Drug-induced myopathy with acute kidney injury (A case report)

Statin-associated muscle symptoms (SAMS) are among the most common side effects of statin therapy. Depending on the severity of muscle damage and the level of creatine phosphokinase (CPK), SAMS can be classified as myalgia, myopathy, myositis, myonecrosis or rhabdomyolysis. Rhabdomyolysis is a rare but severe adverse effect, characterized by non-traumatic muscle necrosis, clinically manifested by myalgia, myoglobinemia, mioglobinuria and, in some cases, by occurrence of acute kidney injury (AKI). While the mechanisms underlying SAMS are not fully understood, several risk factors have been identified – notably, drug interactions between statins and other medications metabolized by cytochrome P450 isoenzymes. This article presents a clinical case of drug-induced myopathy in a patient with focal segmental glomerulosclerosis (FSGS) and recent myocardial infarction (MI) who was treated with atorvastatin and cyclosporine. In July of 2023, a 67-year-old patient N., presented with full-blown nephrotic syndrome (NS), serum creatinine 100 µmol/L. Renal biopsy confirmed the diagnosis of FSGS. Secondary causes were ruled out, and the patient was started on prednisolone 80 mg/day, simvastatin 40 mg/day, and perindopril 2.5 mg/day. After two months, remission of the nephritis was achieved, and prednisolone was gradually tapered; by June of 2024, the dose was decreased to 12.5 mg/day. At this point a rise of proteinuria was observed, followed by the development of acute MI. Treatment was provided according to the clinical guidelines, including the initiation of atorvastatin 80 mg/day and an increase of prednisone in to 20 mg/day. One month later, the nephrotic syndrome relapsed. Pulse glucocorticoids (GC) therapy was administered, and prednisolone dose was increased to 45 mg/day, but without effect. Cyclosporine 200 mg/day was added. During this period, serum creatinine rose to 300 µmol/L, initially interpreted as a manifestation of cyclosporine toxicity, prompting a 50% was reduction. However, the patient subsequently developed progressive muscle weakness, leading to paresis in all extremities, along with marked elevation in CPK and serum myoglobin. Neurological causes were ruled out, and the was diagnosed as severe myopathy associated with combined use of atorvastatin and cyclosporine. Following discontinuation of these drugs, the patient's muscle strength improved, and serum CPK, myoglobin and creatinine levels normalized. Continued steroid monotherapy resulted in nephritis remission. To overcome steroid dependence and maintain remission, the initiation of rituximab is planned. To address the patient’s lipid metabolism disorders, the used of РCSK9 inhibitors is being considered.

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