ArticleFrontiers in cardiovascular medicine2026
A triad of hypertension, heart failure, and glomerular injury in subacute Kawasaki disease: a case report and literature review.
Article in Frontiers in cardiovascular medicine, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD) is the leading cause of acquired pediatric heart disease, characterized by acute systemic vasculitis. We report a 7-year-6-month-old boy with typical KD [meeting the 2017 American Heart Association (AHA) diagnostic criteria] who responded completely to initial intravenous immunoglobulin (IVIG) therapy (2 g/kg), with rapid defervescence and normalized inflammatory markers. Despite this favorable initial response and no coronary abnormalities, he uniquely developed a triad of acute heart failure with cardiomegaly [New York Heart Association (NYHA) class II], severe hypertension (> 99th percentile), and early glomerular injury (elevated urinary albumin-to-creatinine ratio, urinary transferrin, and urinary albumin) during the clinically quiescent subacute phase. This "inflammatory-silent but vascular-loud" phenotype underscores that effective initial treatment and normalization of inflammatory markers do not equate to vascular safety, highlighting persistent endothelial dysfunction as a critical driver of morbidity. The case supports redefining subacute-phase monitoring to include blood pressure surveillance, comprehensive echocardiographic assessment of chamber dimensions and function, and screening for early glomerular injury.
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.