ReviewKidney international reports2021
Complement in Secondary Thrombotic Microangiopathy.
Review in Kidney international reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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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
69 citing papers in PubMed, 107 citations in OpenAlex.
- IPNA clinical practice recommendations for the management of aHUS and secondary TMA in children.Pediatric nephrology (Berlin, Germany) · 2026Article
- Kidney transplant outcomes in patients with complement dysregulation.World journal of transplantation · 2026Article
- Article
- Data-Driven Stratification Reveals 3 Distinct Clinicopathologic Phenotypes in Renal Thrombotic Microangiopathy.Mayo Clinic proceedings. Digital health · 2026Article
- An Unusual Case of Thrombocytopenia and Renal Failure Revealing Malignancy-Associated Thrombotic Microangiopathy.Cureus · 2026Article
- Thrombotic microangiopathy after kidney transplantation: diagnosis and management strategies.Clinical kidney journal · 2026Review
- Biopsy-proven tyrosine kinase inhibitor-associated renal injury: a case series.Clinical kidney journal · 2026Article
- Case Report: Avermectin poisoning-associated hemolytic uremic syndrome.Frontiers in immunology · 2026Article
- Calcium dysregulation in diabetic cardiomyopathy & heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2026Review
- Complement as a driver of immune-vascular heterogeneity across preeclampsia subtypes: toward a precision medicine framework.Frontiers in immunology · 2026Review
- Thrombotic microangiopathy following gene therapy for 5q-spinal muscular atrophy.Gene therapy · 2025Article
- Complement activation in secondary thrombotic microangiopathies.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Pathogenic cytokines in thrombotic microangiopathies: molecular insights and therapeutic targets.Molecular medicine (Cambridge, Mass.) · 2025Review
- Article
- Cytokine storm and microvascular fate: mechanistic insights into endothelial injury in thrombotic microangiopathies.Annals of medicine and surgery (2012) · 2025Review
- Nephrogenomics, precision medicine and the role of genetic testing in adult kidney disease management.Nature reviews. Nephrology · 2025Review
- The complement system in autoimmune diseases: pathogenesis, diagnostic markers, and therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Kidney Complement Immunohistochemistry in Thrombotic Microangiopathy Subtypes.Kidney international reports · 2025Article
- Ten tips for an onco-nephrology clinic.Clinical kidney journal · 2025Review
- The curious case of AAV immunology.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombotic microangiopathy (TMA) is a condition characterized by thrombocytopenia and microangiopathic hemolytic anemia (MAHA) with varying degrees of organ damage in the setting of normal international normalized ratio and activated partial thromboplastin time. Complement has been implicated in the etiology of TMA, which are classified as primary TMA when genetic and acquired defects in complement proteins are the primary drivers of TMA (complement-mediated TMA or atypical hemolytic uremic syndrome, aHUS) or secondary TMA, when complement activation occurs in the context of other disease processes, such as infection, malignant hypertension, autoimmune disease, malignancy, transplantation, pregnancy, and drugs. It is important to recognize that this classification is not absolute because genetic variants in complement genes have been identified in patients with secondary TMA, and distinguishing complement/genetic-mediated TMA from secondary causes of TMA can be challenging and lead to potentially harmful delays in treatment. In this review, we focus on data supporting the involvement of complement in aHUS and in secondary forms of TMA associated with malignant hypertension, drugs, autoimmune diseases, pregnancy, and infections. In aHUS, genetic variants in complement genes are found in up to 60% of patients, whereas in the secondary forms, the finding of genetic defects is variable, ranging from almost 60% in TMA associated with malignant hypertension to less than 10% in drug-induced TMA. On the basis of these findings, a new approach to management of TMA is proposed.
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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.