We are learning more everyday about COVID-19. We know that for most people who contract the disease, recovery will be swift and they will return to normal rather quickly. However, for a small subset of patients, symptoms last much longer. An even smaller group of patients develop further complications such as chronic fatigue or kidney issues.
A study recently examined the role of the kidneys in COVID-19 cases. This study was published in the Nephrology Dialysis Transplantation Journal and included a large sample of patients in Madrid.
COVID-19 and the Kidneys
Coronavirus enter cells using a spike protein which binds to ACE2. Since ACE2 is present in high levels in the airways, COVID-19 has many respiratory affects. ACE2 is also present in the kidneys, which is why some patients develop kidney issues. In a study of the SARS virus that caused the 2003 epidemic, the virus was not found in kidney tissue, even when patients did experience acute kidney injury. However, in a study of two COVID-19 patients, these viral particles were found. This finding is currently being disputed. Was it actually the virus, or similarly structured particles? Regardless, it is clear that research is warranted.
From analysis of autopsies COVID-19 patients it is clear that kidney damage can ensue from the illness. More research is needed for all patients, and specifically those with less severe disease. The researchers in the Madrid study use the term “coronavirus-associated nephropathy” or, COVAN, for simplicity.
Very early research on this issue had many drawbacks such as an overrepresentation of patients with severe disease and the collecting of data retrospectively.
In Wuhan, a study was conducted examining the markers of kidney function. This found that 5.1% of the 701 patient sample had Acute Kidney Injury (AKI). In a subset of 442 patients, hematuria was present in 25% of individuals and proteinuria was found in 40%. A follow up study included 467 patients. 76% of these were patients who had also participated in the first study. In this examination, 10.5% had AKI and 42% were found to have hematuria. Proteinuria was found in 66%.
In New York, a study of 5,449 patients showed 36.6% had AKI. The development of AKI was strongly linked with those who also necessitated mechanical ventilation. For one third of these patients, 46% had hematuria and 26% had proteinuria.
1,603 patients were included in the Madrid study. This investigation included those with more mild disease. 1/5 of the patients who were hospitalized had high creatinine levels, but 40% of these individuals had chronic kidney disease (CKD)
In this sample, more than half of patients had hematuria and approximately 40% of patients had proteinuria. They also found that there was a clear correlation between lost kidney function and short-term mortality, however this is not an association unique to COVID-19.
More noteworthy, they found that hematuria that was a new onset, is associated with higher levels of mortality. It could be that hematuria could be a marker for severe COVID-19.
Ultimately, these researchers believe that the evidence is clear enough to consider COVAN to be a part of COVID-19’s clinical spectrum. But, there are still many things we don’t know. For instance, does kidney tropism as a result of COVID-19 increase an individuals risk for developing CKD down the line?
Further, we don’t know whether asymptomatic patients or those with minor disease will experience detectable proteinuria or hematuria. Researchers explain that if this is the case, unexplained hematuria or proteinuria should call for a COVID-19 test.
We are learning more every day but the research road is long. Hopefully, more data on kidney-related COVID-19 issues will be released soon.
You can read more about this research here.