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Kidney damage associated with COVID-19: from the acute to the chronic phase
Yannick Nlandu1, Elliot Koranteng Tannor2,3, Titilope Bafemika4
1Nephrology Unit, Kinshasa University Hospital, Kinshasa, Democratic Republic of the Congo.
Abstract:
Severe acute respiratory syndrome coronavirus-2 (SARS-COV-2) infection is well established as a systemic disease including kidney damage. The entry point into the renal cell remains the angiotensin-converting enzyme 2 (ACE-2) receptor and the spectrum of renal lesions is broad, with a clear predominance of structural and functional tubular lesions. The most common form of glomerular injury is collapsing glomerulopathy (CG), which is strongly associated with apolipoprotein L1(APOL-1) risk variants. These acute lesions, which are secondary to the direct or indirect effects of SARS-CoV-2, can progress to chronicity and are specific to long COVID-19 in the absence of any other cause. Residual inflammation associated with SARS-CoV-2 infection, in addition to acute kidney injury (AKI) as a transitional state with or without severe histological lesions, may be responsible for greater kidney function decline in mild-to-moderate COVID-19. This review discusses the evidence for renal histological markers of chronicity in COVID-19 patients and triggers of low-grade inflammation that may explain the decline in kidney function in the post-COVID-19 period.
Insights
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes kidney damage primarily through the ACE-2 receptor, leading to tubular lesions and collapsing glomerulopathy. These can become chronic, contributing to long COVID-19 kidney issues.
Area of Science:
- Nephrology
- Virology
- Pathology
Background:
- Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is a systemic disease impacting kidney function.
- Renal damage occurs via the angiotensin-converting enzyme 2 (ACE-2) receptor, with tubular lesions being predominant.
- Collapsing glomerulopathy is a common glomerular injury linked to APOL-1 risk variants.
Purpose of the Study:
- To review evidence of renal histological markers of chronicity in COVID-19 patients.
- To identify triggers of low-grade inflammation post-COVID-19 that impact kidney function.
- To understand the progression of SARS-CoV-2-related kidney damage.
Main Methods:
- Review of existing literature on SARS-CoV-2 and kidney pathology.
- Analysis of histological findings in COVID-19 patients with kidney injury.
- Examination of the role of ACE-2 and APOL-1 in SARS-CoV-2 nephropathy.
Main Results:
- SARS-CoV-2 infection leads to a spectrum of renal lesions, predominantly tubular.
- Acute kidney lesions can progress to chronicity, especially in long COVID-19.
- Residual inflammation and acute kidney injury may cause long-term kidney function decline.
Conclusions:
- Histological markers indicate potential chronicity of kidney damage post-SARS-CoV-2 infection.
- Low-grade inflammation is a key factor in post-COVID-19 kidney function decline.
- Understanding these mechanisms is crucial for managing long-term renal sequelae.
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