Since COVID-19 clearly affects the respiratory system, the effect of the kidneys has not been well studied. This study looks at the kidneys of 26 COVID-19 patient autopsies. The patients passed away from respiratory failure and multiple organ dysfunction syndrome. 9 of the 26 had kidney injury that increased serum creatine and protein in the urine. The tubules of the kidney showed tissue death, red blood cell clusters, SARS-CoV-2 like clusters, and upregulated ACE2. This study shows direct evidence that SARS-CoV-2
SARS-CoV-2 is the name of the virus that causes the disease COVID-19. The common symptoms include cough, fever, and fatigue. But the symptoms can range from nothing to severe respiratory failure. Since the lungs, blood, and immune system are mainly involved in COVID-19, research on the other organs is lacking. Ranges from 1% to 29% of patients in different areas have acute kidney injury with COVID-19.
Families of the patients provided consent for the study, and RT-PCR confirmed these patients were positive for COVID-19. All tissue samples were collected and preserved within 6 hours of fatality.
19 males and 7 females ranging from 39 to 87 years of age were included in the study. All 26 patients had tested positive for COVID-19.
Light microscopy tested for acute tubule injury. This was seen by damage, dilation, or death of the tubule tissue. Red blood cells were found in clusters in the glomerular capillaries, which sometimes caused a blockage in the capillary. In 3 patients, creatine phosphokinase was found in the urine, which can be a sign that the patient’s muscles were damaged and breaking down. Patients with diabetes or hypertension had less healthy glomeruli, and the condition of each glomerulus was varied.
Transmission Electron Microscopy
Coronavirus-like particles were found in the tubules. These particles had spikes matching the spike protein of SARS-CoV-2. Red blood cell clusters causing blockages were found in peritubular capillaries as well.
There was no build up of any inflammatory cells based on this study. White blood cells were found and caused scarring of the capillaries. Staining showed that the peritubular capillaries were almost completely blocked by red blood cells, but no platelets were found.
This study shows there is a wide range of kidney abnormalities in severe COVID-19 patients. This study may be important for less severe COVID-19 patients who have kidney damage. There was damage caused by blockage in tubules and capillaries. Some of the results are similar to how other beta-coronaviruses infect the kidney. The coronavirus-like particles were found in podocytes and matched the spike protein of coronaviruses. Immunohistochemistry shows that SARS-CoV-2 can directly infect the tubules and podocytes of the kidney. This caused acute kidney injury and protein in the urine. The breakdown of damaged skeletal muscle in some patients could be a side effect of the medications they were on, or could be caused by the virus.
SARS-CoV and SARS-CoV-2 have a 79%% resemblance and are both beta-coronaviruses. Since the virus uses ACE2 to enter the cell and there is a high concentration of ACE2 in the kidneys, they could explain some of the damage in the tubules and podocytes.
CD147 is a glycoprotein on the membrane surface that is involved in several kidney diseases. It was recently shown in another study that SARS-CoV-2 can infect cells using CD147. This interaction may be useful to target to treat COVID-19.
Acute kidney injury could have also been caused by low oxygen levels, cytokine storms, secondary infections, and drug interactions. This study was limited by a small sample size, and further research would help confirm the results of this study.