ArticleBMC infectious diseases2026
Is long-term disruption of the renin-angiotensin-aldosterone system associated with long COVID? A retrospective cohort study among healthcare workers.
Article in BMC infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAngiotensin 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.
methodsWe 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.
resultsWe 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.
conclusionNo 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. CLINICAL TRIAL: Not applicable.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.