Severe Rhabdomyolysis and Acute Kidney Injury Following Rosuvastatin Reinitiation During Ticagrelor Therapy: A Case Report and Literature Review
- 1Cardiology, Yeni Klinika, Baku, AZE
- 2Intensive Care Unit, Yeni Klinika, Baku, AZE
- 3Nephrology, Yeni Klinika, Baku, AZE
Abstract
Rhabdomyolysis is a potentially life-threatening condition characterized by skeletal muscle injury, marked elevation of creatine kinase (CK), and potential development of acute kidney injury (AKI). Statins are a well-recognized cause of rhabdomyolysis, although the risk may be influenced by concomitant medications and patient-related factors. We present a case of severe rhabdomyolysis and AKI following initiation of high-intensity rosuvastatin therapy after percutaneous coronary intervention. A 66-year-old woman with type 2 diabetes mellitus, hypertension, and hyperlipidemia was admitted with acute coronary syndrome. Coronary angiography revealed a critical lesion in the left anterior descending artery, and a drug-eluting stent was implanted. Her low-density lipoprotein cholesterol was 184 mg/dL, and her triglycerides were 356 mg/dL. She was discharged on rosuvastatin 40 mg once daily, ticagrelor 90 mg twice daily, aspirin 75 mg once daily, perindopril, and amlodipine. One month later, she developed generalized weakness, fatigue, and severe myalgia. Initial laboratory investigations demonstrated elevated serum creatinine, alanine aminotransferase, and aspartate aminotransferase. Two days later, she developed anuria, severe muscle pain, and dark-red urine. On admission, CK and serum creatinine were markedly elevated. She denied other medication use, toxic exposure, or recent muscle trauma. Rhabdomyolysis with severe AKI was suspected, and she was admitted to the intensive care unit. Rosuvastatin was immediately discontinued, and ticagrelor was replaced with clopidogrel. Despite intravenous hydration and supportive treatment, metabolic acidosis and renal dysfunction worsened, with a serum creatinine level of 6.3 mg/dL, BUN of 82 mg/dL, and bicarbonate of 15 mmol/L. Hemodialysis was initiated. On the fourth day, she developed severe dyspnea and hypoxemia associated with pulmonary congestion, requiring additional consecutive hemodialysis sessions. Cardiac causes of pulmonary edema were excluded by electrocardiography and echocardiography. Her clinical condition subsequently stabilized, and CK and creatinine levels progressively decreased. She was discharged with continued renal monitoring, and serum creatinine decreased to 1.3 mg/dL by the third week after discharge. This case highlights the potential for severe rhabdomyolysis and AKI following high-intensity rosuvastatin therapy, particularly in patients with multiple comorbidities. Early recognition of myalgia, dark urine, oliguria, and markedly elevated CK levels is essential. Prompt discontinuation of the suspected medication, aggressive supportive management, and timely initiation of renal replacement therapy can be crucial in preventing further complications and facilitating recovery.
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BibTeX
@article{alasgarli2026severe,
title = {{Severe Rhabdomyolysis and Acute Kidney Injury Following Rosuvastatin Reinitiation During Ticagrelor Therapy: A Case Report and Literature Review}},
author = {Shahana Alasgarli and Emil Gasimov and Taleh Naghdaliyev and Gulay Mammadova and Anar Karimkhanov},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.117125},
url = {https://europepmc.org/article/PMC/PMC13717536},
note = {CC BY},
}
RIS
TY - JOUR
TI - Severe Rhabdomyolysis and Acute Kidney Injury Following Rosuvastatin Reinitiation During Ticagrelor Therapy: A Case Report and Literature Review
AU - Shahana Alasgarli
AU - Emil Gasimov
AU - Taleh Naghdaliyev
AU - Gulay Mammadova
AU - Anar Karimkhanov
PY - 2026
DA - 2026/09/29
JO - Cureus
DO - 10.7759/cureus.117125
UR - https://europepmc.org/article/PMC/PMC13717536
AB - Rhabdomyolysis is a potentially life-threatening condition characterized by skeletal muscle injury, marked elevation of creatine kinase (CK), and potential development of acute kidney injury (AKI). Statins are a well-recognized cause of rhabdomyolysis, although the risk may be influenced by concomitant medications and patient-related factors. We present a case of severe rhabdomyolysis and AKI following initiation of high-intensity rosuvastatin therapy after percutaneous coronary intervention. A 66-year-old woman with type 2 diabetes mellitus, hypertension, and hyperlipidemia was admitted with acute coronary syndrome. Coronary angiography revealed a critical lesion in the left anterior descending artery, and a drug-eluting stent was implanted. Her low-density lipoprotein cholesterol was 184 mg/dL, and her triglycerides were 356 mg/dL. She was discharged on rosuvastatin 40 mg once daily, ticagrelor 90 mg twice daily, aspirin 75 mg once daily, perindopril, and amlodipine. One month later, she developed generalized weakness, fatigue, and severe myalgia. Initial laboratory investigations demonstrated elevated serum creatinine, alanine aminotransferase, and aspartate aminotransferase. Two days later, she developed anuria, severe muscle pain, and dark-red urine. On admission, CK and serum creatinine were markedly elevated. She denied other medication use, toxic exposure, or recent muscle trauma. Rhabdomyolysis with severe AKI was suspected, and she was admitted to the intensive care unit. Rosuvastatin was immediately discontinued, and ticagrelor was replaced with clopidogrel. Despite intravenous hydration and supportive treatment, metabolic acidosis and renal dysfunction worsened, with a serum creatinine level of 6.3 mg/dL, BUN of 82 mg/dL, and bicarbonate of 15 mmol/L. Hemodialysis was initiated. On the fourth day, she developed severe dyspnea and hypoxemia associated with pulmonary congestion, requiring additional consecutive hemodialysis sessions. Cardiac causes of pulmonary edema were excluded by electrocardiography and echocardiography. Her clinical condition subsequently stabilized, and CK and creatinine levels progressively decreased. She was discharged with continued renal monitoring, and serum creatinine decreased to 1.3 mg/dL by the third week after discharge. This case highlights the potential for severe rhabdomyolysis and AKI following high-intensity rosuvastatin therapy, particularly in patients with multiple comorbidities. Early recognition of myalgia, dark urine, oliguria, and markedly elevated CK levels is essential. Prompt discontinuation of the suspected medication, aggressive supportive management, and timely initiation of renal replacement therapy can be crucial in preventing further complications and facilitating recovery.
SN - 2168-8184
ER -