Some severe patients with new coronary pneumonia will have complications of acute kidney injury, but the relationship is unclear.
A recent study by the School of Medicine of CUHK found that the nucleocapsid protein (N protein) of the new coronavirus can induce acute kidney injury.
The research team confirmed that the N protein of the new coronavirus is pathogenic and can interact with the transforming growth factor-β1 (TGF-β1) signaling molecule Smad3, causing the death of renal tubular epithelial cells and directly causing acute kidney injury.
The team also found that Smad3 inhibitors may be expected to become an "antidote" for the treatment of acute kidney injury in patients with new coronary pneumonia. The results of the study have just been published in the international journal Advanced Science.
The research team of the School of Medicine of CUHK found that Smad3 inhibitors may be expected to be the "antidote" for the treatment of acute kidney injury in patients with new coronary pneumonia.
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According to the Faculty of Medicine of CUHK, acute kidney injury is common in critically ill patients with new coronary pneumonia. Its characteristics include elevated serum creatinine levels, renal tubular necrosis, and kidney inflammation, its incidence and the severity of the new coronary pneumonia, and whether the patients themselves have underlying diseases. Closely related.
More than 40% of critically ill patients have acute kidney injury
According to published data, more than 40% of patients with severe new coronary pneumonia in the intensive care department will have acute kidney injury and have a high mortality rate.
Another study pointed out that acute kidney injury is the second most common complication in critically ill patients with new coronary pneumonia after acute respiratory failure.
However, the mechanism by which the new coronavirus triggers cell death in acute kidney injury is currently unclear.
Dr. Wang Wenbiao and Dr. Chen Junzhe from the Department of Internal Medicine and Therapeutics of the Faculty of Medicine of CUHK, who have carried out related research, pointed out that the kidney is one of the main organs affected by patients with COVID-19, but there is currently no targeted and effective treatment. The cell death mechanism of acute kidney injury is urgent and is the first step in the development of new treatment options.
New coronavirus N protein causes renal tubular necrosis
The research team confirmed through mouse experiments that the new coronavirus N protein is pathogenic, which can induce acute kidney injury by causing renal tubular necrosis and a significant increase in serum creatinine levels, which is especially serious in the case of ischemia.
In addition, the research team found that the new coronavirus N protein interacts with Smad3 signaling molecules to activate the cell death pathway and directly induce acute kidney injury.
When Smad3 in the transforming growth factor-β1 (TGF-β1) signaling pathway is activated, the intracellular death channel can be activated, leading to the death of renal tubular epithelial cells.
The research team further proved that the use of gene knockout technology or drugs to inhibit Smad3 can prevent cell death and acute kidney injury caused by Smad3. Using Smad3 as an inhibitory target is expected to become a new method for the treatment of acute kidney injury caused by new coronary pneumonia.
Lan Huiyao, Professor of Biomedical Research in the Department of Internal Medicine and Therapeutics of CUHK, who led the research, concluded that according to experimental results, the N protein of the new coronavirus can interact with Smad3, leading to acute kidney injury in critically ill patients with new coronary pneumonia. , There is even a chance to evolve into organ fibrosis, such as lung fibrosis.
He mentioned that targeting Smad3 can not only inhibit acute kidney injury, but also become a new treatment strategy for neo-coronary pneumonia-related organ fibrosis, bringing hope to reducing the severity of neo-coronary pneumonia organ damage.
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