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Article ; Online: Fasting influences aquaporin expression, water transport and adipocyte metabolism in the peritoneal membrane.

Costa, Ines P D / Hautem, Nicolas / Schiano, Gugliemo / Uchida, Shinichi / Nishino, Tomoya / Devuyst, Olivier

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2022 Volume 38, Issue 6, Page(s) 1408–1420

Abstract: Background: The water channels aquaporin-1 (AQP1) and AQP7 are abundantly expressed in the peritoneal membrane. While AQP1 facilitates water transport during peritoneal dialysis (PD), the role of AQP7, which mediates glycerol transport during fasting, ... ...

Abstract	Background: The water channels aquaporin-1 (AQP1) and AQP7 are abundantly expressed in the peritoneal membrane. While AQP1 facilitates water transport during peritoneal dialysis (PD), the role of AQP7, which mediates glycerol transport during fasting, remains unknown. Methods: We investigated the distribution of AQP7 and AQP1 and used a mouse model of PD to investigate the role of AQP7 in the peritoneal membrane at baseline and after fasting. Results: Single nucleus RNA-sequencing revealed that AQP7 was mostly detected in mature adipocytes, whereas AQP1 was essentially expressed in endothelial cells. Fasting induced significant decreases in whole body fat, plasma glucose, insulin and triglycerides, as well as higher plasma glycerol and corticosterone levels in mice, paralleled by major decreases in adipocyte size and levels of fatty acid synthase and leptin, and increased levels of hormone-sensitive lipase mRNAs in the peritoneum. Mechanistically, fasting upregulated the expression of AQP1 and AQP7 in the peritoneum, with increased ultrafiltration but no change in small solute transport. Studies based on Aqp1 and Aqp7 knockout mice and RU-486 inhibition demonstrated that the glucocorticoid induction of AQP1 mediates the increase in ultrafiltration whereas AQP7 regulates the size of adipocytes in the peritoneum. Conclusions: Fasting induces a coordinated regulation of lipolytic and lipogenic factors and aqua(glycero)porins in the peritoneum, driving structural and functional changes. These data yield novel information on the specific roles of aquaporins in the peritoneal membrane and indicate that fasting improves fluid removal in a mouse model of PD.
MeSH term(s)	Animals ; Mice ; Peritoneum/metabolism ; Glycerol/metabolism ; Endothelial Cells/metabolism ; Aquaporin 1/genetics ; Adipocytes/metabolism ; Water/metabolism ; Mice, Knockout ; Fasting
Chemical Substances	Glycerol (PDC6A3C0OX) ; Aquaporin 1 (146410-94-8) ; Water (059QF0KO0R)
Language	English
Publishing date	2022-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfac318
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Uromodulin and Vesico-Ureteral Reflux: A Genetic Study.

Maringhini, Silvio / Cusumano, Rosa / Corrado, Ciro / Puccio, Giuseppe / Pavone, Giovanni / D'Alessandro, Maria Michela / Sapia, Maria Chiara / Devuyst, Olivier / Abbate, Serena

Biomedicines

2023 Volume 11, Issue 2

Abstract: Vesicoureteral reflux (VUR) is associated with urinary tract infections (UTI) and renal scars. The kidney damage is correlated with the grade of reflux and the number of UTI, but other factors may also play a role. Uromodulin (UMOD) is a protein produced ...

Abstract	Vesicoureteral reflux (VUR) is associated with urinary tract infections (UTI) and renal scars. The kidney damage is correlated with the grade of reflux and the number of UTI, but other factors may also play a role. Uromodulin (UMOD) is a protein produced by kidney tubular cells, forming a matrix in the lumen. We evaluated whether the common variant rs4293393 in the UMOD gene was associated with febrile UTI (FUTI) and/or scars in a group of children with VUR. A total of 31 patients with primary VUR were enrolled. Renal scars were detected in 16 children; no scar was detected in 15 children. Genotype rs4293393 TC (TC) was present in 8 patients, 7 (88%) had scars; genotype rs4293393 TT (TT) was found in 23 patients, and 9 (39%) had scars. Among children with scars, those with TC compared with those with TT were younger (mean age 77 vs. 101 months), their reflux grade was comparable (3.7 vs. 3.9), and the number of FUTI was lower (2.9 vs. 3.7 per patient). Children with VUR carrying UMOD genotype rs4293393 TC seem more prone to developing renal scars, independent of FUTI.
Language	English
Publishing date	2023-02-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11020509
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Article ; Online: Monogenic Kidney Diseases in Kidney Transplantation.

Gillion, Valentine / Devresse, Arnaud / Olinger, Eric / Dahlqvist, Géraldine / Demoulin, Nathalie / Godefroid, Nathalie / Claes, Kathleen / Devuyst, Olivier / Kanaan, Nada

Kidney international reports

2023 Volume 9, Issue 3, Page(s) 549–568

Abstract: Monogenic kidney diseases are involved in up to 15% of end-stage kidney diseases (ESKDs) in adults, and in 70 % of pediatric patients. When these disorders lead to kidney failure (KF), kidney transplantation (KT) is the preferred mode of replacement ... ...

Abstract	Monogenic kidney diseases are involved in up to 15% of end-stage kidney diseases (ESKDs) in adults, and in 70 % of pediatric patients. When these disorders lead to kidney failure (KF), kidney transplantation (KT) is the preferred mode of replacement therapy. KT requires specific considerations depending on the nature of the genetic disorder, the potential oncological risk, the risk of recurrence in the graft, the possibility of specific complications of immunosuppression, and the issue of living donation. The availability of genetic testing should play an increasing role in the evaluation of patients or related living donor candidates before transplantation, relevant for the pretransplantation and posttransplantation management.
Language	English
Publishing date	2023-12-13
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2023.12.003
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Article ; Online: Allelic effects on uromodulin aggregates drive autosomal dominant tubulointerstitial kidney disease.

Schiano, Guglielmo / Lake, Jennifer / Mariniello, Marta / Schaeffer, Céline / Harvent, Marianne / Rampoldi, Luca / Olinger, Eric / Devuyst, Olivier

EMBO molecular medicine

2023 Volume 15, Issue 12, Page(s) e18242

Abstract: Missense mutations in the uromodulin (UMOD) gene cause autosomal dominant tubulointerstitial kidney disease (ADTKD), one of the most common monogenic kidney diseases. The unknown impact of the allelic and gene dosage effects and fate of mutant uromodulin ...

Abstract	Missense mutations in the uromodulin (UMOD) gene cause autosomal dominant tubulointerstitial kidney disease (ADTKD), one of the most common monogenic kidney diseases. The unknown impact of the allelic and gene dosage effects and fate of mutant uromodulin leaves open the gap between postulated gain-of-function mutations, end-organ damage and disease progression in ADTKD. Based on two prevalent missense UMOD mutations with divergent disease progression, we generated Umod
MeSH term(s)	Animals ; Mice ; Alleles ; Disease Progression ; Kidney/metabolism ; Kidney Diseases/genetics ; Mutation ; Uromodulin/genetics ; Uromodulin/metabolism
Chemical Substances	Uromodulin ; Umod protein, mouse
Language	English
Publishing date	2023-10-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202318242
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Zs.A 6784: Show issues

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Article ; Online: Nlrp2

Rossi, Marianna Nicoletta / Matteo, Valentina / Diomedi-Camassei, Francesca / De Leo, Ester / Devuyst, Olivier / Lamkanfi, Mohamed / Caiello, Ivan / Loricchio, Elena / Bellomo, Francesco / Taranta, Anna / Emma, Francesco / De Benedetti, Fabrizio / Prencipe, Giusi

Frontiers in immunology

2024 Volume 15, Page(s) 1373224

Abstract: Cystinosis is a rare autosomal recessive disorder caused by mutations in ... ...

Abstract	Cystinosis is a rare autosomal recessive disorder caused by mutations in the
MeSH term(s)	Animals ; Humans ; Infant ; Cystinosis/genetics ; Cystinosis/metabolism ; Cystinosis/pathology ; Cystine/metabolism ; Kidney/pathology ; Kidney Diseases/pathology ; RNA, Messenger
Chemical Substances	Cystine (48TCX9A1VT) ; RNA, Messenger
Language	English
Publishing date	2024-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1373224
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Article ; Online: Uromodulin processing in DNAJB11-kidney disease.

Mariniello, Marta / Schiano, Guglielmo / Yoshifuji, Ayumi / Gillion, Valentine / Sayer, John Andrew / Jouret, François / Le Meur, Yannick / Cornec-Le Gall, Emilie / Olinger, Eric Gregory / Devuyst, Olivier

Kidney international

2023 Volume 105, Issue 2, Page(s) 376–380

MeSH term(s)	Humans ; HSP40 Heat-Shock Proteins/genetics ; Mutation ; Nephritis, Interstitial/genetics ; Nephritis, Interstitial/metabolism ; Uromodulin/metabolism
Chemical Substances	DNAJB11 protein, human ; HSP40 Heat-Shock Proteins ; Uromodulin
Language	English
Publishing date	2023-11-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.11.008
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Zs.A 797: Show issues

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Article ; Online: The patient with metabolic alkalosis.

Gillion, Valentine / Jadoul, Michel / Devuyst, Olivier / Pochet, Jean-Michel

Acta clinica Belgica

2018 Volume 74, Issue 1, Page(s) 34–40

Abstract: ... by the gastrointestinal tract (e.g. vomiting) or by the kidney (e.g. use of loop diuretics) or may be due to exogenous base gain ...

Abstract	Metabolic alkalosis defined by the increase of both plasma HCO3- level (>26 mmol/L) and blood arterial pH (>7.43) is quite frequent and usually accompanied by hypokalemia. Its pathogenesis requires both the generation of alkalosis and its maintenance. Generation may be due to excessive hydrogen ion loss by the gastrointestinal tract (e.g. vomiting) or by the kidney (e.g. use of loop diuretics) or may be due to exogenous base gain. Maintenance reflects the inability of the kidney to excrete the excess of bicarbonate because of hypovolemia, chloride depletion, hypokalemia, hyperaldosteronism, renal failure or a combination of these factors. The evaluation of volemic status and measurement of urinary Cl- and plasma levels of renin and aldosterone are crucial to identify the cause(s) of metabolic alkalosis. The cornerstone of treatment is the correction of existing depletions and the prevention of further losses. In vomiting-induced chloride depletion alkalosis, infusion of potassium chloride restores the excretion of bicarbonate by the kidney.
MeSH term(s)	Aged, 80 and over ; Alkalosis/diagnosis ; Alkalosis/etiology ; Alkalosis/therapy ; Diagnosis, Differential ; Female ; Humans
Language	English
Publishing date	2018-10-27
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	390201-8
ISSN	2295-3337 ; 0001-5512 ; 1784-3286
ISSN (online)	2295-3337
ISSN	0001-5512 ; 1784-3286
DOI	10.1080/17843286.2018.1539373
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Ua VI Zs.283: Show issues

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Article ; Online: Clinical practice recommendations for kidney involvement in tuberous sclerosis complex: a consensus statement by the ERKNet Working Group for Autosomal Dominant Structural Kidney Disorders and the ERA Genes & Kidney Working Group.

Mekahli, Djalila / Müller, Roman-Ulrich / Marlais, Matko / Wlodkowski, Tanja / Haeberle, Stefanie / de Argumedo, Marta López / Bergmann, Carsten / Breysem, Luc / Fladrowski, Carla / Henske, Elizabeth P / Janssens, Peter / Jouret, François / Kingswood, John Christopher / Lattouf, Jean-Baptiste / Lilien, Marc / Maleux, Geert / Rozenberg, Micaela / Siemer, Stefan / Devuyst, Olivier /

Schaefer, Franz / Kwiatkowski, David J / Rouvière, Olivier / Bissler, John

Nature reviews. Nephrology

2024

Abstract: Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by the presence of proliferative lesions throughout the body. Management of TSC is challenging because patients have a multifaceted systemic illness with prominent ... ...

Abstract	Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by the presence of proliferative lesions throughout the body. Management of TSC is challenging because patients have a multifaceted systemic illness with prominent neurological and developmental impact as well as potentially severe kidney, heart and lung phenotypes; however, every organ system can be involved. Adequate care for patients with TSC requires a coordinated effort involving a multidisciplinary team of clinicians and support staff. This clinical practice recommendation was developed by nephrologists, urologists, paediatric radiologists, interventional radiologists, geneticists, pathologists, and patient and family group representatives, with a focus on TSC-associated kidney manifestations. Careful monitoring of kidney function and assessment of kidney structural lesions by imaging enable early interventions that can preserve kidney function through targeted approaches. Here, we summarize the current evidence and present recommendations for the multidisciplinary management of kidney involvement in TSC.
Language	English
Publishing date	2024-03-05
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/s41581-024-00818-0
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Zs.MG 107: Show issues

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Article ; Online: Digital Image Analysis of Picrosirius Red Staining: A Robust Method for Multi-Organ Fibrosis Quantification and Characterization.

Courtoy, Guillaume E / Leclercq, Isabelle / Froidure, Antoine / Schiano, Guglielmo / Morelle, Johann / Devuyst, Olivier / Huaux, François / Bouzin, Caroline

Biomolecules

2020 Volume 10, Issue 11

Abstract: Current understanding of fibrosis remains incomplete despite the increasing burden of related diseases. Preclinical models are used to dissect the pathogenesis and dynamics of fibrosis, and to evaluate anti-fibrotic therapies. These studies require ... ...

Abstract	Current understanding of fibrosis remains incomplete despite the increasing burden of related diseases. Preclinical models are used to dissect the pathogenesis and dynamics of fibrosis, and to evaluate anti-fibrotic therapies. These studies require objective and accurate measurements of fibrosis. Existing histological quantification methods are operator-dependent, organ-specific, and/or need advanced equipment. Therefore, we developed a robust, minimally operator-dependent, and tissue-transposable digital method for fibrosis quantification. The proposed method involves a novel algorithm for more specific and more sensitive detection of collagen fibers stained by picrosirius red (PSR), a computer-assisted segmentation of histological structures, and a new automated morphological classification of fibers according to their compactness. The new algorithm proved more accurate than classical filtering using principal color component (red-green-blue; RGB) for PSR detection. We applied this new method on established mouse models of liver, lung, and kidney fibrosis and demonstrated its validity by evidencing topological collagen accumulation in relevant histological compartments. Our data also showed an overall accumulation of compact fibers concomitant with worsening fibrosis and evidenced topological changes in fiber compactness proper to each model. In conclusion, we describe here a robust digital method for fibrosis analysis allowing accurate quantification, pattern recognition, and multi-organ comparisons useful to understand fibrosis dynamics.
MeSH term(s)	Algorithms ; Animals ; Azo Compounds ; Collagen/analysis ; Collagen/metabolism ; Disease Models, Animal ; Fibrosis/classification ; Fibrosis/metabolism ; Fibrosis/pathology ; Image Processing, Computer-Assisted/methods ; Kidney/metabolism ; Kidney/pathology ; Liver/metabolism ; Liver/pathology ; Lung/metabolism ; Lung/pathology ; Male ; Mice, Inbred C57BL ; Pattern Recognition, Automated/methods ; Staining and Labeling
Chemical Substances	Azo Compounds ; C.I. direct red 80 (1294D5G72N) ; Collagen (9007-34-5)
Language	English
Publishing date	2020-11-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10111585
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Article ; Online: The Urinary Excretion of Uromodulin is Regulated by the Potassium Channel ROMK.

Schiano, Guglielmo / Glaudemans, Bob / Olinger, Eric / Goelz, Nadine / Müller, Michael / Loffing-Cueni, Dominique / Deschenes, Georges / Loffing, Johannes / Devuyst, Olivier

Scientific reports

2019 Volume 9, Issue 1, Page(s) 19517

Abstract: Uromodulin, the most abundant protein in normal urine, is produced by cells lining the thick ascending limb (TAL) of the loop of Henle. Uromodulin regulates the activity of the potassium channel ROMK in TAL cells. Common variants in KCNJ1, the gene ... ...

Abstract	Uromodulin, the most abundant protein in normal urine, is produced by cells lining the thick ascending limb (TAL) of the loop of Henle. Uromodulin regulates the activity of the potassium channel ROMK in TAL cells. Common variants in KCNJ1, the gene encoding ROMK, are associated with urinary levels of uromodulin in population studies. Here, we investigated the functional link between ROMK and uromodulin in Kcnj1 knock-out mouse models, in primary cultures of mouse TAL (mTAL) cells, and in patients with Bartter syndrome due to KCNJ1 mutations. Both global and kidney-specific Kcnj1 knock-out mice showed reduced urinary levels of uromodulin paralleled by increased levels in the kidney, compared to wild-type controls. Pharmacological inhibition and genetic deletion of ROMK in mTAL cells caused a reduction in apical uromodulin excretion, reflected by cellular accumulation. In contrast, NKCC2 inhibition showed no effect on uromodulin processing. Patients with Bartter syndrome type 2 showed reduced urinary uromodulin levels compared to age and gender matched controls. These results demonstrate that ROMK directly regulates processing and release of uromodulin by TAL cells, independently from NKCC2. They support the functional link between transport activity and uromodulin in the TAL, relevant for blood pressure control and urinary concentrating ability.
MeSH term(s)	Animals ; Bartter Syndrome/metabolism ; Bartter Syndrome/urine ; Cells, Cultured ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism ; Immunoblotting ; Loop of Henle/metabolism ; Male ; Mice ; Mice, Knockout ; Mutation/genetics ; Potassium Channels, Inwardly Rectifying/urine ; Solute Carrier Family 12, Member 1/metabolism ; Uromodulin/metabolism ; Uromodulin/urine
Chemical Substances	Kcnj1 protein, mouse ; Potassium Channels, Inwardly Rectifying ; Slc12a1 protein, mouse ; Solute Carrier Family 12, Member 1 ; Uromodulin ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) (EC 1.2.1.12)
Language	English
Publishing date	2019-12-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-55771-x
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