AKI has a high incidence, comparable with acute lung injury and severe sepsis, and is associated with higher hospital mortality.

BackgroundStatins are one of the most frequently used drug groups among patients with cardiovascular disease. Muscle pain is very frequent among patients using statins. It is important to distinguish patients with benign muscle pain without significant biochemical correlates from patients with serious myopathies.Case summaryWe present the case of a 68-year-old woman taking atorvastatin in the past 8 months after a coronary bypass grafting, presenting with proximal muscle weakness and pain. Biochemical analysis showed a markedly elevated creatine kinase (CK) (24,159 U/L). Despite discontinuation of the statin and therapy for rhabdomyolysis (IV fluid, mannitol, and sodium bicarbonate), CK levels did not drop as much as expected. Muscle biopsy showed mild inflammatory changes and few necrotic muscle fibres, suggestive for an immune-mediated necrotizing myopathy (IMNM). Serology showed a high anti-HMG-CoA reductase antibody (anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase antibody) titre, diagnostic for an IMNM induced by statins. The patient was treated with corticosteroids and methotrexate. Creatine kinase levels, muscle weakness, and pain gradually improved over the following months.DiscussionIMNM induced by statins is a relatively new entity. It is important to be recognized because it is not a self-limiting adverse effect such as the frequent benign muscle pains caused by statins. Beside discontinuation of the causative statin, aggressive immunosuppressive therapy is mandatory in IMNM. Therefore, it is important to test for anti-HMGCR antibodies and if necessary perform a muscle biopsy in patients taking statins, presenting with muscle weakness, and CK elevations not improving after discontinuation of the statin.

Background: Gemcitabine is a broadly used chemotherapeutic agent that can cause a rare but lifethreatening complication called thrombotic microangiopathy (TMA). Early recognition is crucial as therapy options are limited.Case Description: We report the case of a 46-year-old patient with pancreatic adenocarcinoma who presented with severe anemia and thrombocytopenia as well as acute kidney injury. A diagnosis of gemcitabine-induced TMA was made. He became rapidly transfusion and dialysis dependent. Despite discontinuation of gemcitabine and treatment with high-dose corticotherapy as well as plasmapheresis, no improvement in both renal and hematological parameters was seen. Treatment with eculizumab was initiated. One week after the first administration, the patient no longer required packed cells nor platelet transfusions and one month later, dialysis could be discontinued. After five doses, treatment with eculizumab was stopped. Four months later, his serum creatinine was 1 mg/dL. Conclusions: This case report illustrates the promising beneficial effects of eculizumab in gemcitabineinduced TMA, both regarding transfusion dependence as well as improvement in renal function, thereby allowing further therapy options in patients with an active malignancy.

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