2020•Journal of the American Society of NephrologyRequires access

A Case of Severe Rhabdomyolysis Associated with COVID-19 Infection Without AKI

Genta Uehara, Keisuke Okamoto, Tibor Fülöp, Division of Nephrology

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Abstract

Introduction: We present a case of severe rhabdomyolysis associated with COVID-19 infection without acute kidney injury (AKI). Case Description: A 43 year-old African American male with a history of medicationinduced rhabdomyolysis 6 years ago, renal cell carcinoma status post partial right nephrectomy, hypertension, type 2 diabetes, and morbid obesity presented to emergency department with upper respiratory symptoms, myalgia and discoloration of urine for one week. He reported taking atorvastatin and diltiazem for a long time but has never developed myalgia. There was no family history of myopathies, or binge alcohol intake beforehand. On physical examination, patient was hypertensive, euvolemic, and afebrile, with normal oxygenation. Chest x-ray showed subtle increased interstitial reticulation in the perihilar regions and COVID-19 rapid test returned positive. Laboratory data showed very high creatine kinase (CK) (208,456 U/L). Urinalysis showed trace proteinuria, large blood but only few red blood cells and confirmed myoglobinuria. However, his creatinine was normal (0.8 mg/dL), as well as serum calcium (8.4 mg/dL), phosphate (3.9 mg/dL), and uric acid (5.2mg/dL) levels. Patient was admitted for treatment of assumed severe rhabdomyolysis. COVID-19 was treated conservatively with oxygen supplementation. Atorvastatin and diltiazem were held, and normal saline and isotonic sodium bicarbonate fluids were administered. CK continued to rise with a peak of 499,020 U/L on day 3, but decreased steadily to 58,745 U/L on day 7. Renal function remained stable all the time during the treatment (serum Cr 0.68 - 0.82 mg/dL), with maintained urine output and well-preserved electrolytes and uric acid levels throughout. Discussion: There are increasing number of reports of COVID-19-associated rhabdomyolysis, but risk factors and characteristics are fairly known. The clinical and laboratory manifestations are suggestive of COVID-19 associated rhabodmyolysis rather than statin-induced. We are not aware of any other reports documenting such extreme CK values - with a proper rise and fall of CK - without impacting renal function. As far as we know, this is the first case of COVID-19 associated rhabdomyolysis with peak CK of 499,020 U/L, without AKI and concurrent electrolyte abnormalities. The relationship to COVID-19 vs. individual genetic susceptibility remains to be explored.

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Introduction: We present a case of severe rhabdomyolysis associated with COVID-19 infection without acute kidney injury (AKI). Case Description: A 43 year-old African American male with a history of medicationinduced rhabdomyolysis 6 years ago, renal cell carcinoma status post partial right nephrectomy, hypertension, type 2 diabetes, and morbid obesity presented to emergency department with upper respiratory symptoms, myalgia and discoloration of urine for one week. He reported taking atorvastatin and diltiazem for a long time but has never developed myalgia. There was no family history of myopathies, or binge alcohol intake beforehand. On physical examination, patient was hypertensive, euvolemic, and afebrile, with normal oxygenation. Chest x-ray showed subtle increased interstitial reticulation in the perihilar regions and COVID-19 rapid test returned positive. Laboratory data showed very high creatine kinase (CK) (208,456 U/L). Urinalysis showed trace proteinuria, large blood but only few red blood cells and confirmed myoglobinuria. However, his creatinine was normal (0.8 mg/dL), as well as serum calcium (8.4 mg/dL), phosphate (3.9 mg/dL), and uric acid (5.2mg/dL) levels. Patient was admitted for treatment of assumed severe rhabdomyolysis. COVID-19 was treated conservatively with oxygen supplementation. Atorvastatin and diltiazem were held, and normal saline and isotonic sodium bicarbonate fluids were administered. CK continued to rise with a peak of 499,020 U/L on day 3, but decreased steadily to 58,745 U/L on day 7. Renal function remained stable all the time during the treatment (serum Cr 0.68 - 0.82 mg/dL), with maintained urine output and well-preserved electrolytes and uric acid levels throughout. Discussion: There are increasing number of reports of COVID-19-associated rhabdomyolysis, but risk factors and characteristics are fairly known. The clinical and laboratory manifestations are suggestive of COVID-19 associated rhabodmyolysis rather than statin-induced. We are not aware of any other reports documenting such extreme CK values - with a proper rise and fall of CK - without impacting renal function. As far as we know, this is the first case of COVID-19 associated rhabdomyolysis with peak CK of 499,020 U/L, without AKI and concurrent electrolyte abnormalities. The relationship to COVID-19 vs. individual genetic susceptibility remains to be explored.

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Available abstract

Introduction: We present a case of severe rhabdomyolysis associated with COVID-19 infection without acute kidney injury (AKI). Case Description: A 43 year-old African American male with a history of medicationinduced rhabdomyolysis 6 years ago, renal cell carcinoma status post partial right nephrectomy, hypertension, type 2 diabetes, and morbid obesity presented to emergency department with upper respiratory symptoms, myalgia and discoloration of urine for one week. He reported taking atorvastatin and diltiazem for a long time but has never developed myalgia. There was no family history of myopathies, or binge alcohol intake beforehand. On physical examination, patient was hypertensive, euvolemic, and afebrile, with normal oxygenation. Chest x-ray showed subtle increased interstitial reticulation in the perihilar regions and COVID-19 rapid test returned positive. Laboratory data showed very high creatine kinase (CK) (208,456 U/L). Urinalysis showed trace proteinuria, large blood but only few red blood cells and confirmed myoglobinuria. However, his creatinine was normal (0.8 mg/dL), as well as serum calcium (8.4 mg/dL), phosphate (3.9 mg/dL), and uric acid (5.2mg/dL) levels. Patient was admitted for treatment of assumed severe rhabdomyolysis. COVID-19 was treated conservatively with oxygen supplementation. Atorvastatin and diltiazem were held, and normal saline and isotonic sodium bicarbonate fluids were administered. CK continued to rise with a peak of 499,020 U/L on day 3, but decreased steadily to 58,745 U/L on day 7. Renal function remained stable all the time during the treatment (serum Cr 0.68 - 0.82 mg/dL), with maintained urine output and well-preserved electrolytes and uric acid levels throughout. Discussion: There are increasing number of reports of COVID-19-associated rhabdomyolysis, but risk factors and characteristics are fairly known. The clinical and laboratory manifestations are suggestive of COVID-19 associated rhabodmyolysis rather than statin-induced. We are not aware of any other reports documenting such extreme CK values - with a proper rise and fall of CK - without impacting renal function. As far as we know, this is the first case of COVID-19 associated rhabdomyolysis with peak CK of 499,020 U/L, without AKI and concurrent electrolyte abnormalities. The relationship to COVID-19 vs. individual genetic susceptibility remains to be explored.

Key concepts: Rhabdomyolysis, Medicine, myalgia, Internal medicine, Myoglobinuria, Urinalysis, Gastroenterology, Acute kidney injury

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