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Complement activation in IgA nephropathy

Seminars in immunopathology, 2021-10, Vol.43 (5), p.679-690

2021

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Pathologic Classification of Diabetic Nephropathy

Journal of the American Society of Nephrology, 2010-04, Vol.21 (4), p.556-563

2010

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C3 glomerulopathy - understanding a rare complement-driven renal disease

Nature reviews. Nephrology, 2019-03, Vol.15 (3), p.129-143

2019

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A Multicenter Study of the Predictive Value of Crescents in IgA Nephropathy

Journal of the American Society of Nephrology, 2017-02, Vol.28 (2), p.691-701

2017

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A novel CFHR5 fusion protein causes C3 glomerulopathy in a family without Cypriot ancestry

Kidney international, 2014-04, Vol.85 (4), p.933-937

2014

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Clusters Not Classifications: Making Sense of Complement-Mediated Kidney Injury

Journal of the American Society of Nephrology, 2018-01, Vol.29 (1), p.9-12

2018

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Eculizumab as rescue therapy in severe resistant lupus nephritis

Rheumatology (Oxford, England), 2015-12, Vol.54 (12), p.2286-2288

2015

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The Origin of Renal Fibroblasts and Progression of Kidney Disease

The American journal of pathology, 2010, Vol.176 (1), p.22-24

Cook, H. Terence

2010

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Recent insights into C3 glomerulopathy

Nephrology, dialysis, transplantation, 2013-07, Vol.28 (7), p.1685-1693

2013

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Spleen tyrosine kinase inhibition is an effective treatment for established vasculitis in a pre-clinical model

Kidney international, 2020-06, Vol.97 (6), p.1196-1207

2020

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Acute Iron Deprivation Reprograms Human Macrophage Metabolism and Reduces Inflammation In Vivo

Cell reports (Cambridge), 2019-07, Vol.28 (2), p.498-511.e5

2019

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Dense Deposit Disease and C3 Glomerulopathy

Seminars in nephrology, 2013-11, Vol.33 (6), p.493-507

2013

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C3 Glomerulopathy: Clinicopathologic Features and Predictors of Outcome

Clinical journal of the American Society of Nephrology, 2014-01, Vol.9 (1), p.46-53

2014

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Inhibition of spleen tyrosine kinase decreases donor specific antibody levels in a rat model of sensitization

Scientific reports, 2022-02, Vol.12 (1), p.3330-3330, Article 3330

2022

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The Development of Atypical Hemolytic Uremic Syndrome Depends on Complement C5

Journal of the American Society of Nephrology, 2011, Vol.22 (1), p.137-145

2011

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IL-10-producing regulatory B cells induced by IL-33 (BregIL-33 ) effectively attenuate mucosal inflammatory responses in the gut

Journal of autoimmunity, 2014-05, Vol.50 (100), p.107-122

2014

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Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice

The Journal of clinical investigation, 2019-03, Vol.129 (3), p.1061-1075

2019

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Correlation of disease activity in proliferative glomerulonephritis with glomerular spleen tyrosine kinase expression

Kidney international, 2015-07, Vol.88 (1), p.52-60

2015

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Live Imaging of Monocyte Subsets in Immune Complex-Mediated Glomerulonephritis Reveals Distinct Phenotypes and Effector Functions

Journal of the American Society of Nephrology, 2020-11, Vol.31 (11), p.2523-2542

2020

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Acute Presentation and Persistent Glomerulonephritis Following Streptococcal Infection in a Patient With Heterozygous Complement Factor H–Related Protein 5 Deficiency

American journal of kidney diseases, 2012-07, Vol.60 (1), p.121-125

2012

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Inhibition of Hypoxia Inducible Factor Hydroxylases Protects Against Renal Ischemia-Reperfusion Injury

Journal of the American Society of Nephrology, 2008, Vol.19 (1), p.39-46

2008

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Mucosal inflammation at the respiratory interface: a zebrafish model

American journal of physiology. Lung cellular and molecular physiology, 2016-03, Vol.310 (6), p.L551-L561

2016

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Phagocytosis is the main CR3-mediated function affected by the lupus-associated variant of CD11b in human myeloid cells

PloS one, 2013-02, Vol.8 (2), p.e57082-e57082

2013

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Complement activation in IgA nephropathy

Pathologic Classification of Diabetic Nephropathy

Revision of the International Society of Nephrology/Renal Pathology Society classification for lupus nephritis: clarification of definitions, and modified National Institutes of Health activity and chronicity indices

C3 glomerulopathy - understanding a rare complement-driven renal disease

A Multicenter Study of the Predictive Value of Crescents in IgA Nephropathy

A novel CFHR5 fusion protein causes C3 glomerulopathy in a family without Cypriot ancestry

Clusters Not Classifications: Making Sense of Complement-Mediated Kidney Injury

Eculizumab as rescue therapy in severe resistant lupus nephritis

The Origin of Renal Fibroblasts and Progression of Kidney Disease

Recent insights into C3 glomerulopathy

Spleen tyrosine kinase inhibition is an effective treatment for established vasculitis in a pre-clinical model

Acute Iron Deprivation Reprograms Human Macrophage Metabolism and Reduces Inflammation In Vivo

Dense Deposit Disease and C3 Glomerulopathy

C3 Glomerulopathy: Clinicopathologic Features and Predictors of Outcome

Inhibition of spleen tyrosine kinase decreases donor specific antibody levels in a rat model of sensitization

The Development of Atypical Hemolytic Uremic Syndrome Depends on Complement C5

IL-10-producing regulatory B cells induced by IL-33 (BregIL-33 ) effectively attenuate mucosal inflammatory responses in the gut

Identification of a mutation in complement factor H-related protein 5 in patients of Cypriot origin with glomerulonephritis

Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice

Correlation of disease activity in proliferative glomerulonephritis with glomerular spleen tyrosine kinase expression

Live Imaging of Monocyte Subsets in Immune Complex-Mediated Glomerulonephritis Reveals Distinct Phenotypes and Effector Functions

Acute Presentation and Persistent Glomerulonephritis Following Streptococcal Infection in a Patient With Heterozygous Complement Factor H–Related Protein 5 Deficiency

Inhibition of Hypoxia Inducible Factor Hydroxylases Protects Against Renal Ischemia-Reperfusion Injury

Mucosal inflammation at the respiratory interface: a zebrafish model

Phagocytosis is the main CR3-mediated function affected by the lupus-associated variant of CD11b in human myeloid cells

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