Mr N, 46 years old gentle man with End Stage Renal Disease, due to chronic hypertension underwent live related renal transplantation on 1.12.2023. His renal donor was his wife. It was a blood group incompatible transplantation. His blood group was O and his wife’s blood group was A. He underwent pre transplantation desensitization that included Rituximab, plasmapheresis and conventional triple immuno suppression comprising of Tacrolimus, Mycophenolate and steroids.
He had no other co-morbids and his surgery was uneventful. The kidney started functioning immediately and in 48 hours post transplantation. Protocol ultra-sonogram screening on the third day was normal and his Tacrolimus trough level was 18.6 ng/dl. (High)
On day 5 post transplantation, he had giddiness while attempting to walk. His heart rate was 206 / mt and ECG revealed Supra-Ventricular Tachycardia. His blood pressure dropped to 80 / 60n mm Hg. He was treated with DC shock and IV amiodarone. His heart rate stabilised.
He was euhydrated, there was no obvious bleeding from anywhere and was no signs of sepsis. His Tacrolimus level was 23.5 ng/ml. His ECHO was normal.
The question is what is the reason for this episode? With no routine reasons available, could it be due to the immuno suppressive medications post-transplant? With such high level, can Tacrolimus cause this phenomenon?
Adverse cardiovascular events such as chest pain, palpitation, electrocardiographic abnormalities, or decrease in left ventricular ejection fraction were reported in few clinical trials post transplantation. Many of them were related to the immuno suppression – tacrolimus in recipients of kidney transplantation. Symptomatic events were closely related with elevated drug concentrations in the relatively early phase after transplantation, especially in the range of 20- 60 ng / ml. (1)
Endogan et al reported Sinus tachycardia in 8 out of 31 children and young adults within 30 days post transplantation. (2). Bo-Ra Kim et al reported life-threatening arrhythmia after renal transplantation due to tacrolimus and cautioned careful monitoring.
The exact mechanism is not known, but thought to be due to autonomic nervous system related, calcium signalling, and mitochondrial functional alterations (4)
He was switched over to Cyclosporin from Tacrolimus and he was carefully monitored subsequently. His amiodorone was continued and there were no further episodes of tachyarythmia.
Dr R Balasubramaniyam Chief Of Nephrology, Kauvery Hospital, Chennai
