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Article ; Online: BLISS in the Treatment of Lupus Nephritis.

Thurman, Joshua M

Clinical journal of the American Society of Nephrology : CJASN

2021 Volume 16, Issue 6, Page(s) 969–971

MeSH term(s)	Antibodies, Monoclonal, Humanized/therapeutic use ; Clinical Trials as Topic ; Humans ; Immunosuppressive Agents/therapeutic use ; Lupus Nephritis/drug therapy ; Treatment Outcome
Chemical Substances	Antibodies, Monoclonal, Humanized ; Immunosuppressive Agents ; belimumab (73B0K5S26A)
Language	English
Publishing date	2021-02-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.17991120
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Article ; Online: Rhabdomyolysis and complement-once again, epithelial cells take center stage.

Thurman, Joshua M

Kidney international

2021 Volume 99, Issue 3, Page(s) 537–539

Abstract: Rhabdomyolysis is frequently associated with kidney injury. Unfortunately, there are no specific treatments for this condition, and patient care primarily consists of supportive measures. In this edition of Kidney International, Boudhabhay et al. ... ...

Abstract	Rhabdomyolysis is frequently associated with kidney injury. Unfortunately, there are no specific treatments for this condition, and patient care primarily consists of supportive measures. In this edition of Kidney International, Boudhabhay et al. demonstrate that myoglobin released from injured skeletal muscle cells triggers tubulointerstitial complement activation. In a mouse model of the disease, interventions that scavenged free heme or that prevented complement activation ameliorated kidney injury, raising the possibility that these strategies may be effective treatments for the condition.
MeSH term(s)	Acute Kidney Injury ; Animals ; Complement Activation ; Epithelial Cells ; Humans ; Mice ; Myoglobin ; Rhabdomyolysis/therapy
Chemical Substances	Myoglobin
Language	English
Publishing date	2021-02-26
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2020.10.045
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Zs.A 797: Show issues

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Article ; Online: The role of complement in kidney disease.

Petr, Vojtech / Thurman, Joshua M

Nature reviews. Nephrology

2023 Volume 19, Issue 12, Page(s) 771–787

Abstract: 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 ... ...

Abstract	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.
MeSH term(s)	Humans ; Complement System Proteins/metabolism ; Kidney Diseases/metabolism ; Complement Activation ; Kidney/metabolism ; Kidney Glomerulus/pathology ; Autoimmune Diseases
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2023-09-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-023-00766-1
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Article ; Online: Complement and the Kidney: An Overview.

Thurman, Joshua M

Advances in chronic kidney disease

2020 Volume 27, Issue 2, Page(s) 86–94

Abstract: The complement cascade was first recognized as a downstream effector system of antibody-mediated cytotoxicity. Consistent with this view, it was discovered in the 1960s that complement is activated in the glomeruli of patients with immune complex ... ...

Abstract	The complement cascade was first recognized as a downstream effector system of antibody-mediated cytotoxicity. Consistent with this view, it was discovered in the 1960s that complement is activated in the glomeruli of patients with immune complex glomerulonephritis. More recently, research has shown that complement system has many additional functions relating to regulation of the immune response, homeostasis, and metabolism. It has also become clear that the complement system is important to the pathogenesis of many non-immune complex mediated kidney diseases. In fact, in atypical hemolytic uremic syndrome and C3 glomerulopathy, uncontrolled complement activation is the primary driver of disease. Complement activation generates multiple pro-inflammatory fragments, and if not properly controlled it can cause fulminant tissue injury. Furthermore, the mechanisms of complement activation and complement-mediated injury vary from disease to disease. Many new drugs that target the complement cascade are in clinical development, so it is important to fully understand the biology of the complement system and its role in disease.
Language	English
Publishing date	2020-06-09
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ISSN	1548-5609 ; 1548-5595
ISSN (online)	1548-5609
ISSN	1548-5595
DOI	10.1053/j.ackd.2019.10.003
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Zs.A 4627: Show issues

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Article ; Online: The Immune System and Idiopathic Nephrotic Syndrome.

Campbell, Ruth E / Thurman, Joshua M

Clinical journal of the American Society of Nephrology : CJASN

2022 Volume 17, Issue 12, Page(s) 1823–1834

Abstract: Idiopathic nephrotic syndrome often responds to immunosuppressive treatment. Nevertheless, this syndrome-and the drugs used to treat it-remain important causes of patient morbidity. Idiopathic nephrotic syndrome is usually caused by minimal change ... ...

Abstract	Idiopathic nephrotic syndrome often responds to immunosuppressive treatment. Nevertheless, this syndrome-and the drugs used to treat it-remain important causes of patient morbidity. Idiopathic nephrotic syndrome is usually caused by minimal change disease or FSGS, diseases that primarily affect the podocytes. In spite of decades of research, the underlying causes of both diseases remain incompletely understood. There is, however, a large body of observational and experimental data linking the immune system with both minimal change disease and FSGS, including associations with systemic infections and hematologic malignancies. Perhaps most compellingly, many different immunomodulatory drugs are effective for treating idiopathic nephrotic syndrome, including biologic agents that have well-defined immune targets. In fact, the unexpected efficacy of targeted therapeutic agents has provided important new insights into the pathogenesis of these diseases. Given the large number of drugs that are available to deplete or block specific cells and molecules within the immune system, a better understanding of the immunologic causes of idiopathic nephrotic syndrome may lead to better diagnostic and therapeutic approaches.
MeSH term(s)	Humans ; Nephrotic Syndrome/drug therapy ; Nephrotic Syndrome/pathology ; Nephrosis, Lipoid/drug therapy ; Nephrosis, Lipoid/complications ; Glomerulosclerosis, Focal Segmental/drug therapy ; Immune System/pathology
Language	English
Publishing date	2022-10-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.07180622
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Article ; Online: The susceptibility of the kidney to alternative pathway activation-A hypothesis.

Thurman, Joshua M / Harrison, Richard A

Immunological reviews

2022 Volume 313, Issue 1, Page(s) 327–338

Abstract: The glomerulus is often the prime target of dysregulated alternative pathway (AP) activation. In particular, AP activation is the key driver of two severe kidney diseases: atypical hemolytic uremic syndrome and C3 glomerulopathy. Both conditions are ... ...

Abstract	The glomerulus is often the prime target of dysregulated alternative pathway (AP) activation. In particular, AP activation is the key driver of two severe kidney diseases: atypical hemolytic uremic syndrome and C3 glomerulopathy. Both conditions are associated with a variety of predisposing molecular defects in AP regulation, such as genetic variants in complement regulators, autoantibodies targeting AP proteins, or autoantibodies that stabilize the AP convertases (C3- and C5-activating enzymes). It is noteworthy that these are systemic AP defects, yet in both diseases pathologic complement activation primarily affects the kidneys. In particular, AP activation is often limited to the glomerular capillaries. This tropism of AP-mediated inflammation for the glomerulus points to a unique interaction between AP proteins in plasma and this particular anatomic structure. In this review, we discuss the pre-clinical and clinical data linking the molecular causes of aberrant control of the AP with activation in the glomerulus, and the possible causes of this tropism. Based on these data, we propose a model for why the kidney is so uniquely and frequently targeted in patients with AP defects. Finally, we discuss possible strategies for preventing pathologic AP activation in the kidney.
MeSH term(s)	Humans ; Complement Pathway, Alternative/genetics ; Complement C3/genetics ; Complement C3/metabolism ; Kidney ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Atypical Hemolytic Uremic Syndrome/genetics ; Atypical Hemolytic Uremic Syndrome/pathology ; Autoantibodies
Chemical Substances	Complement C3 ; Autoantibodies
Language	English
Publishing date	2022-11-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13168
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Article ; Online: Complement inhibitors in pediatric kidney diseases: new therapeutic opportunities.

Antonucci, Luca / Thurman, Joshua M / Vivarelli, Marina

Pediatric nephrology (Berlin, Germany)

2023 Volume 39, Issue 5, Page(s) 1387–1404

Abstract: Historically, the complement system (classical, lectin, alternative, and terminal pathways) is known to play a crucial role in the etiopathogenesis of many kidney diseases. Direct or indirect activation in these settings is revealed by consumption of ... ...

Abstract	Historically, the complement system (classical, lectin, alternative, and terminal pathways) is known to play a crucial role in the etiopathogenesis of many kidney diseases. Direct or indirect activation in these settings is revealed by consumption of complement proteins at the serum level and kidney tissue deposition seen by immunofluorescence and electron microscopy. The advent of eculizumab has shown that complement inhibitors may improve the natural history of certain kidney diseases. Since then, the number of available therapeutic molecules and experimental studies on complement inhibition has increased exponentially. In our narrative review, we give a summary of the main complement inhibitors that have completed phase II and phase III studies or are currently used in adult and pediatric nephrology. The relevant full-text works, abstracts, and ongoing trials (clinicaltrials.gov site) are discussed. Data and key clinical features are reported for eculizumab, ravulizumab, crovalimab, avacopan, danicopan, iptacopan, pegcetacoplan, and narsoplimab. Many of these molecules have been shown to be effective in reducing proteinuria and stabilizing kidney function in different complement-mediated kidney diseases. Thanks to their efficacy and target specificity, these novel drugs may radically improve the outcome of complement-mediated kidney diseases, contributing to an improvement in our understanding of their underlying pathophysiology.
MeSH term(s)	Adult ; Child ; Humans ; Complement Inactivating Agents/therapeutic use ; Complement Inactivating Agents/pharmacology ; Complement C3/metabolism ; Glomerulonephritis, Membranoproliferative/drug therapy ; Atypical Hemolytic Uremic Syndrome/drug therapy ; Kidney Diseases/drug therapy ; Complement Activation
Chemical Substances	Complement Inactivating Agents ; Complement C3
Language	English
Publishing date	2023-09-21
Publishing country	Germany
Document type	Review ; Journal Article
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-023-06120-8
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Zs.A 2196: Show issues

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Article ; Online: Alternative pathway diagnostics

Thurman, Joshua M. / Fremeaux‐Bacchi, Veronique

Immunological Reviews. 2023 Jan., v. 313, no. 1, p. 225-238

2023 , Page(s) 225–238

Abstract: Uncontrolled alternative pathway activation is the primary driver of several diseases, and it contributes to the pathogenesis of many others. Consequently, diagnostic tests to monitor this arm of the complement system are increasingly important. Defects ... ...

Abstract	Uncontrolled alternative pathway activation is the primary driver of several diseases, and it contributes to the pathogenesis of many others. Consequently, diagnostic tests to monitor this arm of the complement system are increasingly important. Defects in alternative pathway regulation are strong risk factors for disease, and drugs that specifically block the alternative pathway are entering clinical use. A range of diagnostic tests have been developed to evaluate and monitor the alternative pathway, including assays to measure its function, expression of alternative pathway constituents, and activation fragments. Genetic studies have also revealed many disease‐associated variants in alternative pathway genes that predict the risk of disease and prognosis. Newer imaging modalities offer the promise of non‐invasively detecting and localizing pathologic complement activation. Together, these various tests help in the diagnosis of disease, provide important prognostic information, and can help guide therapy with complement inhibitory drugs.
Keywords	complement ; diagnostic techniques ; pathogenesis ; prognosis ; risk ; therapeutics
Language	English
Dates of publication	2023-01
Size	p. 225-238
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	REVIEW
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13156
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Article ; Online: Complement Biomarkers of Hemolytic Uremic Syndrome-If Not One Thing, Maybe Another.

Thurman, Joshua M

Mayo Clinic proceedings

2018 Volume 93, Issue 10, Page(s) 1337–1339

MeSH term(s)	Atypical Hemolytic Uremic Syndrome ; Biomarkers ; Complement System Proteins ; Humans
Chemical Substances	Biomarkers ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2018-10-04
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	124027-4
ISSN	1942-5546 ; 0025-6196
ISSN (online)	1942-5546
ISSN	0025-6196
DOI	10.1016/j.mayocp.2018.08.024
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Article ; Online: The susceptibility of the kidney to alternative pathway activation—A hypothesis

Thurman, Joshua M. / Harrison, R. A.

Immunological Reviews 2023 Jan., v. 313, no. 1, p. 327-338

2023 , Page(s) 327–338

Abstract	The glomerulus is often the prime target of dysregulated alternative pathway (AP) activation. In particular, AP activation is the key driver of two severe kidney diseases: atypical hemolytic uremic syndrome and C3 glomerulopathy. Both conditions are associated with a variety of predisposing molecular defects in AP regulation, such as genetic variants in complement regulators, autoantibodies targeting AP proteins, or autoantibodies that stabilize the AP convertases (C3‐ and C5‐activating enzymes). It is noteworthy that these are systemic AP defects, yet in both diseases pathologic complement activation primarily affects the kidneys. In particular, AP activation is often limited to the glomerular capillaries. This tropism of AP‐mediated inflammation for the glomerulus points to a unique interaction between AP proteins in plasma and this particular anatomic structure. In this review, we discuss the pre‐clinical and clinical data linking the molecular causes of aberrant control of the AP with activation in the glomerulus, and the possible causes of this tropism. Based on these data, we propose a model for why the kidney is so uniquely and frequently targeted in patients with AP defects. Finally, we discuss possible strategies for preventing pathologic AP activation in the kidney.
Keywords	autoantibodies ; complement ; glomerulopathy ; hemolytic uremic syndrome ; inflammation ; kidneys ; models
Language	English
Dates of publication	2023-01
Size	p. 327-338.
Publishing place	John Wiley & Sons, Inc
Document type	Article ; Online
Note	REVIEW
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13168
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