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.

Renal Failure
|April 1, 2024
PubMed

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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