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.