ReviewJournal of the American Society of Nephrology : JASN2015
Kidney Disease Caused by Dysregulation of the Complement Alternative Pathway: An Etiologic Approach.
Review in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Meta-analysis of Transcriptomic Data from Lung Autopsy and Cellular Models of SARS-CoV-2 Infection.Biochemical genetics · 2024Pooled it
- Long-term eculizumab treatment failure in C3 glomerulonephritis: two case reports.Clinical kidney journal · 2026Article
- Complement Profiling in Glomerular Disease: Insights from Laser Microdissection and Mass Spectrometry.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- C3 Glomerulopathy Diagnosis, Current Treatments, and Emerging Therapies.Kidney medicine · 2026Review
- A young woman with membranoproliferative glomerulonephritis and persistent hypocomplementemia: a case report.BMC nephrology · 2026Article
- Diagnosis and treatment of complement-mediated thrombotic microangiopathies: consensus of the Genetic Diseases Committee of the Chilean Society of Nephrology.BMC nephrology · 2026Review
- Immune complex handling in transplantation: central roles for complement factor H, animal models, and translational implications.Frontiers in immunology · 2026Review
- Urine Complement Factor Ba Identifies Persistent Acute Kidney Injury and Organ Failures in Critically Ill Adults.Kidney international reports · 2025Article
- Unbiased kidney-centric molecular categorization of chronic kidney disease as a step towards precision medicine.Kidney international · 2024Article
- Carfilzomib-induced thrombotic microangiopathy (TMA): an under-recognised spectrum of disease from microangiopathic haemolysis to subclinical TMA.Blood cancer journal · 2023Article
- Recurrent C3 Glomerulonephritis along with BK-Virus-Associated Nephropathy after Kidney Transplantation: A Case Report.Medicina (Kaunas, Lithuania) · 2023Article
- Overlap of C3 Glomerulopathy and Thrombotic Microangiopathy: A Case Series.Kidney international reports · 2023Article
- Improvement of hemolytic anemia with GBT1118 is renoprotective in transgenic sickle mice.Blood advances · 2022Article
- Macrophage Depletion Reduces Disease Pathology in Factor H-Dependent Immune Complex-Mediated Glomerulonephritis.Journal of immunology research · 2022Article
- Extracellular vesicles mediate cellular interactions in renal diseases-Novel views of intercellular communications in the kidney.Journal of cellular physiology · 2021Review
- Article
- A rare cause of postinfectious glomerulonephritis: Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
- Identification of key signaling pathways induced by SARS-CoV2 that underlie thrombosis and vascular injury in COVID-19 patients.Journal of leukocyte biology · 2021Review
- Thrombotic Microangiopathy, an Unusual Form of Monoclonal Gammopathy of Renal Significance: Report of 3 Cases and Literature Review.Frontiers in immunology · 2021Review
- Treatment of C3 Glomerulopathy in Adult Kidney Transplant Recipients: A Systematic Review.Medical sciences (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidney diseases caused by genetic or acquired dysregulation of the complement alternative pathway (AP) are traditionally classified on the basis of clinical presentation (atypical hemolytic uremic syndrome as thrombotic microangiopathy), biopsy appearance (dense deposit disease and C3 GN), or clinical course (atypical postinfectious GN). Each is characterized by an inappropriate activation of the AP, eventuating in renal damage. The clinical diversity of these disorders highlights important differences in the triggers, the sites and intensity of involvement, and the outcome of the AP dysregulation. Nevertheless, we contend that these diseases should be grouped as disorders of the AP and classified on an etiologic basis. In this review, we define different pathophysiologic categories of AP dysfunction. The precise identification of the underlying abnormality is the key to predict the response to immune suppression, plasma infusion, and complement-inhibitory drugs and the outcome after transplantation. In a patient with presumed dysregulation of the AP, the collaboration of the clinician, the renal pathologist, and the biochemical and genetic laboratory is very much encouraged, because this enables the elucidation of both the underlying pathogenesis and the optimal therapeutic approach.
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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.