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The role of complement in kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

Authors: Vivarelli, Marina; Barratt, Jonathan; Beck, Laurence; Fakhouri, Fadi; Gale, Daniel; Goicoechea de Jorge, Elena; Mosca, Marta; +61 Authors

The role of complement in kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

Abstract

Uncontrolled complement activation can cause or contribute to glomerular injury in multiple kidney diseases. Although complement activation plays a causal role in atypical hemolytic uremic syndrome and C3 glomerulopathy, over the past decade, a rapidly accumulating body of evidence has shown a role for complement activation in multiple other kidney diseases, including diabetic nephropathy and several glomerulonephritides. The number of available complement inhibitor therapies has also increased during the same period. In 2022, Kidney Diseases: Improving Global Outcomes (KDIGO) convened a Controversies Conference, "The Role of Complement in Kidney Disease," to address the expanding role of complement dysregulation in the pathophysiology, diagnosis, and management of various glomerular diseases, diabetic nephropathy, and other forms of hemolytic uremic syndrome. Conference participants reviewed the evidence for complement playing a primary causal or secondary role in progression for several disease states and considered how evidence of complement involvement might inform management. Participating patients with various complement-mediated diseases and caregivers described concerns related to life planning, implications surrounding genetic testing, and the need for inclusive implementation of effective novel therapies into clinical practice. The value of biomarkers in monitoring disease course and the role of the glomerular microenvironment in complement response were examined, and key gaps in knowledge and research priorities were identified.

Keywords

MESH: Kidney Diseases / diagnosis, MESH: Complement Inactivating Agents / therapeutic use, MESH: Biomarkers / blood, [SDV]Life Sciences [q-bio], Kidney Glomerulus, Komplement-Inhibitor Komplement-vermittelte Verletzung glomeruläre Schädigung, glomerular injury., MESH: Atypical Hemolytic Uremic Syndrome / diagnosis, MESH: Atypical Hemolytic Uremic Syndrome / therapy, MESH: Complement System Proteins / metabolism, Complement Activation, complement inhibitor, MESH: Complement System Proteins / immunology, MESH: Glomerulonephritis / therapy, Life sciences, [SDV] Life Sciences [q-bio], Disease Progression, MESH: Disease Progression, Kidney Diseases, ddc:570, complement inhibitor complement-mediated injury glomerular injury, Biologie, MESH: Diabetic Nephropathies / diagnosis, 570, 610, MESH: Glomerulonephritis / immunology, MESH: Complement Activation / immunology, MESH: Diabetic Nephropathies / therapy, 616, Humans, MESH: Kidney Diseases / therapy, MESH: Humans, MESH: Diabetic Nephropathies / etiology, MESH: Glomerulonephritis / diagnosis, Complement System Proteins, Congresses as Topic, MESH: Kidney Glomerulus / pathology, glomerular injury, complement inhibitor; complement-mediated injury; glomerular injury, Komplement-Inhibitor Komplement-vermittelte Verletzung glomeruläre Schädigung ; complement inhibitor complement-mediated injury glomerular injury, Complement Inactivating Agents, MESH: Kidney Glomerulus / immunology, Biowissenschaften, Biologie, MESH: Atypical Hemolytic Uremic Syndrome / immunology, MESH: Diabetic Nephropathies / immunology, complement-mediated injury, Biowissenschaften, MESH: Kidney Diseases / immunology, MESH: Congresses as Topic, Biomarkers, ddc: ddc:570

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
76
Top 1%
Top 10%
Top 1%
Green
hybrid