Acute necrotizing glomerulonephritis associated with COVID-19 infection: report of two pediatric cases

Basiratnia, Mitra; Derakhshan, Dorna; Yeganeh, Babak Shirazi; Derakhshan, Ali

doi:10.1007/s00467-021-04944-w

Cited by 19 publications

(23 citation statements)

References 12 publications

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“…Despite indirect signs, SARS-CoV-2 RNA by RT-PCR in kidney tissue and urine were undetected in our patient. This is in line with the only other pediatric report by Basiratnia et al [ 10 ]. However, the presence of the virus at a concentration level below the threshold of detection cannot be excluded.…”

Section: Discussionsupporting

confidence: 93%

“…The histological findings mimicking viral particles in the first kidney biopsy and the evidence of a global worsening of the histological features of the second one suggest an association between SARS-CoV-2 infection and the severity of kidney inflammation. An acute exacerbation of a pre-existing kidney disease following COVID-19 was hypothesized also in one of the 2 cases described by Basiratnia et al [ 10 ]. The better prognosis of our case may be related to the absence of general and respiratory involvement.…”

Section: Discussionmentioning

confidence: 93%

“…AKI is the most feared kidney complication in children with COVID-19, but there is no consensus regarding its best management. To date, kidney biopsies are reported only in two children with COVID-19-associated AKI [ 10 ], showing an acute necrotizing glomerulonephritis in both cases. EM was not available.…”

Section: Discussionmentioning

confidence: 99%

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Kidney involvement and histological findings in two pediatric COVID-19 patients

et al. 2021

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Background Histological findings of kidney involvement have been rarely reported in pediatric patients with SARS-CoV-2 infection. Here, we describe clinical, laboratory, and histological findings of two pediatric cases with almost exclusive kidney involvement by SARS-CoV-2. Results A 10-year-old girl with IgA vasculitis nephritis underwent kidney biopsy, showing diffuse and segmental mesangial-proliferative glomerulonephritis, and steroid therapy was initiated. After the worsening of the clinical picture, including an atypical skin rash, she was diagnosed with SARS-CoV-2. The re-evaluation of initial biopsy showed cytoplasmatic blebs and virus-like particles in tubular cells at electron microscopy. Despite SARS-CoV-2 clearance and the intensification of immunosuppression, no improvement was observed. A second kidney biopsy showed a crescentic glomerulonephritis with sclerosis, while virus-like particles were no longer evident. The second patient was a 12-year-old girl with a 3-week history of weakness and weight loss. Rhinitis was reported the month before. No medications were being taken. Blood and urine analysis revealed elevated serum creatinine, hypouricemia, low molecular weight proteinuria, and glycosuria. A high SARS-CoV-2-IgG titre was detected. Kidney biopsy showed acute tubular-interstitial nephritis. Steroid therapy was started with a complete resolution of kidney involvement. Conclusion We can speculate that in both cases SARS-CoV-2 played a major role as inflammatory trigger of the kidney damage. Therefore, we suggest investigating the potential kidney damage by SARS-CoV-2 in children. Moreover, SARS-CoV-2 can be included among infectious agents responsible for pediatric acute tubular interstitial nephritis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 93%

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Kidney involvement and histological findings in two pediatric COVID-19 patients

et al. 2021

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“…As in other organs, it remains unclear if AKI is largely due to hemodynamic changes and cytokine release or if the virus also leads to direct cytotoxicity. Kidney histopathology examined in an autopsy series of 42 patients who died with COVID-19 showed varying degrees of acute tubular necrosis, collapsing focal segmental glomerulosclerosis [ 85 , 86 , 87 , 88 , 89 , 90 , 91 , 102 , 103 , 104 , 105 , 106 , 107 , 108 ], interstitial infiltration by lymphocytes, tubular epithelial cell necrosis, fibrinoid necrosis of blood vessels, and microthrombi in small vessels. There were also erythrocyte casts in some of the tubules (erythrocyturia), as well as ballooned glomeruli with mild mesangial expansion akin to diabetic nephropathy class IIa [ 80 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 ].…”

Section: Discussionmentioning

confidence: 99%

Multi-Organ Histopathological Changes in a Mouse Hepatitis Virus Model of COVID-19

Paidas

Mohamed

Norenberg

et al. 2021

Viruses

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Infection with SARS-CoV-2, the virus responsible for the global COVID-19 pandemic, causes a respiratory illness that can severely impact other organ systems and is possibly precipitated by cytokine storm, septic shock, thrombosis, and oxidative stress. SARS-CoV-2 infected individuals may be asymptomatic or may experience mild, moderate, or severe symptoms with or without pneumonia. The mechanisms by which SARS-CoV-2 infects humans are largely unknown. Mouse hepatitis virus 1 (MHV-1)-induced infection was used as a highly relevant surrogate animal model for this study. We further characterized this animal model and compared it with SARS-CoV-2 infection in humans. MHV-1 inoculated mice displayed death as well as weight loss, as reported earlier. We showed that MHV-1-infected mice at days 7–8 exhibit severe lung inflammation, peribronchiolar interstitial infiltration, bronchiolar epithelial cell necrosis and intra-alveolar necrotic debris, alveolar exudation (surrounding alveolar walls have capillaries that are dilated and filled with red blood cells), mononuclear cell infiltration, hyaline membrane formation, the presence of hemosiderin-laden macrophages, and interstitial edema. When compared to uninfected mice, the infected mice showed severe liver vascular congestion, luminal thrombosis of portal and sinusoidal vessels, hepatocyte degeneration, cell necrosis, and hemorrhagic changes. Proximal and distal tubular necrosis, hemorrhage in interstitial tissue, and the vacuolation of renal tubules were observed. The heart showed severe interstitial edema, vascular congestion, and dilation, as well as red blood cell extravasation into the interstitium. Upon examination of the MHV-1 infected mice brain, we observed congested blood vessels, perivascular cavitation, cortical pericellular halos, vacuolation of neuropils, darkly stained nuclei, pyknotic nuclei, and associated vacuolation of the neuropil in the cortex, as well as acute eosinophilic necrosis and necrotic neurons with fragmented nuclei and vacuolation in the hippocampus. Our findings suggest that the widespread thrombotic events observed in the surrogate animal model for SARS-CoV-2 mimic the reported findings in SARS-CoV-2 infected humans, representing a highly relevant and safe animal model for the study of the pathophysiologic mechanisms of SARS-CoV-2 for potential therapeutic interventions.

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“…After the adult de novo ANCA-associated glomerulonephritis and COVID-19 cases, two pediatric patients with COVID-19-related necrotizing glomerulonephritis have been reported [ 5 , 7 ]. In our differential diagnosis, we also considered ANCA-associated vasculitis based on the nodular lesions on thorax CT and the rapidly progressing GN.…”

Section: Discussionmentioning

confidence: 99%