Hyperurikämie und Kristall-induzierte Nephropathien
Zusammenfassung der Projektergebnisse
Due to the mutually reinforcing results and the large number of published work, the topic of soluble and crystalline uric acid (asymptomatic and symptomatic hyperuricemia) on the effector functions of immune cells including macrophages, neutrophils and monocytes in kidney disease could be further developed in the context of sterile inflammation. These findings are of translational importance and provided evidence for previously unexplained clinical observations, e.g. in gouty arthritis. The applicant has set up new collaborations, has been asked to present on this topic at meetings and congresses, and has become an independent group leader. The novel implications and research findings will be now extended beyond this subject, for example the applicant received DFG funding to investigate the antioxidative and immunoregulatory function of soluble uric acid in CKD with emphasize on infections (secondary immunodeficiency related to kidney disease) as well as is involved in one sub-project as project leader in the DFG Transregioinitiative on neutrophils to identify mechanisms that are associated with soluble metabolites and neutrophil functions during crystal-induced kidney injury.
Projektbezogene Publikationen (Auswahl)
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Sodium glucose transporter-2 inhibition has no renoprotective effects on non-diabetic chronic kidney disease. Physiol Rep. 2017;pii: e13228
Ma Q, Steiger S & Anders HJ
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The macrophage phenotype and inflammasome component NLRP3 contributes to nephrocalcinosis-related chronic kidney disease independent from IL-1-mediated tissue injury. Kidney Int. 2018 Mar;93(3):656-669
Anders HJ, Suarez-Alvarez B, Grigorescu M, Foresto-Neto O, Steiger S, Desai J, Marschner JA, Honarpisheh M, Shi C, Jordan J, Müller L, Burzlaff N, Bäuerle T, Mulay SR
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Anti-Transforming Growth Factor β IgG Elicits a Dual Effect on Calcium Oxalate Crystallization and Progressive Nephrocalcinosis-Related Chronic Kidney Disease. Front Immunol. 2018 Mar 29;9:619
Steiger S, Grill JF, Ma Q, Bäuerle T, Jordan J, Smolle M, Böhland C, Lech M, Anders HJ
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Only Hyperuricemia with Crystalluria, but not Asymptomatic Hyperuricemia, Drives Progression of Chronic Kidney Disease. J Am Soc Nephrol. 2020 Dec;31(12):2773-2792
Sellmayr M, Hernandez Petzsche MR, Ma Q, Krüger N, Liapis H, Brink A, Lenz B, Angelotti ML, Gnemmi V, Kuppe C, Kim H, Bindels EMJ, Tajti F, Saez-Rodriguez J, Lech M, Kramann R, Romagnani P, Anders HJ, Steiger S
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Soluble Uric Acid Is an Intrinsic Negative Regulator of Monocyte Activation in Monosodium Urate Crystal-Induced Tissue Inflammation. J Immunol. 2020 Aug 1;205(3):789-800
Ma Q, Honarpisheh M, Li C, Sellmayr M, Lindenmeyer M, Böhland C, Romagnani P, Anders HJ, Steiger S
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Genetic Background but Not Intestinal Microbiota After Co-Housing Determines Hyperoxaluria-Related Nephrocalcinosis in Common Inbred Mouse Strains. Front Immunol. 2021 Apr 21;12:673423
Ma Q, Grigorescu M, Schreiber A, Kettritz R, Lindenmeyer M, Anders HJ, Steiger S
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Asymptomatic hyperuricemia promotes recovery from ischemic organ injury by modulating the phenotype of macrophages. Cells. 2022 Feb 11;11(4):626
Gnemmi V, Li Q, Ma Q, De Chiara L, Carangelo G, Li C, Molina-Van den Bosch M, Romagnani P, Anders HJ, Steiger S
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Soluble uric acid inhibits β2 integrin-mediated neutrophil recruitment in innate immunity. Blood. 2022 Mar 18
Ma Q, Immler R, Pruenster M, Sellmayr M, Li C, von Brunn A, von Brunn B, Ehmann R, Wölfel R, Napoli M, Li Q, Romagnani P, Böttcher RT, Sperandio M, Anders HJ, Steiger S
