Is long-term disruption of the renin-angiotensin-aldosterone system associated with LC?A retrospective cohort study healthcare workers,2026,Lange-Tal

[Chandelier]

Full title: Is long-term disruption of the renin-angiotensin-aldosterone system associated with long COVID? A retrospective cohort study among healthcare workers

Is long-term disruption of the renin-angiotensin-aldosterone system associated with long COVID? A retrospective cohort study among healthcare workers - BMC Infectious Diseases

Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin aldosterone system (RAAS), is the main receptor for SARS-CoV-2 entry into huma

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Is long-term disruption of the renin-angiotensin-aldosterone system associated with long COVID? A retrospective cohort study among healthcare workers

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Authors: Tali Lange-Tal, Neta Tuvia, Sophie Lazar, Yarra Farajh, Tomer Bernstine, Zaid Abassi, Michael Edelstein, Kamal Abu Jabal

Abstract​

Background​

Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin aldosterone system (RAAS), is the main receptor for SARS-CoV-2 entry into human cells.
The occurrence of long-term symptoms post-COVID 19 infection (Long COVID, LC) is an important public health issue with an unclear etiological mechanism.
We aimed to determine whether LC was associated with long-term RAAS disruption.

Methods​

We recruited a cohort of healthcare workers (HCWs) from Ziv Medical Center in Safed, Israel, who were uninfected and unvaccinated at baseline, and who later became infected with SARS-CoV-2.
We measured serum circulating levels of four RAAS components (ACE, ACE2, Ang1-7 and AngII) using commercially available ELISA assays at three time points, using serum samples regularly collected from consenting hospital workers during the COVID-19 pandemic: pre-infection, 3–6 months post-infection, and a year post-infection.
Post-serum collection we determined LC status using an online survey based on self-reported, LC-compatible symptoms not explained by alternative diagnoses.
We excluded participants with conditions or medications interfering with the RAAS (e.g. hypertension, chronic kidney disease, antihypertensives, antidiuretics).
At each time point we compared the levels of each of the four RAAS components between those infected and reporting LC and those infected not reporting LC using Mann Whitney U tests and Wilcoxon signed-rank tests, corrected for multiple testing.

Results​

We included 38 LC positive and 38 LC negative participants.
Age/gender distribution was similar in both groups.
NO STATISTICALLY SIGNIFICANT DIFFERENCES IN ANY OF THE FOUR RAAS MARKERS WERE OBSERVED BETWEEN LC CASES AND controls AT EITHER 3–6 MONTHS OR 12 MONTHS POST-INFECTION IN OUR STUDY SAMPLE.

Conclusion​

No evidence was detected within the limits of the study design and sample size to conclude that long-term disruption of RAAS is a significant contributor to LC pathophysiology.


Web | DOI | BMC Infectious Diseases

 

[MEMarge]

Good to see null results published

 

[Eleanor]

They started with a cohort of 'approximately 1000' and ended up with 76 participants,

38 of whom reported experiencing LC and 38 of whom did not (Figure 1). This numerical balance occurred by chance and was not the result of any deliberate matching or selection.

 

[Eleanor]

Participants were considered LC positive if they had at least one LC-compatible symptom [4] that emerged within three months of disease onset, persisted for at least two months, and could not be explained by an alternative diagnosis

participants classified as LC-positive may have reported non-specific symptoms unrelated to infection, resulting in misclassification and potentially biasing the results toward the null. To mitigate this risk, we ensured that a) there was no alternative explanation for symptoms and b) the onset of symptoms occurred after infection. Using more specific criteria, such as symptom clusters, would have further reduced the risk of misclassification, but this would have required a larger sample size than the limited number of participants available in our study.