MO323MEDICATION INDUCED RELAPSE OF FGSG

Abstract

Abstract Background and Aims 31-year-old female with past medical history of Multiple Sclerosis diagnosed with Minimal Change Disease (MCD) in 2011. At diagnosis she had proteinuria that exceeded 7 g per day. She was treated with steroids and went into complete remission. In 2017 presented again with nephrotic syndrome and on repeat biopsy she was diagnosed with Focal Segmental Glomerulosclerosis (FSGS). She was restarted on steroids and had some improvement but despite 20 weeks of high dose steroids did not achieve remission. After every attempt of tapering, she would relapse. Method Other treatments tried without success were tacrolimus, cyclophosphamide and rituximab. Mild improvement with tacrolimus but stopped after a grand mal seizure. The lowest achievable steroid dose was 20mg daily. She was started on combination therapy tacrolimus and mycophenolate mofetil and was able to come off steroids and went into remission. Results After a few months of remission, she began to relapse. It was noted after extensive investigation that she had been placed on cabergolin for hyperprolactinemia by her endocrinologist at the time she began to relapse. Cabergolin was stopped and she went into remission again. We present the first case of FSGS relapse due to cabergolin. Conclusion Cabergoline is metabolized by hydrolysis and has limited cytochrome P450 (CYP) metabolism. Despite limited CYP metabolism, cabergoline does have an interaction with clarithromycin, a known inhibitor of CYP and p-glycoprotein. One rat study suggest that mycophenolate is a substrate for p-glycoprotein, so it is possible that there is some competitive inhibition. This would explain why the patient relapsed while on cabergoline and in remission after stopping it.