#1882 Unseen Hazards: Rhabdomyolysis in CKD patients due to ticagrelor and colchicine

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Abstract Background and Aims Rhabdomyolysis (RM) is a medical condition characterized by the release of intracellular elements into the bloodstream following muscle injury. It manifests with symtoms as muscle pain (MP), weakness (W), and dark urine, which are associated with elevated levels of creatine kinase (CK) in the blood. Among the various forms of RM, drug-induced RM (DIR) is particulary notable due to its idiosyncratic nature, making it challenging to study and predict. However, this risk of DIR may be significantly higher when given the widespread use of both exclusive and combined drug therapies. Method Description of a case series involving four patients diagnosed with drug-induced rhabdomyolysis (DIR) at our center from July 2020 to November 2024. Data were collected from electronic medical records (Tables 1 and 2). Case 1 An 86-year-old female (F) presented to the hospital (H) with general malaise, asthenia (A), and MP. Blood tests (BT) confirmed rhabdomyolysis (RM), hepatic injury (HI), and acute kidney injury (AKI) with preserved urine output (UO). Six weeks earlier, she was hospitalized for non-ST elevation myocardial infarction (NSTEMI) and underwent percutaneous coronary intervention (PCI) with stent placement (SP). Ticagrelor (T) and rosuvastatin (R) was initiated. Following the RM diagnosis, T and R were discontinued, and conservative treatment was given, with resolution of RM and HI, but only partial renal function (RF) recovery. Case 2 An 87-yo (F) was electively admitted for coronary angiography due to angina pectoris and underwent Percutaneous CI with SP. T was added to her chronic medication, which included R. After 10 days, she developed severe MP and A. BT showed elevated CK, AST and ALT, as well as AKI. Hemodialysis (HD) was initiated but poorly tolerated, leading to bradycardia and cardiac arrest, ultimately resulting in her death. Case 3 A 64 yo man with end stage renal disease (CKD) on peritoneal dialysis (PD) started colchicine (Co) therapy for acute pericarditis. Two months later, he was admitted to the H for lower limb W, and exercise-MP. BT indicated RM with associated HI and initial thrombocytopenia. Atorvastatin (A) was discontinued, and PD continued with limited benefits. An MRI showed myositis, with negative autoimmune investigations. Co therapy was discontinued, and HD initiated due to reduced UO. His condition was further complicated by severe pneumonia and melena, leading to hemodynamic and respiratory instability, culminating in the patient's death. Case 4 A 56 yo F with Stage III CKD due to previous preeclampsia, presented to the H with marked W and MP after excessive sweating from work conditions. BT indicated RM, AKI and HI. The patient was on chronic Co therapy for gout, not adjusted for RF. After other causes of RM were ruled out, the condition was attributed to Co, and the medication was discontinued. This led to a gradual decrease in CK levels and resolution of HI. However, renal dysfunction persisted, necessitating the initiation of HD. Results In all cases, muscle toxicity was caused drugs. In the A and B cases, this was due to the combination of R and T, which share some metabolic pathways. In C case the combined use of A and Co resulted in severe muscle damage. Lastly, in the D case, severe dehydration led to AKI and in additional drug accumulation. In our case series, the renal outcome was unfavorable, with progression of known CKD in B,C and D cases: two required HD, and one resulted in the loss of residual UO. In terms of survival, two patients died due to complications related to their H stay, rather than directly from the drugs or RM. Conclusion RM is a rare but severe condition commonly associated with statin use, but less well-known in relation to T and Co. Patients with CKD are at higher risk due to the partial renal metabolism of these drugs. Despite adjusting drug dosages based on RF, reduced cytochrome functionality is a hidden danger that must be considered to identify patients at risk of RM. Additionally, worsening of RF in CKD patients increases toxicity risks, as drug dosages are not always properly adjusted.

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