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Acute Kidney Injury Following Exposure to Calcineurin Inhibitors in a Patient with Idiopathic Membranous Nephropathy
Maciej Goździk1,2, Agnieszka Płuciennik2, Anna Zawiasa-Bryszewska1,2
1Department of Clinical Pharmacology, 1st Chair of Internal Medicine, Medical University of Łódź, ul. Kopcińskiego 22, 90-153, Lodz, Poland.
Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in non-diabetic adult patients; 75% of adult patients with MN suffer from primary idiopathic membranous nephropathy (IMN). The treatment of choice is immunosuppressive therapy, with a combination of steroids and cyclophosphamide (CYF) or chlorambucil or, as second-line treatment, calcineurin inhibitors (CNIs). One of the main concerns associated with the usage of CNIs is their potential to induce nephrotoxicity. We report a case of acute kidney injury that developed on two separate occasions within days of the administration of CNIs in a 57-year-old male patient treated for MN. The patient was qualified for first-line treatment with prednisone and CYF. Due to insufficient response and bad tolerance of CYF infusions, the immunosuppressive regimen was modified and CNIs were introduced, starting with cyclosporine A (CsA). On the third day of treatment, a severe decrease in diuresis and kidney function occurred and CsA was discontinued, resulting in a return to baseline kidney function. After 2 months, the situation repeated after attempting to introduce tacrolimus.
Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in non-diabetic adult patients; 75% of adult patients with MN suffer from primary idiopathic membranous nephropathy (IMN). The treatment of choice is immunosuppressive therapy, with a combination of steroids and cyclophosphamide (CYF) or chlorambucil or, as second-line treatment, calcineurin inhibitors (CNIs). One of the main concerns associated with the usage of CNIs is their potential to induce nephrotoxicity. We report a case of acute kidney injury that developed on two separate occasions within days of the administration of CNIs in a 57-year-old male patient treated for MN. The patient was qualified for first-line treatment with prednisone and CYF. Due to insufficient response and bad tolerance of CYF infusions, the immunosuppressive regimen was modified and CNIs were introduced, starting with cyclosporine A (CsA). On the third day of treatment, a severe decrease in diuresis and kidney function occurred and CsA was discontinued, resulting in a return to baseline kidney function. After 2 months, the situation repeated after attempting to introduce tacrolimus.
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