Kidney damage associated with COVID-19: from the acute to the chronic phase.

Publication date: Dec 01, 2024

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.

Concepts Keywords
Coronavirus acute kidney injury
Enzyme chronic kidney disease
Glomerulopathy COVID-19
Kidney Kidney damage
SARS-CoV-2

Semantics

Type Source Name
disease MESH COVID-19
disease MESH infection
disease IDO cell
drug DRUGBANK Angiotensin II
disease MESH long COVID
disease MESH inflammation
disease MESH acute kidney injury
disease MESH chronic kidney disease

Original Article

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