key: cord-296271-85io9yvy
authors: Chong, Woon H.; Saha, Biplab
title: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Associated With Rhabdomyolysis and Acute Kidney Injury (AKI)
date: 2020-07-28
journal: Am J Med Sci
DOI: 10.1016/j.amjms.2020.07.032
sha: 
doc_id: 296271
cord_uid: 85io9yvy

nan

coronavirus pandemic since it was first recognized in December 2019 in Wuhan, China. The prevalence of acute kidney injury (AKI) in SARS-CoV-2 is 15%. 1 A study of 701 SARS-CoV-2 patients by Cheng and colleagues demonstrated that in-hospital mortality increased by almost three-fold in those who had AKI. 2 We report a patient with SARS-CoV-2 who developed AKI likely secondary to rhabdomyolysis and discuss the possible association between cytokine storm as the etiology.

A 37-year-old male without any medical history presented with a 2-day history of dyspnea and fatigue. He was diagnosed with SARS-CoV-2 confirmed by real-time reverse transcription-polymerase chain reaction (RT-PCR) nasopharyngeal swab. Physical examination revealed no evidence of swelling or tenderness of his extremities. He was subsequently intubated for acute hypoxic respiratory failure (AHRF) secondary to SARS-CoV-2 pneumonia. His pertinent labs are summarized in Table 1 . His creatine kinase (CK) on admission was 17,000 and peaked at 35,000 IU/L. Inflammatory markers, such as lactate dehydrogenase (LDH), white blood cell count (WBC), and C-reactive protein (CRP), were markedly elevated since his admission. He was diagnosed with rhabdomyolysis and hydrated aggressively with intravenous fluids. He required renal replacement therapy (RRT) on day five of hospitalization due to poor urine output and worsening AHRF. No other predisposing factors for rhabdomyolysis were identified, such as drugs, toxins, electrolyte abnormalities, or other infections. He died 12-days later despite therapies involving hydroxychloroquine, azithromycin, dexamethasone, tocilizumab, and convalescent plasma.

SARS-CoV-2 belongs to the same family of coronavirus that caused the severe acute respiratory syndrome coronavirus (SARS-CoV) 2003 epidemic. A case series of SARS-CoV-related rhabdomyolysis showed the development of AKI with peak CK levels ranging from 7,500 to 340,000 IU/L. 3 Jin and colleagues were the first to describe a 60-year-old man who was admitted with RT-PCR confirmed SARS-CoV-2 pneumonia and developed rhabdomyolysis on day 9 th of hospital admission. His renal function was within normal limits, and his peak laboratory values of CK, LDH, and CRP were markedly elevated at 12,000 IU/L, 2,347 IU/L, and 206 mg/L, respectively. 4 He did not develop AKI and improved with hydration and supportive care. Peak CK has been shown to have a poor correlation with the incidence of AKI, where a retrospective study on influenza-related rhabdomyolysis showed 82% of patients developed AKI with peak CK 20,000 IU/L and less. 5 Rhabdomyolysis can be the initial presentation or occur at any time during the SARS-CoV-2 disease course. Clinicians should be aware that although aggressive fluid administration has been frequently applied to prevent AKI in rhabdomyolysis, SARS-CoV-2 patients are at risk of developing worsening ARHF from fluid overload, especially in the setting of AKI with oliguria.

Generalized muscle pain and fatigue are common presenting symptoms in SARS-CoV-2.

However, this can be difficult to assess in critically ill patients, especially when they are intubated and sedated on a mechanical ventilator. Unlike other inflammatory markers 6 (white blood cell count, platelet count, lactate dehydrogenase [LDH], c-reactive protein, ferritin, and Ddimer) used for prognostication of SARS-Cov-2, CK levels are rarely monitored. Therefore, rhabdomyolysis can be easily misdiagnosed. A retrospective study of 171 SARS-CoV-2 patients showed that CK of more than 185 IU/L, AKI, and requirement of RRT was associated with an increase in mortality. 1 In the same cohort of patients who had elevated CK and developed AKI, they were more likely to have elevated inflammatory markers of LDH, d-dimer, ferritin, and procalcitonin. This may suggest a connection between excessive immune cytokine response leading to rhabdomyolysis and AKI. We postulate that the possible etiologies of SARS-CoV-2related rhabdomyolysis could be 1) direct viral invasion of muscles, 2) release of viral-toxins causing myositis, or 3) overwhelming immune response to the virus leading to cytokine storm with resulting myositis 2 .

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. The Lancet

Kidney disease is associated with in-hospital death of patients with COVID-19

Rhabdomyolysis associated with probable SARS

Rhabdomyolysis as Potential Late Complication Associated with COVID-19

Infectious Etiologies of Rhabdomyolysis: Three Case Reports and Review

A rapid advice guideline for the diagnosis and treatment of 2019 novel coronavirus (2019-nCoV) infected pneumonia (standard version)

Acknowledgments: WC had full access to the data. WC and BS were involved in writing the manuscript.