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E-Poster Submission Deadline
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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Abstract titles should be brief and reflect the content of the abstract.
Kidney transplantation in Atypical Hemolytic Uremic syndrome is dreaded with recurrence of micro-angiopathy in the graft kidney resulting in graft loss. The present treatment for prevention of recurrence is use of Eculizimab, a humanised monoclonal antibody which targets complement system blocking complement protein C5. However it is a costly therapy. So we used alternative protocol of pre-transplantation plasmapheresis , basiliximab induction and triple immunosuppression using tacrolimus , prednisolone and mycophenolate sodium.
23 year old male medical student presented with severe headache, malignant hypertension, seizures, diminished vision, and breathlessness at rest. Past history revealed that he underwent surgery for Achalasia Cardia in early childhood.
Vital parameters were: pulse 128 beats per minute, BP 240/136 mm Hg , respiration rate 36 per minute, SPO2 76% with high flow oxygen mask , he was afebrile.
Urine routine showed massive proteinuria , micro-hematuria, Fundus examination showed hypertensive retinopathy with intravitreal bleed. Echocardiography revealed left ventricular hypertrophy with ejection fraction 38%.
He had features of pulmonary edema needing mechanical ventilation and hemodialysis. With daily hemodialysis with fluid removal with ultrafiltration, pulmonary edema was controlled. MRI brain showed multiple tiny foci of micro-hemorrhages in subcortical and cortex of bilateral frontal , parietal and temporal lobes. CSF was normal.
Clinical exome sequencing revealed Homozygous 113.54 kb deletion on chromosome 1 encompassing CFHR1/CFHR3 region, confirming genetic aHUS susceptibility.
After explaining the risks associated with recurrence of aHUS following transplantation , related kidney transplantation was done. Mother donated the kidney. She had 6/12 HLA match. Her pre-transplant evaluation was normal , flow cytometry cross match was negative.
4 sessions of Pre-transplant plasmapheresis was performed. Induction was with Basiliximab. Triple drug immuno-suppression was used, namely tacrolimus 3mg twice daily (adjusted as per tacrolimus level), mycophenolate sodium 360mg twice daily, prednisolone 40mg once daily in tapering dosages, reaching 5 mg once a day in 10 weeks.
Transplantation was uneventful. Urination was immediate. Graft function normalised within 5 days. Patient was discharged in 10 days with normal graft function. Tacrolimus dosages were adjusted as per tacrolimus level. Blood pressure was under control with minimal antihypertensive drugs.
There was rise in creatinine level after 15 days post transplant. Apparently patient had not taken enough fluids orally fearing previous pre-transplant episodes of pulmonary edema. Urine routine was normal, there was no proteinuria. Platelet count was normal.Lactic dehydrogenase was normal, peripheral smear did not show schistocytes. There were no features of hemolytic uremic syndrome. Graft biopsy was done. It revealed mild changes of tubular injury. It did not reveal any features of microangiopathy. Patient was counselled and after adequate fluid intake, serum creatinine level started coming down. Presently serum creatinine came down from 2.2 mg/dl to 1.6 mg/dl.
Despite severe baseline complications including PRES and malignant hypertension pre-transplant, transplantation achieved immediate graft function. Tacrolimus levels reached 6.88 ng/ml on day 3. No aHUS recurrence observed clinically, biochemically or histologically on graft biopsy. Patient maintained stable renal function with controlled blood pressure on reduced antihypertensive regimen.
This case demonstrates successful renal transplantation in genomically-confirmed aHUS with severe neurological and cardiovascular manifestations using cost-effective tacrolimus-plasmapheresis protocol as alternative to eculizumab. The CFHR1/CFHR3 deletion represents high recurrence risk, yet excellent early outcomes were achieved.
This approach offers viable treatment of genomically-confirmed aHUS with pre-transplantation plasmapheresis, basiliximab and triple immunosuppression (Tacrolimus, mycophenolate ,prednisolone) for resource-limited settings while maintaining transplant success comparable to standard protocols of using eculizimab.
