussion : Early subtherapeutic tacrolimus levels (below 6-7 ng/mL) on the first post-transplant week are associated with markedly increased acute rejection risk.Genetic polymorphisms, particularly CYP3A5 expressers carrying the *1 allele, require higher tacrolimus doses due to enhanced metabolism. CYP3A5 *1 expressers need 1.5-2 times higher doses for therapeutic targets. Severe erosive esophagitis (grade D) likely impaired tacrolimus absorption through mechanisms like gastrointestinal inflammation and altered mucosal integrity. Lansoprazole inhibit CYP3A4 metabolism, typically increasing tacrolimus levels, but in CYP2C19 poor metabolizer genotypes, PPIs paradoxically reduce tacrolimus concentrations. The gut microbiota influences tacrolimus pharmacokinetics, GERD may alter bacterial composition and affect drug absorption and metabolism. P-glycoprotein mediates intestinal efflux of tacrolimus, and inflammatory conditions may enhance this transporter activity, further reducing bioavailability. Non-pharmacokinetic factors also contributed to rejection risk. Pre-transplant DSA against HLA DPA1, despite negative virtual crossmatch, reflects alloimmune memory and increases susceptibility to acute rejection when immunosuppression is inadequate. The 99% cPRA indicates extensive HLA sensitization, further increasing immunological risk.
Achieving adequate tacrolimus levels during the early post-transplant period is crucial to prevent TCMR, especially in patients with pre-existing DSA and high immunological risk. Severe erosive esophagitis likely impaired tacrolimus absorption, exacerbated by drug-drug interactions and genetic polymorphisms affecting drug metabolism. Proactive strategies include CYP3A5 genotyping, pre-transplant gastrointestinal disorder treatment, drug interaction monitoring, aggressive dose adjustments based on early monitoring, and alternative calcineurin inhibitors in refractory cases.
