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Article ; Online: Primary glomerulonephritis

Jürgen Floege

Kidney Research and Clinical Practice, Vol 32, Iss 3, Pp 103-

A review of important recent discoveries

2013 Volume 110

Abstract: The publication of the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines on the treatment of glomerular diseases in 2012 marked a milestone in this field, as it is the first time that comprehensive guidelines are provided for such disease ... ...

Abstract	The publication of the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines on the treatment of glomerular diseases in 2012 marked a milestone in this field, as it is the first time that comprehensive guidelines are provided for such disease entities. The current review focuses on major findings, both pathogenesis related and clinical, in the primary glomerulonephritis that have been made after the guidelines came into effect.
Keywords	Focal segmental glomerulosclerosis ; IgA nephropathy ; Membranoproliferative glomerulonephritis ; Membranous glomerulonephritis ; Minimal change disease ; Internal medicine ; RC31-1245 ; Specialties of internal medicine ; RC581-951
Language	English
Publishing date	2013-09-01T00:00:00Z
Publisher	The Korean Society of Nephrology
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cardiac Remodeling in Chronic Kidney Disease

Nadine Kaesler / Anne Babler / Jürgen Floege / Rafael Kramann

Toxins, Vol 12, Iss 3, p

2020 Volume 161

Abstract: Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart ... ...

Abstract	Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
Keywords	uremia ; uremic cardiomyopathy ; organ crosstalk ; cardiorenal syndrome ; chronic kidney disease ; left-ventricular hypertrophy ; heart failure ; cardiac fibrosis ; Medicine ; R
Subject code	610
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Impact of sucroferric oxyhydroxide on the oral and intestinal microbiome in hemodialysis patients

Mohamed M. H. Abdelbary / Christoph Kuppe / Sareh Said-Yekta Michael / Thilo Krüger / Jürgen Floege / Georg Conrads

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 15

Abstract: Abstract Hyperphosphatemia is a consequence of chronic kidney disease associated with mineral/bone impairment, increased cardiovascular events and mortality. Therapeutically, most dialysis patients have to take phosphate binders. Here, we investigated ... ...

Abstract	Abstract Hyperphosphatemia is a consequence of chronic kidney disease associated with mineral/bone impairment, increased cardiovascular events and mortality. Therapeutically, most dialysis patients have to take phosphate binders. Here, we investigated effects of the Fe(3+)-based phosphate binder sucroferric oxyhydroxide (SFOH) on the oral and gastrointestinal microbiome of 11 hemodialysis patients. Saliva, dental plaque and stool were collected at baseline, one and four weeks of SFOH intake and subjected to 16S rRNA gene (V3-V4 region) directed Illumina MiSeq-based analysis. Total Fe, Fe(2+) and Fe(3+) were determined in stool and saliva. Overall, the microbiome did not change significantly. However, some patient-, sample- and taxon-specific differences were noted, which allowed patients to be divided into those with a shift in their microbiome (6/11) and those without a shift (5/11). Total Fe and Fe(2+) were highest after one week of SFOH, particularly in patients who exhibited a shift in microbiome composition. Eight bacterial taxa showed significant unidirectional changes during treatment. In-depth microbiome analysis revealed that taxa that significantly benefited from iron plethora had no iron-binding siderophores or alternatives, which was in contrast to taxa that significantly declined under iron plethora. Patients with microbiome-shift were significantly younger and had higher serum phosphate concentrations. In conclusion, this study sheds light on the impact of iron on the microbiome of hemodialysis patients.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: New Aspects of Kidney Fibrosis–From Mechanisms of Injury to Modulation of Disease

Marcus J. Moeller / Rafael Kramann / Twan Lammers / Bernd Hoppe / Eicke Latz / Isis Ludwig-Portugall / Peter Boor / Jürgen Floege / Christian Kurts / Ralf Weiskirchen / Tammo Ostendorf

Frontiers in Medicine, Vol

2022 Volume 8

Abstract: Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative ... ...

Abstract	Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative Research Center “Organ Fibrosis: From Mechanisms of Injury to Modulation of Disease” (referred to as SFB/TRR57) was hosted from 2009 to 2021 by the Medical Faculties of RWTH Aachen University and the University of Bonn. This consortium had the ultimate goal of discovering new common but also different fibrosis pathways in the liver and kidneys. It finally successfully identified new mechanisms and established novel therapeutic approaches to interfere with hepatic and renal fibrosis. This review covers the consortium's key kidney-related findings, where three overarching questions were addressed: (i) What are new relevant mechanisms and signaling pathways triggering renal fibrosis? (ii) What are new immunological mechanisms, cells and molecules that contribute to renal fibrosis?, and finally (iii) How can renal fibrosis be modulated?
Keywords	renal fibrosis ; myofibroblast ; parietal epithelial cell ; inflammasome ; crystals ; lupus erythematodes ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: MicroRNAs in Chronic Kidney Disease

Linsey J. F. Peters / Jürgen Floege / Erik A. L. Biessen / Joachim Jankowski / Emiel P. C. van der Vorst

International Journal of Molecular Sciences, Vol 21, Iss 6547, p

Four Candidates for Clinical Application

2020 Volume 6547

Abstract: There are still major challenges regarding the early diagnosis and treatment of chronic kidney disease (CKD), which is in part due to the fact that its pathophysiology is very complex and not clarified in detail. The diagnosis of CKD commonly is made ... ...

Abstract	There are still major challenges regarding the early diagnosis and treatment of chronic kidney disease (CKD), which is in part due to the fact that its pathophysiology is very complex and not clarified in detail. The diagnosis of CKD commonly is made after kidney damage has occurred. This highlights the need for better mechanistic insight into CKD as well as improved clinical tools for both diagnosis and treatment. In the last decade, many studies have focused on microRNAs (miRs) as novel diagnostic tools or clinical targets. MiRs are small non-coding RNA molecules that are involved in post-transcriptional gene regulation and many have been studied in CKD. A wide array of pre-clinical and clinical studies have highlighted the potential role for miRs in the pathogenesis of hypertensive nephropathy, diabetic nephropathy, glomerulonephritis, kidney tubulointerstitial fibrosis, and some of the associated cardiovascular complications. In this review, we will provide an overview of the miRs studied in CKD, especially highlighting miR-103a-3p, miR-192-5p, the miR-29 family and miR-21-5p as these have the greatest potential to result in novel therapeutic and diagnostic strategies.
Keywords	MicroRNAs ; kidney fibrosis ; chronic kidney disease ; clinical application ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate.

Anne Babler / Carlo Schmitz / Andrea Buescher / Marietta Herrmann / Felix Gremse / Theo Gorgels / Juergen Floege / Willi Jahnen-Dechent

PLoS ONE, Vol 15, Iss 2, p e

2020 Volume 0228938

Abstract: Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly ...

Abstract	Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly severe soft tissue calcifications, while fetuin-A deficient C57BL/6 mice remain healthy. We employed molecular genetic analysis to identify risk factors of calcification in fetuin-A deficient mice. We sought to identify pharmaceutical therapeutic targets that could be influenced by dietary of parenteral supplementation. We studied the progeny of an intercross of fetuin-A deficient DBA/2 and C57BL/6 mice to identify candidate risk genes involved in calcification. We determined that a hypomorphic mutation of the Abcc6 gene, a liver ATP transporter supplying systemic pyrophosphate, and failure to regulate the Trpm6 magnesium transporter in kidney were associated with severity of calcification. Calcification prone fetuin-A deficient mice were alternatively treated with parenteral administration of fetuin-A dietary magnesium supplementation, phosphate restriction, or by or parenteral pyrophosphate. All treatments markedly reduced soft tissue calcification, demonstrated by computed tomography, histology and tissue calcium measurement. We show that pathological ectopic calcification in fetuin-A deficient DBA/2 mice is caused by a compound deficiency of three major extracellular and systemic inhibitors of calcification, namely fetuin-A, magnesium, and pyrophosphate. All three of these are individually known to contribute to stabilize protein-mineral complexes and thus inhibit mineral precipitation from extracellular fluid. We show for the first time a compound triple deficiency that can be treated by simple dietary or parenteral supplementation. This is of special importance in patients with advanced CKD, who commonly exhibit reduced serum fetuin-A, magnesium and pyrophosphate levels.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hypoglycemia following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function.

Armando Coca / Ana Lucia Valencia / Jesus Bustamante / Alicia Mendiluce / Jürgen Floege

PLoS ONE, Vol 12, Iss 2, p e

2017 Volume 0172961

Abstract: BACKGROUND:Hypoglycemia is a serious complication following the administration of insulin for hyperkalemia. We determined the incidence of hypoglycemia and severe hypoglycemia (blood glucose <70 or ≤40 mg/dl, respectively) in a cohort of AKI and non- ... ...

Abstract	BACKGROUND:Hypoglycemia is a serious complication following the administration of insulin for hyperkalemia. We determined the incidence of hypoglycemia and severe hypoglycemia (blood glucose <70 or ≤40 mg/dl, respectively) in a cohort of AKI and non-dialysis dependent CKD patients who received an intravenous infusion of insulin plus glucose to treat hyperkalemia. METHODS:We retrospectively reviewed charts of all AKI and non-dialysis dependent CKD patients who received 10 U of insulin plus 50 g glucose to treat hyperkalemia from December 1, 2013 to May 31, 2015 at our Department. RESULTS:One hundred sixty four episodes of hyperkalemia were treated with insulin plus glucose and were eligible for analysis. Serum potassium levels dropped by 1.18 ± 1.01 mmol/l. Eleven treatments (6.1%) resulted in hypoglycemia and two (1.2%) in severe hypoglycemia. A lower pretreatment blood glucose tended to associate with a higher subsequent risk of hypoglycemia. Age, sex, renal function, an established diagnosis of diabetes or previous treatment were not associated with the development of this complication. We did not register any significant adverse events. CONCLUSION:Our intravenous regimen combining an infusion of insulin plus glucose effectively reduced serum potassium levels compared to previous studies and associated a low risk of symptomatic hypoglycemia and other complications.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Next-Generation Morphometry for pathomics-data mining in histopathology

David L. Hölscher / Nassim Bouteldja / Mehdi Joodaki / Maria L. Russo / Yu-Chia Lan / Alireza Vafaei Sadr / Mingbo Cheng / Vladimir Tesar / Saskia V. Stillfried / Barbara M. Klinkhammer / Jonathan Barratt / Jürgen Floege / Ian S. D. Roberts / Rosanna Coppo / Ivan G. Costa / Roman D. Bülow / Peter Boor

Nature Communications, Vol 14, Iss 1, Pp 1-

2023 Volume 14

Abstract: Pathology diagnostics still rely on tissue morphology assessment by trained experts. Here, the authors perform deep-learning-based segmentation followed by large-scale feature extraction of histological images, i.e., next-generation morphometry, to ... ...

Abstract	Pathology diagnostics still rely on tissue morphology assessment by trained experts. Here, the authors perform deep-learning-based segmentation followed by large-scale feature extraction of histological images, i.e., next-generation morphometry, to enable outcome-relevant and disease-specific pathomics analysis of non-tumor kidney pathology.
Keywords	Science ; Q
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury

Yuki Sato / Akiko Oguchi / Yuji Fukushima / Kyoko Masuda / Naoya Toriu / Keisuke Taniguchi / Takahisa Yoshikawa / Xiaotong Cui / Makiko Kondo / Takeshi Hosoi / Shota Komidori / Yoko Shimizu / Harumi Fujita / Li Jiang / Yingyi Kong / Takashi Yamanashi / Jun Seita / Takuya Yamamoto / Shinya Toyokuni /

Yoko Hamazaki / Masakazu Hattori / Yasunobu Yoshikai / Peter Boor / Jürgen Floege / Hiroshi Kawamoto / Yasuhiro Murakawa / Nagahiro Minato / Motoko Yanagita

The Journal of Clinical Investigation, Vol 132, Iss

2022 Volume 2

Abstract: Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling ... ...

Abstract	Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
Keywords	Inflammation ; Nephrology ; Medicine ; R
Subject code	570
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Disruption of CUL3-mediated ubiquitination causes proximal tubule injury and kidney fibrosis

Turgay Saritas / Catherina A. Cuevas / Mohammed Z. Ferdaus / Christoph Kuppe / Rafael Kramann / Marcus J. Moeller / Jürgen Floege / Jeffrey D. Singer / James A. McCormick

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 14

Abstract: Abstract Cullin 3 (CUL3) is part of the ubiquitin proteasomal system and controls several cellular processes critical for normal organ function including the cell cycle, and Keap1/Nrf2 signaling. Kidney tubule-specific Cul3 disruption causes ... ...

Abstract	Abstract Cullin 3 (CUL3) is part of the ubiquitin proteasomal system and controls several cellular processes critical for normal organ function including the cell cycle, and Keap1/Nrf2 signaling. Kidney tubule-specific Cul3 disruption causes tubulointerstitial fibrosis, but little is known about the mechanisms. Therefore, we tested the hypothesis that dysregulation of the cell cycle and Keap1/Nrf2 pathway play a role in initiating the kidney injury upon Cul3 disruption. Cul3 deletion increased expression of cyclin E and p21, associated with uncontrolled proliferation, DNA damage, and apoptosis, all of which preceded proximal tubule injury. The cdk2-cyclin E inhibitor roscovitine did not prevent the effects of Cul3 deletion, but instead exacerbated the kidney injury. Injury occurred despite accumulation and activation of CUL3 substrate Keap1/Nrf2, proposed to be protective in kidney injury. Cul3 disruption led to progressive interstitial inflammation, functionally relevant renal fibrosis and death. Finally, we observed reduced CUL3 expression in several AKI and CKD mouse models and in fibrotic human kidney tissue. These data establish CUL3 knockout mice as a novel genetic CKD model in which dysregulation of the cell cycle may play a primary role in initiating tubule injury, and that CUL3 dysregulation could contribute to acute and fibrotic kidney disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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