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  1. Article ; Online: Urinary biomarkers in kidney disease.

    Canki, Esra / Kho, Esther / Hoenderop, Joost G J

    Clinica chimica acta; international journal of clinical chemistry

    2024  Volume 555, Page(s) 117798

    Abstract: Background: Chronic kidney disease (CKD) affects many people worldwide and early diagnosis is essential for successful treatment and improved outcome. Unfortunately, current methods are insufficient especially for early disease detection. However, ... ...

    Abstract Background: Chronic kidney disease (CKD) affects many people worldwide and early diagnosis is essential for successful treatment and improved outcome. Unfortunately, current methods are insufficient especially for early disease detection. However, advances in the analytical methods for urinary biomarkers may provide a unique opportunity for diagnosis and management of CKD. This review explores evolving technology and highlights the importance of early marker detection in these patients.
    Approach: A search strategy was set up using the terms CKD, biomarkers, and urine. The search included 53 studies comprising 37 biomarkers. The value of these biomarkers for CKD are based on their ability to diagnose CKD, monitor progression, assess mortality and nephrotoxicity.
    Results: KIM-1 was the best marker for diagnosis as it increased with the development of incident CKD. DKK3 increased in patients with declining eGFR, whereas UMOD decreased in those with declining kidney function. Unfortunately, none fulfilled all criteria to adequately assess mortality and nephrotoxicity.
    Conclusion: New developments in the field of urinalysis using smart toilets may open several possibilities for urinary biomarkers. This review explored which biomarkers could be used for CKD disease detection and management.
    MeSH term(s) Humans ; Creatinine ; Renal Insufficiency, Chronic/diagnosis ; Kidney ; Biomarkers ; Urinalysis ; Acute Kidney Injury/diagnosis ; Disease Progression
    Chemical Substances Creatinine (AYI8EX34EU) ; Biomarkers
    Language English
    Publishing date 2024-01-26
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 80228-1
    ISSN 1873-3492 ; 0009-8981
    ISSN (online) 1873-3492
    ISSN 0009-8981
    DOI 10.1016/j.cca.2024.117798
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  2. Article ; Online: Correction to: Mechanisms of ion transport regulation by HNF1β in the kidney: beyond transcriptional regulation of channels and transporters.

    Tholen, Lotte E / Hoenderop, Joost G J / de Baaij, Jeroen H F

    Pflugers Archiv : European journal of physiology

    2022  Volume 474, Issue 8, Page(s) 917

    Language English
    Publishing date 2022-05-20
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-022-02706-7
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  3. Article ; Online: Inhibition of pannexin-1 does not restore electrolyte balance in precystic Pkd1 knockout mice.

    van Megen, Wouter H / van Houtert, Teun J / Bos, Caro / Peters, Dorien J M / de Baaij, Jeroen H F / Hoenderop, Joost G J

    Physiological reports

    2024  Volume 12, Issue 7, Page(s) e15956

    Abstract: Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney disease (ADPKD), which is characterized by the formation of fluid-filled cysts in the kidney. In a subset of ADPKD patients, reduced blood calcium ( ... ...

    Abstract Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney disease (ADPKD), which is characterized by the formation of fluid-filled cysts in the kidney. In a subset of ADPKD patients, reduced blood calcium (Ca
    MeSH term(s) Animals ; Humans ; Mice ; Adenosine Triphosphate/metabolism ; Kidney/metabolism ; Mice, Knockout ; Mutation ; Polycystic Kidney, Autosomal Dominant/metabolism ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism ; TRPP Cation Channels/pharmacology ; Water-Electrolyte Balance
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; TRPP Cation Channels ; polycystic kidney disease 1 protein ; Panx1 protein, mouse
    Language English
    Publishing date 2024-04-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15956
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  4. Article ; Online: Mechanisms of proton pump inhibitor-induced hypomagnesemia.

    Gommers, Lisanne M M / Hoenderop, Joost G J / de Baaij, Jeroen H F

    Acta physiologica (Oxford, England)

    2022  Volume 235, Issue 4, Page(s) e13846

    Abstract: Proton pump inhibitors (PPIs) reliably suppress gastric acid secretion and are therefore the first-line treatment for gastric acid-related disorders. Hypomagnesemia (serum magnesium [ ... ...

    Abstract Proton pump inhibitors (PPIs) reliably suppress gastric acid secretion and are therefore the first-line treatment for gastric acid-related disorders. Hypomagnesemia (serum magnesium [Mg
    MeSH term(s) Colon/metabolism ; Gastrointestinal Microbiome ; Homeostasis ; Magnesium/metabolism ; Magnesium/pharmacology ; Proton Pump Inhibitors/adverse effects
    Chemical Substances Proton Pump Inhibitors ; Magnesium (I38ZP9992A)
    Language English
    Publishing date 2022-06-14
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13846
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  5. Book ; Thesis: Towards a comprehensive molecular model of active calcium reabsorption

    Hoenderop, Justinus Gerardus Johannes

    2000  

    Author's details door Justinus Gerardus Johannes Hoenderop
    Language English
    Size 155 S. : Ill., graph. Darst.
    Publishing country Netherlands
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Nijmegen, Kath. Univ., Diss., 2000
    Note Zsfassung in niederländ. Sprache
    HBZ-ID HT012788749
    ISBN 90-901-3600-2 ; 978-90-901-3600-4
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2000 E 2222 order for loan Magazin

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  6. Article ; Online: Liver and spleen predominantly mediate calciprotein particle clearance in a rat model of chronic kidney disease.

    Zeper, Lara W / Bos, Caro / Leermakers, Pieter A / Franssen, Gerben M / Raavé, René / Hoenderop, Joost G J / de Baaij, Jeroen H F

    American journal of physiology. Renal physiology

    2024  Volume 326, Issue 4, Page(s) F622–F634

    Abstract: Calciprotein particles (CPPs) provide an efficient mineral buffering system to prevent the complexation of phosphate and calcium in the circulation. However, in chronic kidney disease (CKD), the phosphate load exceeds the mineral buffering capacity, ... ...

    Abstract Calciprotein particles (CPPs) provide an efficient mineral buffering system to prevent the complexation of phosphate and calcium in the circulation. However, in chronic kidney disease (CKD), the phosphate load exceeds the mineral buffering capacity, resulting in the formation of crystalline CPP2 particles. CPP2 have been associated with cardiovascular events and mortality. Moreover, CPP2 have been demonstrated to induce calcification in vitro. In this study, we examined the fate of CPP2 in a rat model of CKD. Calcification was induced in Sprague-Dawley rats by 5/6 nephrectomy (5/6-Nx) combined with a high-phosphate diet. Control rats received sham surgery and high-phosphate diet. Twelve weeks after surgery, kidney failure was significantly induced in 5/6-Nx rats as determined by enhanced creatinine and urea plasma levels and abnormal kidney histological architecture. Subsequently, radioactive and fluorescent (FITC)-labeled CPP2 ([
    MeSH term(s) Rats ; Animals ; Spleen/metabolism ; Calcium/metabolism ; Fluorescein-5-isothiocyanate ; Tissue Distribution ; Rats, Sprague-Dawley ; Vascular Calcification/diagnostic imaging ; Vascular Calcification/etiology ; Minerals ; Liver/metabolism ; Phosphates ; Renal Insufficiency, Chronic/pathology
    Chemical Substances Calcium (SY7Q814VUP) ; Fluorescein-5-isothiocyanate (I223NX31W9) ; Minerals ; Phosphates
    Language English
    Publishing date 2024-02-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00239.2023
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  7. Article ; Online: Mechanisms of ion transport regulation by HNF1β in the kidney: beyond transcriptional regulation of channels and transporters.

    Tholen, Lotte E / Hoenderop, Joost G J / de Baaij, Jeroen H F

    Pflugers Archiv : European journal of physiology

    2022  Volume 474, Issue 8, Page(s) 901–916

    Abstract: Hepatocyte nuclear factor 1β (HNF1β) is a transcription factor essential for the development and function of the kidney. Mutations in and deletions of HNF1β cause autosomal dominant tubule interstitial kidney disease (ADTKD) subtype HNF1β, which is ... ...

    Abstract Hepatocyte nuclear factor 1β (HNF1β) is a transcription factor essential for the development and function of the kidney. Mutations in and deletions of HNF1β cause autosomal dominant tubule interstitial kidney disease (ADTKD) subtype HNF1β, which is characterized by renal cysts, diabetes, genital tract malformations, and neurodevelopmental disorders. Electrolyte disturbances including hypomagnesemia, hyperuricemia, and hypocalciuria are common in patients with ADTKD-HNF1β. Traditionally, these electrolyte disturbances have been attributed to HNF1β-mediated transcriptional regulation of gene networks involved in ion transport in the distal part of the nephron including FXYD2, CASR, KCNJ16, and FXR. In this review, we propose additional mechanisms that may contribute to the electrolyte disturbances observed in ADTKD-HNF1β patients. Firstly, kidney development is severely affected in Hnf1b-deficient mice. HNF1β is required for nephron segmentation, and the absence of the transcription factor results in rudimentary nephrons lacking mature proximal tubule, loop of Henle, and distal convoluted tubule cluster. In addition, HNF1β is proposed to be important for apical-basolateral polarity and tight junction integrity in the kidney. Interestingly, cilia formation is unaffected by Hnf1b defects in several models, despite the HNF1β-mediated transcriptional regulation of many ciliary genes. To what extent impaired nephron segmentation, apical-basolateral polarity, and cilia function contribute to electrolyte disturbances in HNF1β patients remains elusive. Systematic phenotyping of Hnf1b mouse models and the development of patient-specific kidney organoid models will be essential to advance future HNF1β research.
    MeSH term(s) Animals ; Electrolytes ; Hepatocyte Nuclear Factor 1-beta/metabolism ; Ion Transport ; Kidney/metabolism ; Membrane Transport Proteins ; Mice ; Nephrons/metabolism ; Transcription Factors/metabolism
    Chemical Substances Electrolytes ; Hnf1b protein, mouse ; Membrane Transport Proteins ; Transcription Factors ; Hepatocyte Nuclear Factor 1-beta (138674-15-4)
    Language English
    Publishing date 2022-05-13
    Publishing country Germany
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-022-02697-5
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  8. Article: Genome-wide association study of serum magnesium in type 2 diabetes.

    Oost, Lynette J / Slieker, Roderick C / Blom, Marieke T / 't Hart, Leen M / Hoenderop, Joost G J / Beulens, Joline W J / de Baaij, Jeroen H F

    Genes & nutrition

    2024  Volume 19, Issue 1, Page(s) 2

    Abstract: People with type 2 diabetes have a tenfold higher prevalence of hypomagnesemia, which is suggested to be caused by low dietary magnesium intake, medication use, and genetics. This study aims to identify the genetic loci that influence serum magnesium ... ...

    Abstract People with type 2 diabetes have a tenfold higher prevalence of hypomagnesemia, which is suggested to be caused by low dietary magnesium intake, medication use, and genetics. This study aims to identify the genetic loci that influence serum magnesium concentration in 3466 people with type 2 diabetes. The GWAS models were adjusted for age, sex, eGFR, and HbA1c. Associated traits were identified using publicly available data from GTEx consortium, a human kidney eQTL atlas, and the Open GWAS database. The GWAS identified a genome-wide significant locus in TAF3 (p = 2.9 × 10
    Language English
    Publishing date 2024-01-26
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2416599-2
    ISSN 1865-3499 ; 1555-8932
    ISSN (online) 1865-3499
    ISSN 1555-8932
    DOI 10.1186/s12263-024-00738-5
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    In stock of ZB MED Bonn / Germany

    Z 7828: Show issues

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  9. Article ; Online: Transcription factor HNF1β controls a transcriptional network regulating kidney cell structure and tight junction integrity.

    Tholen, Lotte E / Latta, Femke / Martens, Joost H A / Hoenderop, Joost G J / de Baaij, Jeroen H F

    American journal of physiology. Renal physiology

    2022  Volume 324, Issue 2, Page(s) F211–F224

    Abstract: Mutations in the hepatocyte nuclear factor (HNF)1β gene ( ...

    Abstract Mutations in the hepatocyte nuclear factor (HNF)1β gene (
    MeSH term(s) Mice ; Animals ; Transcription Factors/metabolism ; Gene Regulatory Networks ; Tight Junctions/metabolism ; Kidney/metabolism ; Epithelial Cells/metabolism ; Hepatocyte Nuclear Factors/genetics ; Hepatocyte Nuclear Factors/metabolism ; Electrolytes/metabolism ; Hepatocyte Nuclear Factor 1-beta/genetics
    Chemical Substances Transcription Factors ; Hepatocyte Nuclear Factors ; Electrolytes ; Hepatocyte Nuclear Factor 1-beta (138674-15-4)
    Language English
    Publishing date 2022-12-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00199.2022
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  10. Article ; Online: Title: Jealous protons sour another happy marriage; the story of how TRPV5 and PI(4,5)P

    van Goor, Mark K C / van der Wijst, Jenny / Hoenderop, Joost G J

    Cell calcium

    2022  Volume 105, Page(s) 102609

    Abstract: TRPV5 is a highly selective calcium channel that finetunes urinary calcium excretion by reabsorbing calcium from the pro-urine. New structural findings show how PTH and pH control TRPV5 activity by altering the binding of endogenous ligands calmodulin ... ...

    Abstract TRPV5 is a highly selective calcium channel that finetunes urinary calcium excretion by reabsorbing calcium from the pro-urine. New structural findings show how PTH and pH control TRPV5 activity by altering the binding of endogenous ligands calmodulin and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P
    MeSH term(s) Calcium/metabolism ; Calcium Channels/metabolism ; Marriage ; Protons ; TRPV Cation Channels/metabolism
    Chemical Substances Calcium Channels ; Protons ; TRPV Cation Channels ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-05-31
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2022.102609
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