Rhabdomyolysis and acute kidney injury in severe COVID-19 infection

Taxbro, Knut; Kahlow, Hannes; Wulcan, Hannes; Fornarve, Anna

doi:10.1136/bcr-2020-237616

Cited by 50 publications

(53 citation statements)

References 10 publications

(16 reference statements)

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“…of patients with data] 164 (392) [38] 315 (273) [8] 171 (609) [16] 58 (206) [14] 175 (567) [10] Highest, median (IQR) [No. of patients with data] 600 (748) [38] 359 (583) [9] 694 (706) [16] 808 (1374) [14] 485 (885) [11] Creatine…”

Section: Key Pointsmentioning

confidence: 99%

Association Between SARS-CoV-2 Infection and Immune-Mediated Myopathy in Patients Who Have Died

et al. 2021

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IMPORTANCE Myalgia, increased levels of creatine kinase, and persistent muscle weakness have been reported in patients with COVID-19.OBJECTIVE To study skeletal muscle and myocardial inflammation in patients with COVID-19 who had died. DESIGN, SETTING, AND PARTICIPANTSThis case-control autopsy series was conducted in a university hospital as a multidisciplinary postmortem investigation. Patients with COVID-19 or other critical illnesses who had died between March 2020 and February 2021 and on whom an autopsy was performed were included. Individuals for whom informed consent to autopsy was available and the postmortem interval was less than 6 days were randomly selected. Individuals who were infected with SARS-CoV-2 per polymerase chain reaction test results and had clinical features suggestive of COVID-19 were compared with individuals with negative SARS-CoV-2 polymerase chain reaction test results and an absence of clinical features suggestive of COVID-19. MAIN OUTCOMES AND MEASURES Inflammation of skeletal muscle tissue was assessed by quantification of immune cell infiltrates, expression of major histocompatibility complex (MHC) class I and class II antigens on the sarcolemma, and a blinded evaluation on a visual analog scale ranging from absence of pathology to the most pronounced pathology. Inflammation of cardiac muscles was assessed by quantification of immune cell infiltrates. RESULTS Forty-three patients with COVID-19 (median [interquartile range] age, 72 [16] years; 31 men [72%]) and 11 patients with diseases other than COVID-19 (median [interquartile range] age, 71 [5] years; 7 men [64%]) were included. Skeletal muscle samples from the patients who died with COVID-19 showed a higher overall pathology score (mean [SD], 3.4 [1.8] vs 1.5 [1.0]; 95% CI, 0-3; P < .001) and a higher inflammation score (mean [SD], 3.5 [2.1] vs 1.0 [0.6]; 95% CI, 0-4; P < .001). Relevant expression of MHC class I antigens on the sarcolemma was present in 23 of 42 specimens from patients with COVID-19 (55%) and upregulation of MHC class II antigens in 7 of 42 specimens from patients with COVID-19 (17%), but neither were found in any of the controls. Increased numbers of natural killer cells (median [interquartile range], 8 [8] vs 3 [4] cells per 10 high-power fields; 95% CI, 1-10 cells per 10 high-power fields; P < .001) were found. Skeletal muscles showed more inflammatory features than cardiac muscles, and inflammation was most pronounced in patients with COVID-19 with chronic courses. In some muscle specimens, SARS-CoV-2 RNA was detected by reverse transcription-polymerase chain reaction, but no evidence for a direct viral infection of myofibers was found by immunohistochemistry and electron microscopy. CONCLUSIONS AND RELEVANCEIn this case-control study of patients who had died with and without COVID-19, most individuals with severe COVID-19 showed signs of myositis ranging from mild to severe. Inflammation of skeletal muscles was associated with the duration of illness and was more pronounced than cardiac inflammation. Det...

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Section: Key Pointsmentioning

confidence: 99%

Association Between SARS-CoV-2 Infection and Immune-Mediated Myopathy in Patients Who Have Died

et al. 2021

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“…Exposure to myotoxic medication could be identified in 18 patients. Myotoxic drugs these patients were taking at the time rhabdomyolysis occurred included azithromycin, hydroxy-chloroquine, placitaxel [5], propofol [6], imastinib, piperacillin and meropenem, hydrochlorothiazide, and acetaminophen (Table). Typical clinical manifestations of rhabdomyolysis (myalgia, dark urine, fever, fatigue, vomiting, diarrhoea) were reported in 20 patients and remained unreported in 10 cases.…”

Section: Resultsmentioning

confidence: 99%

SARS-CoV-2 associated rhabdomyolysis in 32 patients

Finsterer¹,

Scorza²

2021

Turk J Med Sci

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Background/aim: This mini-review aims at summarising and discussing previous and recent findings concerning the clinical manifestations, therapeutic management, and outcome of SARS-CoV-2 associated rhabdomyolysis. Materials and methods: literature search in the PubMed database applying appropriate search terms. Results: identified were 26 articles reporting SARS-CoV-2 associated rhabdomyolysis in 32 patients. Age ranged from 16 to 80 years. Four patients were female and 25 male. Onset of rhabdomyolysis was prior to onset of COVID-19 in 7 patients, and after onset of COVID-19 in the remaining patients. Exposure to myotoxic medication was identified in 18 patients. Myotoxic drugs these patients were taking at the time rhabdomyolysis included azithromycin, hydroxy-chloroquine, placitaxel, propofol, imastinib, piperacillin and meropenem, hydrochlorothiazide, and acetaminophen. Peak creatine-kinase values ranged from 328 to >427656 U/l. The outcome was unreported in 8 cases, favourable in 15 cases, incomplete in 3 cases, and lethal in 6 cases. Conclusions: SARS-CoV-2 associated rhabdomyolysis is rare, may be most frequently due to side effects of myotoxic anti-COVID-19 drugs, and only rarely due to virus myositis, and may have a favourable outcome in most patients.

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“…36,37 COVID-19 not only causes intrarenal inflammation and increased vascular permeability, but also leads to intravascular volume depletion and cardiomyopathy, thereby precipitating cardio-renal syndrome. 38 Other proposed mechanisms for COVID-associated kidney injury include direct cytopathic effects of SARS-CoV-2 on the podocytes and renal tubules 39 and the consequences of multi-organ dysfunction such as acute tubular necrosis secondary to rhabdomyolysis, 40 renal medullary hypoxia secondary to ARDS and renal compartment syndrome due to high peak airway pressure, and intraabdominal hypertension. 41 Our finding that Black patients with COVID-19 had approximately 2.2 times increased odds of developing inhospital AKI after adjusting for potential confounders has confirmed those of the previous studies in different populations that reported 1.2-2.0 times increased odds of AKI among Black COVID-19 patients.…”

Section: Discussionmentioning

confidence: 99%

Self-identified Race and COVID-19-Associated Acute Kidney Injury and Inflammation: a Retrospective Cohort Study of Hospitalized Inner-City COVID-19 Patients

et al. 2021

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Background Black individuals have been disproportionately affected by the coronavirus disease 2019 (COVID-19). However, it remains unclear whether there are any biological factors that predispose Black patients to COVID-19-related morbidity and mortality. Objective To compare in-hospital morbidity, mortality, and inflammatory marker levels between Black and White hospitalized COVID-19 patients. Design and Participants This single-center retrospective cohort study analyzed data for Black and White patients aged ≥18 years hospitalized with a positive SARS-CoV-2 PCR test between March 1, 2020, and August 4, 2020. Main Measures The exposure was self-identified race documented in the medical record. The primary outcome of was in-hospital death. Secondary outcomes included intensive care unit admission, hospital morbidities, and inflammatory marker levels. Key Results A total of 1,424 Black and White patients were identified. The mean ± SD age was 56.1 ± 17.4 years, and 663 (44.5%) were female. There were 683 (48.0%) Black and 741 (52.0%) White patients. In the univariate analysis, Black patients had longer hospital stays (8.1 ± 10.2 vs. 6.7 ± 8.3 days, p = 0.011) and tended to have higher rates of in-hospital death (11.0% vs. 7.3%), myocardial infarction (6.9% vs. 4.5%), pulmonary embolism (PE; 5.0% vs. 2.3%), and acute kidney injury (AKI; 39.4% vs. 23.1%) than White patients (p <0.05). However, after adjusting for potential confounders, only PE (adjusted odds ratio [aOR] 2.07, 95% CI, 1.13–3.79) and AKI (aOR 2.16, 95% CI, 1.57–2.97) were statistically significantly associated with Black race. In comparison with White patients, Black patients had statistically significantly higher peak plasma D-dimer (standardized β = 0.10), erythrocyte sedimentation rate (standardized β = 0.13), ferritin (standardized β = 0.09), and lactate dehydrogenase (standardized β = 0.11), after adjusting for potential confounders (p<0.05). Conclusions Black hospitalized COVID-19 patients had increased risks of developing PE and AKI and higher inflammatory marker levels compared with White patients. This observation may be explained by differences in the prevalence and severity of underlying comorbidities and other unmeasured biologic risk factors between Black and White patients. Future research is needed to investigate the mechanism of these observed differences in outcomes of severe COVID-19 infection in Black versus White patients. Supplementary Information The online version contains supplementary material available at 10.1007/s11606-021-06931-1.

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Rhabdomyolysis and acute kidney injury in severe COVID-19 infection

Cited by 50 publications

References 10 publications

Association Between SARS-CoV-2 Infection and Immune-Mediated Myopathy in Patients Who Have Died

Association Between SARS-CoV-2 Infection and Immune-Mediated Myopathy in Patients Who Have Died

SARS-CoV-2 associated rhabdomyolysis in 32 patients

Self-identified Race and COVID-19-Associated Acute Kidney Injury and Inflammation: a Retrospective Cohort Study of Hospitalized Inner-City COVID-19 Patients

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