Acute Kidney Injury in a Man With COVID-19
James Matera, DO
Practicing Nephrologist, Senior Vice President for Medical Affairs, and Chief Medical Officer
CentraState Medical Center
Freehold, New Jersey
Matera J. Acute kidney injury in a man with COVID-19. Consultant360. Published online December 2, 2020.
A 54-year-old man presented to the emergency department with a 3-day history of fevers (up to 38.6°C), chills, nausea, anosmia, and dyspnea. He had been to a gathering of more than 100 people 3 days prior to developing these symptoms. Several people had tested positive for COVID-19 from that gathering. The patient had a positive COVID-19 antigen test.
On admission, the patient’s respiratory rate was 28 breaths/min, his oxygen saturation as measured by pulse oximetry was only 90% despite the administration of 4 L/min of oxygen via a nasal cannula, his D-dimer level was elevated to 2678 µg/mL, and his baseline creatinine level was elevated at 1.2 mg/dL on admission.
The patient was placed in the prone position and started on high-flow oxygen, but his condition deteriorated, and he required mechanical ventilation. Medications given at the time were intravenous (IV) dexamethasone, 6 mg daily; remdesivir; prophylactic anticoagulation; histamine-2 receptor antagonists, and IV fluids. Results of 24-hour urine studies revealed 6.2 g of proteinuria (reference range: <300 mg/24 h) with a total urine volume of 700 mL/24 h (reference range: 1500-2500 mL/24 h).
He developed oliguria 48 hours into the treatment course. Remdesivir was discontinued, and convalescent plasma was given. His creatinine level increased from 1.2 mg/dL on admission to 2.2 mg/dL on hospital day 3, 4.6 mg/dL on hospital day 5, and 5.3 mg/dL on hospital day 6. Continuous renal replacement therapy (CRRT) was started. Due to his critical illness, renal biopsy could not be performed.
The SARS-CoV-2 virus gains entry into cells via angiotensin-converting enzyme 2 (ACE2) receptors in the lungs, kidney, heart, and intestinal cells. The kidney has multiple ACE2 receptors and can be a target for COVID-19 infection.
Incidence of acute kidney injury (AKI) in patients with COVID-19 varies from 0.5% to 57.0% in reports since the pandemic started. The median time from admission to AKI is 7 to 14 days. AKI portends a higher mortality risk in patients with COVID-19 infection, reported at 35% in the United States and up to 55% in patients receiving renal replacement therapy.
Etiologies for AKI have been postulated, including:
- Cytotoxic effect with tubular and podocyte injury
- Cytokines and hyperinflammation
- Often with altered prothrombin time/partial thromboplastin time, elevated D-dimer levels, and elevated levels of fibrin degradation products
- Collapsing glomerulopathy
- Also described with HIV infections due to tubuloreticular inclusions
- Also suspected to be in high-risk patients who express the apolipoprotein L1 gene (APOL1)
- Abdominal compartment syndrome
- Cardiorenal syndrome, especially in patients with heart failure with reduced ejection fraction and other major cardiovascular issues
- Postobstructive AKI, which appears to be less common
Treatment for COVID-19–associated AKI is supportive, using renal replacement therapy as needed. Frequent system clotting, especially in CRRT, can predispose to poor overall flows and management in AKI.
Always remember that patients with underlying CKD and those with kidney failure often have comorbid conditions, making them much more susceptible to COVID-19.
Our patient died from COVID-19 on hospital day 25, remaining on CRRT the entire time. An autopsy was not performed to help discern the nature of the AKI.
- Hassanein M, Radhakrishnan Y, Sedor J, et al. COVID-19 and the kidney. Cleve Clin J Med. 2020,87(10):619-631. https://doi.org/10.3949/ccjm.87a.20072