2.0 Impact of COVID-19 on kidney conditions
The global spread of COVID-19 has left nephrologists and their patients
with challenging decisions in the treatment and management of kidney
conditions such as acute kidney injury, chronic kidney disease, diabetic
nephropathy, renal cancer, kidney infarction, end-stage kidney disease,
nephrotic syndrome, dialysis and kidney transplantation. It has been
widely reported that SARS-CoV-2 enters its host cell by binding to
angiotensin-converting enzyme 2 (ACE2), a cell-surface protein found in
a host of tissues and organs including the kidney (Kuba et al., 2005;
Alhene-Gelas and Drueke, 2020). In addition, transmembrane protease
serine 2 (TMPRSS2), which is also expressed in the kidney, facilitates
the fusion of the virus and cellular membranes by cleaving the spike (S)
protein of the virus (Pan et al., 2020). In the kidney, colocalization
of ACE2 and TMPRSS were found in the podocytes and the proximal straight
tubule cells as the host cells for COVID-19 infection due to their
increased expression of these proteins (Pan et al., 2020; Wu et al.,
2021). Interestingly, RNA-sequencing data revealed that ACE2 expression
in the kidneys was almost 100-fold greater than in the lungs, suggesting
that COVID-19-related kidney injury is significantly through
ACE2-dependent pathways (Cheng et al., 2020). ACE2 is an enzyme of the
renin-angiotensin-aldosterone-system that converts angiotensin II to
angiotensin I, a vasodilator which counteracts the effects of
angiotensin II. As illustrated in figure 1, the attachment and
proliferation of the virus in the kidneys lead to an increase in kidney
function parameters such as creatinine, along with hematuria,
proteinuria and other urine abnormalities. Furthermore, kidney
structures such as the glomeruli are also inflamed and destroyed. These
changes in the kidneys progressively lead to renal failure, needing
kidney replacement therapy such as dialysis and transplantation in
patients with renal manifestations of COVID-19 infection.