ArticleMayo Clinic proceedings. Digital health2026
Data-Driven Stratification Reveals 3 Distinct Clinicopathologic Phenotypes in Renal Thrombotic Microangiopathy.
Article in Mayo Clinic proceedings. Digital health, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To define phenotypic subgroups of thrombotic microangiopathy (TMA) by integrating clinicopathologic data to identify patterns suggestive of pathogenic features and etiologies. Patients and Methods: We retrospectively analyzed 283 patients with biopsy-confirmed renal TMA between January 1, 2010, and December 31, 2020. Sixty-four clinicopathologic variables were applied in consensus clustering. Results: Three distinct clusters were identified. Cluster 1 (n=78), predominantly women (n=50, 64%), was enriched for drug-induced (n=23, 29%), lupus-associated (n=9, 12%), and post-bone marrow transplant TMA (n=8, 10%). It showed wide immune-complex staining (IgM, C3, κ, and λ) and subendothelial deposits (n=16, 21%), suggestive of immune-associated injury. Cluster 2 (n=92) included the oldest patients (54±18 years) and was dominated by drug-induced TMA (n=21, 23%; one-third owing to vascular endothelial growth factor inhibitor bevacizumab) and monoclonal gammopathy-associated TMA (n=10, 11%). It showed marked endothelial damage (n=65, 71%) and mesangiolysis (n=66, 72%) with little immune staining, suggesting a toxic-related injury. Cluster 3 (n=113) exhibited the worst outcomes, with 80% (24/30) progressing to renal failure, compared with 31% (12/39) in cluster 1 and 34% (16/47) in cluster 2. This cluster was characterized by the youngest age (45±14 years), mostly males (n=67, 59%), severe hypertension (n=75, 66%), and low estimated glomerular filtration rate (10 mL/min/1.73 m Conclusion: Integrative clustering of clinical and histologic data in TMA identified 3 clinicopathologic phenotypes that may suggest underlying immune-, toxic-, or severe vascular lesion-related drivers. These findings support data-driven classification that may help prioritize diagnostic and therapeutic considerations.
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.