Post by Nadica (She/Her) on Aug 12, 2024 2:12:33 GMT
How SARS-CoV-2 Responsible For Severe Kidney Injuries Post-Covid? All You Need to Know - Published Aug 11, 2024
Researchers have found that deposits of SARS-CoV-2 protein are contributing to an autoimmune condition where the body attacks the tiny filtering units in the kidneys
The SARS-CoV-2 virus, responsible for the deadly Covid-19 pandemic, is worsening kidney injuries with protein depositions, according to a study. Researchers from the Capital Medical University and Chifeng University in China found that deposits of SARS-CoV-2 protein in kidneys are contributing to the “occurrence and recurrence of membranous nephropathy (MN)” — an autoimmune condition where the body attacks the tiny filtering units (glomeruli) in the kidneys.
SARS-CoV-2’s Effect on Kidney Function
The study included 38 patients with biopsy-proven MN who developed new onset proteinuria — elevated protein in the urine — after Covid, and 100 patients with primary MN diagnosed before the pandemic as controls. “Thirteen of 38 patients were found positive for the SARS-CoV-2 nucleocapsid protein. Compared with control patients, the clinical manifestations were more severe in patients after Covid infection,” the team said, in the paper published in the Kidney International Reports.
Those with positive SARS-CoV-2 protein levels “had a higher proportion of nephrotic syndrome, lower level of serum albumin, and greater severity of renal interstitial fibrosis than those of patients with negative SARS-CoV-2” protein levels. “Our study suggests that SARS-CoV-2 infection may contribute to the deposition of viral protein under epithelial cells and lead to podocyte (kidney cells) injury,” the researchers said.
MN is the most common pathological type of adult nephrotic syndrome — a kidney disorder that causes the body to excrete too much protein in the urine. It is characterised by the deposition of immune complexes under glomerular epithelial cells, which include specific antigens, IgG, and complement membrane attack complexes (MAC). Approximately 70 per cent of MN are considered primary, while the remaining 30 per cent are secondary to various etiologies, including infections such as hepatitis virus as one of the important secondary causes.
While previous studies showed SARS-CoV-2 primarily in renal tubular epithelial cells of Covid patients with kidney injury, the new study, for the first time, observed deposits of SARS-CoV-2 nucleocapsid protein along the glomerular basement membrane.
Yet researchers noted that “the relationship between the SARS-CoV-2 protein deposition and the pathogenesis of MN remains unclear”. They called for further investigation.
Researchers have found that deposits of SARS-CoV-2 protein are contributing to an autoimmune condition where the body attacks the tiny filtering units in the kidneys
The SARS-CoV-2 virus, responsible for the deadly Covid-19 pandemic, is worsening kidney injuries with protein depositions, according to a study. Researchers from the Capital Medical University and Chifeng University in China found that deposits of SARS-CoV-2 protein in kidneys are contributing to the “occurrence and recurrence of membranous nephropathy (MN)” — an autoimmune condition where the body attacks the tiny filtering units (glomeruli) in the kidneys.
SARS-CoV-2’s Effect on Kidney Function
The study included 38 patients with biopsy-proven MN who developed new onset proteinuria — elevated protein in the urine — after Covid, and 100 patients with primary MN diagnosed before the pandemic as controls. “Thirteen of 38 patients were found positive for the SARS-CoV-2 nucleocapsid protein. Compared with control patients, the clinical manifestations were more severe in patients after Covid infection,” the team said, in the paper published in the Kidney International Reports.
Those with positive SARS-CoV-2 protein levels “had a higher proportion of nephrotic syndrome, lower level of serum albumin, and greater severity of renal interstitial fibrosis than those of patients with negative SARS-CoV-2” protein levels. “Our study suggests that SARS-CoV-2 infection may contribute to the deposition of viral protein under epithelial cells and lead to podocyte (kidney cells) injury,” the researchers said.
MN is the most common pathological type of adult nephrotic syndrome — a kidney disorder that causes the body to excrete too much protein in the urine. It is characterised by the deposition of immune complexes under glomerular epithelial cells, which include specific antigens, IgG, and complement membrane attack complexes (MAC). Approximately 70 per cent of MN are considered primary, while the remaining 30 per cent are secondary to various etiologies, including infections such as hepatitis virus as one of the important secondary causes.
While previous studies showed SARS-CoV-2 primarily in renal tubular epithelial cells of Covid patients with kidney injury, the new study, for the first time, observed deposits of SARS-CoV-2 nucleocapsid protein along the glomerular basement membrane.
Yet researchers noted that “the relationship between the SARS-CoV-2 protein deposition and the pathogenesis of MN remains unclear”. They called for further investigation.