#3387 Hepatitis, acute kidney injury and myositis due to atorvastatin

Abstract Background and Aims A 77 year old male patient consulted the emergency department due to a new onset of jaundice without other clinical symptoms besides asthenia. Patient had a medical history of high blood pressure, dyslipidemia, type 2 diabetes and alcohol use disorder. He had no medical history of chronic liver disease or chronic kidney disease. Two months prior to the admission, the patient had been hospitalized in cardiology 2 months prior for an aortic valve replacement and quadruple CABG, with introduction of statins. During current hospitalisation, patient developed acute kidney injury, followed by acute myositis. Method An exhaustive work-up including full viral and bacterial screening and auto-immune testing was performed. Hepatic iconography (MRCP), kidney ultrasound and quadriceps MRI were also realised. Liver and kidney biopsies were performed. Results Initial blood tests showed cytolysis (AST > 35x ULN and ALT > 30x ULN) and hyperbilirubinemia (8.42 mg/dL). Two days after admission, he developed an acute kidney injury (Plasmatic Creatinine up to 8.43 mg/dL) complicated by hypervolemia and metabolic acidosis, which required hemodialysis. Surprisingly, six days after admission, he developed an elevation of Creatinine Phosphokinase up to 40855 U/L. We quickly stopped nephrotoxic therapy and excluded urinary tract obstruction, but despite that, the renal function kept getting worse. Auto-immune screening was negative, with immunoglobins and complement were within normal limits. Also, leptospirosis and hantavirus research were negative on 2 times. Urinary sediment showed no leucocyturia or hematuria, while urinary chemistry showed tubular proteinuria (P/C 1912 mg/g creat, ACR 841 mg/g creat), with negative Bence-Jones. Kidney biopsy showed rhabdomyolysis. Extended hepatic viral work-up was negative. MRCP showed no signs of hepatic parenchym or bile duct pathology. Liver biopsy showed sign of acute hepatitis, with toxic/pharmacologic as first hypothesis. As previously said, patient had negative auto-immune screening, including anti-HMGCOA antibodies were negative. Muscle MRI showed acute sign of quadriceps myositis. It is important to note that EKG and transthoracic ultrasound showed no sign of myocardial infarction. After discontinuation of Atorvastatin, liver test and Creatinine Kinase returned to normal levels. Patient still required hemodialysis after discharge from the hospital, a potential normalization of renal function is expected within 6 to 8 weeks. Conclusion Our patient showed a rare case of hepatitis, myositis and acute kidney injury after introduction of atorvastatin. As we know, this is the first case of acute kidney injury caused by statins with a delay of elevation of creatinine kinase. It shows the necessity to monitor the patients after introduction of statins to prevent the occurrence of side effect, although generally minor, but in some cases lead to major medical conditions.