ReviewInnere Medizin (Heidelberg, Germany)2024
[What is proven in the treatment of complement-mediated kidney diseases?]
Review in Innere Medizin (Heidelberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement-mediated kidney diseases encompass a complex group of diseases that are primarily caused by dysregulation of the complement system. The complement system is a crucial component of the innate immune system consisting of soluble and membrane-bound proteins. The complement system is essential for the defence against pathogens and homeostasis but its uncontrolled activation can lead to an exaggerated cellular response to immunogenic, inflammatory and metabolic stimuli. For example, glomerular deposition of immune complexes can activate the complement system and contribute to the progression of kidney diseases. The most well-known complement-mediated kidney diseases are atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy, which falls under the group of membranoproliferative glomerulonephritis (MPGN). Diagnosing these diseases requires detailed investigations with respect to triggering factors, including genetic analyses and the measurement of specific complement factors. New therapeutic approaches with drugs targeting complement system activation are now offering promising treatment options. These medications fundamentally differ from other immunosuppressive drugs and specifically target the pathological processes within the complement system. This article provides an overview of the mechanisms of complement regulation, the pathophysiological foundations of complement-mediated kidney diseases and the latest diagnostic and therapeutic advances. The goal is to provide a deeper understanding of these complex conditions and to emphasize the importance of an interdisciplinary approach in treatment and research.
Indexed as
Identifiers
39557672What 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.