Bruton’s tyrosine kinase inhibition attenuates disease progression by reducing renal immune cell invasion in mice with hemolytic-uremic syndrome

Kröller, Sarah; Wissuwa, Bianka; Dennhardt, Sophie; Krieg, Nadine; Thiemermann, Christoph; Daniel, Christoph; Amann, Kerstin; Gunzer, Florian; Coldewey, Sina M.

doi:10.3389/fimmu.2023.1105181

Cited by 5 publications

(3 citation statements)

References 51 publications

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“…Burton kinase inhibitors (BTKi) inhibit the Burton kinase gene present in B lymphocytes and by doing so allow modulation of these cells in malignant processes involving them. These agents are approved by US FDA for treatments of chronic lymphocytic lymphoma (CLL) and mantle cell lymphoma (MCL) [8 ▪ ,42,43]. There are also other investigations in to the role of these agents in multiple sclerosis as well as in hemolytic uremic syndrome.…”

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

“…There are also other investigations in to the role of these agents in multiple sclerosis as well as in hemolytic uremic syndrome. These new class of agents are not uniformly nephrotoxic as well [8 ▪ ,42,43] (see Fig. 1 for general overview of signaling systems touched by VEGFi/TKI/JAK-stat agents/ and BTKi).…”

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

“…,42,43]. There are also other investigations in to the role of these agents in multiple sclerosis as well as in hemolytic uremic syndrome.…”

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confidence: 99%

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Onconephrology: mitigation of renal injury in chemotherapy administration

Selamet,

Ahdoot,

Salasnek

et al. 2023

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of review Onconephrology was first coined as a name for the intersection of cancer medicine and nephrology in the early 2010s. It was recognized then that beyond and understanding of kidney physiology, a new generation of nephrologists skilled in both molecular biology and precision medicine were needed to deal with the challenges of emerging cancer therapies. Stem cell transplants, biologic agents, adjuvants blocking basic cellular signaling pathways, immunotherapy were found to promote novel anticancer outcomes, but also to pose new risks to the kidneys. The field rapidly overlapped with emerging expertise in vascular glomerular disease, glomerular disease, and the same biologic agents now applied to auto immune systemic and kidney diseases. Recent findings Many categories of chemotherapeutic agents have been discovered to have adverse renal side effects. In this review, we address classic chemotherapeutic nephrotoxicity and oncologic clinical situations leading to acute kidney injury. We also review the frontiers of nephrotoxicity reported with cell cycle inhibitors, diverse classes of tyrosine kinase inhibitors, immune checkpoint inhibitors, chimeric antigen receptor T-cell therapy, anticancer vaccines, and thrombotic microangiopathies triggered by malignancy and chemotherapy. The aim will be to focus on published strategies to mitigate nephrotoxicity. Summary As onconephrology expands into its own field, it gives birth to new subdisciplines. An understanding that patient populations want the benefits of chemotherapy without the renal (and other) systemic toxicities is emerging. A need to develop a new class of molecular and genetic experts in onconephrology to mitigate nephrotoxicity from chemotherapy is apparent and urgent.

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Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

Section: Novel Onconephrology Approaches For More Novel Agentsmentioning

confidence: 99%

See 1 more Smart Citation

Onconephrology: mitigation of renal injury in chemotherapy administration

Selamet,

Ahdoot,

Salasnek

et al. 2023

Current Opinion in Nephrology &Amp; Hypertension

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The immune regulatory role of lymphangiogenesis in kidney disease

Lu,

Ma,

Ren

et al. 2024

J Transl Med

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The renal lymphatic system is critical for maintaining kidney homeostasis and regulating the immune response inside the kidney. In various kidney pathological situations, the renal lymphatic network experiences lymphangiogenesis, which is defined as the creation of new lymphatic vessels. Kidney lymphangiogenesis controls immunological response inside the kidney by controlling lymphatic flow, immune cell trafficking, and immune cell regulation. Ongoing study reveals lymphangiogenesis’s different architecture and functions in numerous tissues and organs. New research suggests that lymphangiogenesis in kidney disorders may regulate the renal immune response in various ways. The flexibility of lymphatic endothelial cells (LECs) improves the kidney’s immunological regulatory function of lymphangiogenesis. Furthermore, current research has shown disparate findings regarding its impact on distinct renal diseases, resulting in contradictory outcomes even within the same kidney condition. The fundamental causes of the various effects of lymphangiogenesis on renal disorders remain unknown. In this thorough review, we explore the dual impacts of renal lymphangiogenesis on several kidney pathologies, with a particular emphasis on existing empirical data and new developments in understanding its immunological regulatory function in kidney disease. An improved understanding of the immunological regulatory function of lymphangiogenesis in kidney diseases might help design novel medicines targeting lymphatics to treat kidney pathologies.

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Transition from acute kidney injury to chronic kidney disease in a long-term murine model of Shiga toxin-induced hemolytic-uremic syndrome

Wegener,

Dennhardt,

Loeffler

et al. 2024

Front. Immunol.

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IntroductionUp to 40% of patients with typical hemolytic–uremic syndrome (HUS), characterized by microangiopathic hemolytic anemia and acute kidney injury (AKI), develop long-term consequences, most prominently chronic kidney disease (CKD). The transition from AKI to CKD, particularly in the context of HUS, is not yet fully understood. The objective of this study was to establish and characterize a Shiga toxin (Stx)-induced long-term HUS model to facilitate the study of mechanisms underlying the AKI-to-CKD transition.MethodsC57BL/6J mice were subjected to 5, 10, 15, or 20 ng/kg Stx on days 0, 3, and 6 of the experiment and were sacrificed on day 14 or day 21 to identify the critical time of turnover from the acute to the chronic state of HUS disease.ResultsAcute disease, indicated by weight loss, plasma neutrophil gelatinase-associated lipocalin (NGAL) and urea, and renal neutrophils, diminished after 14 days and returned to sham level after 21 days. HUS-associated hemolytic anemia transitioned to non-hemolytic microcytic anemia along with unchanged erythropoietin levels after 21 days. Renal cytokine levels indicated a shift towards pro-fibrotic signaling, and interstitial fibrosis developed concentration-dependently after 21 days. While Stx induced the intrarenal invasion of pro-inflammatory M1 and pro-fibrotic M2 macrophages after 14 days, pro-fibrotic M2 macrophages were the dominant phenotype after 21 days.ConclusionIn conclusion, we established and characterized the first Stx-induced long-term model of HUS. This tool facilitates the study of underlying mechanisms in the early AKI-to-CKD transition following HUS and allows the testing of compounds that may protect patients with AKI from developing subsequent CKD.

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Bruton’s tyrosine kinase inhibition attenuates disease progression by reducing renal immune cell invasion in mice with hemolytic-uremic syndrome

Cited by 5 publications

References 51 publications

Onconephrology: mitigation of renal injury in chemotherapy administration

Onconephrology: mitigation of renal injury in chemotherapy administration

The immune regulatory role of lymphangiogenesis in kidney disease

Transition from acute kidney injury to chronic kidney disease in a long-term murine model of Shiga toxin-induced hemolytic-uremic syndrome

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