COVID-19-associated acute cortical necrosis

How to cite this article:
Etta PK, Madhavi T. COVID-19-associated acute cortical necrosis. Indian J Pathol Microbiol 2023;66:229-30

Dear Editor,

Coronavirus disease 2019 (COVID-19) has been associated with acute kidney injury (AKI) in about 30-40% of hospitalized patients. It can result in systemic inflammation, cytokine storm, microcirculatory dysfunction, and hypercoagulable state with resultant arterial and venous thrombosis. Thrombotic microangiopathy (TMA) can rarely result from COVID-19 infection and can precipitate acute cortical necrosis (ACN). We describe a case of COVID-19 associated AKI due to ACN without evidence of TMA.

A 38-year-old man was hospitalized elsewhere with COVID-19 pneumonia of moderate severity requiring supplemental oxygen. His baseline renal function tests at admission were normal. Inflammatory markers and d-dimer (1600 ng/mL) were elevated modestly. He was started on antibiotics, corticosteroids, and anticoagulants. During the hospital stay, he was detected to have hospital-acquired AKI. His hemodynamic parameters were well maintained. He did not require ICU stay. There was no exposure to nephrotoxic drugs including remdesivir. His urine output gradually reduced and required four sessions of hemodialysis. After about 2 weeks of hospital stay, he was discharged with the advice of close follow up. He remained oliguric thereafter, requiring intermittent hemodialysis for about another week. At the end of 3 weeks, he started recovering and urine output gradually improved to around 1 L per day. Serum creatinine remained around 3.5 mg/dl and became dialysis independent. Urine examination showed 1+ albuminuria, with no active sediments. A kidney biopsy was performed at the end of 1 month due to persistent AKI. Light microscopy showed widespread areas of patchy cortical necrosis with ghost outlines of necrotic tubules and intervened areas of acute tubular injury with dilatation, vacuolization, flattening, and denudation of lining epithelium. The viable glomeruli were normal. There was no evidence of TMA [Figure 1]. The patient was continued on supportive care under close follow up.

Figure 1: Light microscopy examination of the kidney biopsy specimens showing areas of acute tubular injury with vacuolization, flattening, and denudation of lining epithelium (thick arrows) and patchy cortical necrosis with ghost outlines of necrotic tubules (thin arrows) (hematoxylin and eosin stain, ×5)

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ACN is characterized by patchy or diffuse coagulative necrosis of all the elements of the renal cortex resulting from significantly diminished renal arterial perfusion and ischemia due to vascular spasm and microvascular injury. The common predisposing factors for ACN are severe and prolonged hypotension, vascular insults (vascular thrombosis, thromboembolism, vasculitis, surgical factors), disseminated intravascular coagulation (DIC), infections (sepsis, angioinvasive infections like Aspergillus and Mucormycosis), immunological (systemic lupus erythematosus and antiphospholipid syndrome), TMA, and envenomation. Several pathogenetic mechanisms and risk factors of AKI in COVID-19 include microcirculatory dysfunction, systemic inflammation, cytokine storm, mechanical ventilation, hypoxemia, hypotension, metabolic acidosis, fluid overload, hypercoagulability with vascular thrombosis, and use of nephrotoxic drugs. The SARS-CoV-2 virus can also result in direct pathological injury to kidneys. The distinctive microvascular abnormalities described in COVID-19 are endothelial dysfunction, inflammation, disruption of intercellular junctions, and microthrombi formation. The various pathologies of COVID-19 associated AKI include acute tubular injury, acute tubular necrosis, acute interstitial nephritis, TMA, collapsing glomerulopathy, and other glomerular pathologies.[1] ACN has been described very rarely in these patients, mostly in association with TMA which is thought to be triggered by SARS-CoV-2 infection.[2],[3],[4] Recent evidence links the emergence of antiphospholipid antibodies (aPLs) with thrombotic complications in COVID-19.[5],[6] Some other factors such as DIC and heparin-induced thrombocytopenia can also induce microvascular thrombosis in these patients. Vaccine-induced immune thrombotic thrombocytopenia that has been described with certain SARS-CoV-2 vaccines (especially ChAdOx1 nCoV-19 adenoviral vector vaccine) can also trigger multifocal thrombosis.

Our patient was detected to have ACN without evidence of TMA or large vessel thrombosis. It could probably be triggered by COVID-19 associated microcirculatory dysfunction, cytokine storm, and microvascular thrombosis. We could not evaluate for aPLs in our patients. There were no other predisposing factors for ACN in our case. Due to the patchy nature of ACN in our patient, the renal function has recovered partially which was enough to stop dialysis. This case illustrates that ACN can result rarely due to systemic effects of COVID-19 infection and it may not always be associated with TMA. It remains to be evaluated whether aPLs are involved in the pathogenesis of the ACN in COVID-19. The cause of ACN, in this case, remains undetermined, however, the history of recent COVID-19 infection may indicate an indirect effect of COVID-19 in its pathogenesis. Multiple pathogenic events related to COVID-19 can be implicated.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

References

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