The role of complement in kidney disease
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F23%3A00084359" target="_blank" >RIV/00023001:_____/23:00084359 - isvavai.cz</a>
Result on the web
<a href="https://www.nature.com/articles/s41581-023-00766-1" target="_blank" >https://www.nature.com/articles/s41581-023-00766-1</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/s41581-023-00766-1" target="_blank" >10.1038/s41581-023-00766-1</a>
Alternative languages
Result language
angličtina
Original language name
The role of complement in kidney disease
Original language description
The complement cascade comprises soluble and cell surface proteins and is an important arm of the innate immune system. Once activated, the complement system rapidly generates large quantities of protein fragments that are potent mediators of inflammatory, vasoactive and metabolic responses. Although complement is crucial to host defence and homeostasis, its inappropriate or uncontrolled activation can also drive tissue injury. For example, the complement system has been known for more than 50 years to be activated by glomerular immune complexes and to contribute to autoimmune kidney disease. Notably, the latest research shows that complement is also activated in kidney diseases that are not traditionally thought of as immune-mediated, including haemolytic-uraemic syndrome, diabetic kidney disease and focal segmental glomerulosclerosis. Several complement-targeted drugs have been approved for the treatment of kidney disease, and additional anti-complement agents are being investigated in clinical trials. These drugs are categorically different from other immunosuppressive agents and target pathological processes that are not effectively inhibited by other classes of immunosuppressants. The development of these new drugs might therefore have considerable benefits in the treatment of kidney disease. The complement system is often involved in immune-driven kidney injury. In this Review, the authors discuss complement activation in a variety of kidney diseases, including conditions not traditionally considered to be immune-mediated, and the potential of complement therapeutics for the treatment of kidney disease. The complement system is activated in kidney diseases of different aetiologies, including diseases involving immune complex formation, thrombotic microangiopathy, C3 glomerulopathy, glomerulosclerosis and acute kidney injury.Experimental and clinical evidence suggests that the complement cascade contributes to injury in diseases that are not traditionally regarded as immune mediated, including diabetic kidney disease and focal segmental glomerulosclerosis.The mechanisms of complement activation, including the activation pathways involved, vary among different kidney diseases, as do their downstream pathological effects.Deposition of immune complexes in the glomerular capillaries, the high local concentration of complement proteins and the delicate system of complement regulation within the kidney might all contribute to its unique susceptibility to complement-mediated injury.Many complement-inhibiting drugs have been approved, and additional agents targeting different components along the complement cascade are being investigated in clinical trials.Complement-inhibiting drugs target immune system pathways that are not directly blocked by other immunosuppressive agents.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30217 - Urology and nephrology
Result continuities
Project
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Continuities
N - Vyzkumna aktivita podporovana z neverejnych zdroju
Others
Publication year
2023
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Nature Reviews Nephrology
ISSN
1759-5061
e-ISSN
1759-507X
Volume of the periodical
19
Issue of the periodical within the volume
12
Country of publishing house
DE - GERMANY
Number of pages
17
Pages from-to
771-787
UT code for WoS article
001071106200002
EID of the result in the Scopus database
2-s2.0-85171889254