tetano
Editor, Senior Moderator
Ren Fail
. 2024 Dec;46(1):2316885.
doi: 10.1080/0886022X.2024.2316885. Epub 2024 Apr 1. Kidney damage associated with COVID-19: from the acute to the chronic phase
Yannick Nlandu[SUP] 1 [/SUP], Elliot Koranteng Tannor[SUP] 2 3 [/SUP], Titilope Bafemika[SUP] 4 [/SUP], Jean-Robert Makulo[SUP] 1 [/SUP]
Affiliations
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.
Keywords: COVID-19; Kidney damage; SARS-CoV-2; acute kidney injury; chronic kidney disease.
. 2024 Dec;46(1):2316885.
doi: 10.1080/0886022X.2024.2316885. Epub 2024 Apr 1. Kidney damage associated with COVID-19: from the acute to the chronic phase
Yannick Nlandu[SUP] 1 [/SUP], Elliot Koranteng Tannor[SUP] 2 3 [/SUP], Titilope Bafemika[SUP] 4 [/SUP], Jean-Robert Makulo[SUP] 1 [/SUP]
Affiliations
- PMID: 38561236
- DOI: 10.1080/0886022X.2024.2316885
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.
Keywords: COVID-19; Kidney damage; SARS-CoV-2; acute kidney injury; chronic kidney disease.