At the beginning of the COVID-19 series (here), we mentioned that we will cover COVID-19’s effects on human kidney cells. In our previous post, we focused on lung cells. In this post, we will focus on COVID-19’s attacks on the kidney. This topic was triggered by a recent study that focused on 26 patients’ autopsies (1).

Many patients with kidney diseases are at higher risks for infections. For example, patients on dialysis can have weaker immune systems; patients with kidney transplants have taken immunosuppressive medications. Since the COVID-19 outbreak, clinicians have also become aware of the damaging effects on the kidney (2). According to an article from the Washington Post recently: “almost half the people hospitalized because of COVID-19 have blood or protein in their urine, indicating early damage to their kidneys” (5). Furthermore, early hospital data showed that 14-30% of ICU patients showed kidney dysfunction; some required dialysis or kidney replacement therapy (5).

Acute kidney injury (AKI) is one of the most challenging complications of COVID-19.  Initial reports showed that kidney dysfunctions or renal failures occur in 0.5–7% of cases and in 2.9–23% of ICU patients. Nine of the 26 showed clinical signs of kidney injury that included increased serum creatinine and/or new-onset proteinuria (1). By light microscopy, diffuse proximal tubule injury with the loss of brush border, non-isometric vacuolar degeneration, and even necrosis was observed (1). Additional mechanisms of kidney damages are found in a new study that describes cytokine damage, organ crosstalk and systemic effects (4).

Tubular spikes (from COVID-19) were also observed in the podocytes (1). Distal tubules and collecting ducts showed only occasional cellular swelling and edematous expansion of the interstitial space without significant inflammation. Occasional podocytes vacuolation and even detachment from the glomerular basement membrane was noted. Notably, podocytes are particularly vulnerable to viral and bacterial attacks, and podocytes injury easily induces heavy proteinuria (1,3).

Previously, we discussed that Angiotensin-converting enzyme II (ACE2) is the presumed genetic target of COVID-19. Early histology reports showed that Angiotensin-converting enzyme II (ACE2) stained mainly proximal tubules and podocytes (1, 3). TMPRSS2 is a second gene implicated in COVID-19 viral particle attacks and is co-expressed with ACE2 in podocytes (3).

Functional roles of proximal tubules and podocytes?

In our previous blog post (here), we described the structural and functional roles of proximal tubules and podocytes. Also, we summarized their roles in kidney diseases. In brief:

1) Podocytes belong to the kidney glomerulus and is a major contributor of the ultrafiltration machinery. In several kidney diseases, podocytes are the hallmark of proteinuric kidney diseases. 

2) Proximal tubule area lies in the kidney cortex; it is the site of reabsorption in the nephron including glucose, amino acids, ions, small proteins/peptides (via endocytosis) and calcium. Renal cell carcinoma (a type of kidney cancer) arise from the proximal tubules.


1) Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China Su, Hua et al. Kidney International, Volume 0, Issue 0

2) Guan W-J et al., (2020) Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med.

3) Pan, X., Xu, D., Zhang, H. et al. Identification of a potential mechanism of acute kidney injury during the COVID-19 outbreak: a study based on single-cell transcriptome analysis. Intensive Care Med (2020).

4) Ronco, C., Reis, T. Kidney involvement in COVID-19 and rationale for extracorporeal therapies. Nat Rev Nephrol (2020).

5) Washington Post article: <>

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