The Coronavirus is not a single thing, it is a group of closely related viruses sharing similar “spikes” on their surface that make up their own family (group of Beta Envelope Coronaviruses) distinct from influenza or the norovirus. The novel 2019-Coronavirus (Covid19) is likely up to three closely related strains, and shares a comparable overall fatality to the Spanish Flu that wiped out around 50 million in 1918-1919 (about 2.5% overall mortality), although this has varied between the Princess Diamond and Italy, and showing diverse mortality and symptomatic profiles.
One cluster of symptoms that really divides the Coronavirus from Influenza has been barely discussed; kidney damage also known as renal impairment. Although this may not mean anything to most people, the kidneys are some of the most important organs and are responsible for filtering your blood. The fact that this symptom is exclusive within the otherwise shared symptoms means it should be common knowledge in the time of a global pandemic where the ability to differentiate the coronavirus from a cold or flu is vital.
The first publication to find that the Coronavirus can lead to kidney damage was in 2005, from a sample of 536 patients with SARS, 36 (6.7%) developed acute renal impairment occurring at a median duration of 20 days (range 5-48 days) after the onset of viral infection. This actually fits roughly with the data from the Coronavirus as in Italy approximately 3-9% of novel Coronavirus victims suffer acute kidney injury (AKI). Although this doesn’t sound like a high proportion, it is possible that the damage is simply mild in most patients, with one unpublished study showing all 27/27 of Coronapositive patients showing kidney abnormalities in a CT scan, although only 19% had elevated creatinine levels.
The fact is that MERS, another Coronavirus, was already shown to induce kidney failure and damage at a higher rate than earlier coronaviruses after only 11 days versus the 20 days as seen for SARS, with the SARS Coronavirus showing almost equal propagation in the kidney as in the bronchial tubes. This shows that the kidneys, and not just the lungs, are a source of infection and attack. The fact that all CT scans showed renal abnormalities is a potential cause for alarm.
The mechanism that SARS impacts the kidneys is likely similar to that of the related MERS, meaning it mimics kidney problems through upregulation of Smad7 and fibroblast growth factor 2 (FGF2) expression in both kidney and lung cells and leading to cell death. Its effect in the kidney is also increased due to the fact that the SARS coronavirus keeps the cells from doubling and so the organs cannot regenerate during the infection. This means that this not simply a respiratory sickness, but equivalently a renal/kidney illness, and since the lungs are in steady “crosstalk” with the kidneys and negative impacts to one often lead to issues in the other.
It is possible that part of the “shortness of breath” experienced by patients of Covid19 is due to reduced kidney function leading to lower oxygen levels in the blood and making the antagonism of the virus to the lungs and bronchial tubes more extreme. The respiratory problems from the Covid19 coronavirus are no joke, and indeed ⅔ of patients in the ICU are there with respiratory problems. That said, there remain ⅓ of patients without major respiratory issues and those with respiratory issues are likely having them exacerbated, or made worse, by the simultaneous infection of the kidneys following likely the same avenue of attack as in the lungs.
The new SARS coronavirus is not simply a “cold” or a “flu” as neither of these infections attacks your kidneys, and in the ways that it is similar to the flu it is still more intense and aggressive in many instances. Indeed we may need to worry about kidney failure of both those with respiratory as well as those with “asymptomatic” cases down the road, and the combination of both is often seen in those who die from the infection.
For a full list of all the tissues where SARS has been found, this has luckily already been investigated by Chinese scientists: “lung, trachea/bronchus, stomach, small intestine, distal convoluted renal tubule, sweat gland, parathyroid, pituitary, pancreas, adrenal gland, liver, and cerebrum”
The exact action in the other organs is not clear, for instance, there is no evidence of neurodegeneration regarding the cerebrum, although this could explain the headaches. The SARS-Cov1 findings regarding infection of the intestines appear to be applicable to SARS-Cov2 as well, with viral RNA found in the faeces up to 5 weeks after testing negative via throat swab. Considering the environmental persistence of Sars-Cov2 (Covid19) is equal to that of SARS-Cov1, it is reasonable to suspect this is essentially clinically classic SARS with improved transmission. This is a very valid reason to take existing research regarding SARS seriously, even before it is replicated in SARS-Cov2.
One reason for concern from this data is the transmission via sweat, due to infection of the sweat glands, similar as with Hepatitis C. It is also worth wondering whether there are virus-induced changes to behavior considering the infection of the adrenal gland and cerebrum.
In this context, it is advisable to not drink alcohol until this crisis has passed as that increases stress to the kidneys, and may be contributing to the higher death rates seen in France, Spain, and Italy when compared with Germany or Singapore. It is also worth wondering whether the higher death rate seen in the Netherlands is due to the fact that THC tends to lower your body’s viral immune response, and thus can potentially leave the body less able to react to the coronavirus infection, and overall smoking makes your lungs easier targets.
No matter who you are, it is worth being careful with regard to the new Covid19 (Sars-Cov2) coronavirus. It is no joke, and you owe it to yourself and your fellow humans to be careful, reserved, and overall stay home during this pandemic.
