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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: Advancements in kidney organoids and tubuloids to study (dys)function.

    Dilmen, E / Orhon, I / Jansen, J / Hoenderop, J G J

    Trends in cell biology

    2023  Volume 34, Issue 4, Page(s) 299–311

    Abstract: The rising prevalence of kidney diseases urges the need for novel therapies. Kidney organoids and tubuloids are advanced in vitro models and have recently been described as promising tools to study kidney (patho)physiology. Recent developments have shown ...

    Abstract The rising prevalence of kidney diseases urges the need for novel therapies. Kidney organoids and tubuloids are advanced in vitro models and have recently been described as promising tools to study kidney (patho)physiology. Recent developments have shown their application in disease modeling, drug screening, and nephrotoxicity. These applications rely on their ability to mimic (dys)function in vitro including endocrine activity and drug, electrolyte, and water transport. This review provides an overview of these emerging kidney models and focuses on the most recent developments that utilize their functional capabilities. In addition, we cover current limitations and provide future perspectives for this rapidly evolving field, including what these functional properties mean for translational and personalized medicine now and in the future.
    MeSH term(s) Humans ; Kidney ; Organoids
    Language English
    Publishing date 2023-10-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2023.09.005
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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: 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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  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: 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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  7. 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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  8. 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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  9. Article ; Online: Magnesium in chronic haemodialysis (MAGIC-HD): a study protocol for a randomised controlled trial to determine feasibility and safety of using increased dialysate magnesium concentrations to increase plasma magnesium concentrations in people treated with haemodialysis.

    Leenders, Nicoline H J / Douma, Caroline E / Hoenderop, Joost G J / Vervloet, Marc G

    BMJ open

    2022  Volume 12, Issue 11, Page(s) e063524

    Abstract: Introduction: People treated with haemodialysis are at increased risk for all-cause and cardiovascular mortality. Plasma magnesium concentration has been inversely associated with these risks. Therefore, plasma magnesium may be a new modifiable risk ... ...

    Abstract Introduction: People treated with haemodialysis are at increased risk for all-cause and cardiovascular mortality. Plasma magnesium concentration has been inversely associated with these risks. Therefore, plasma magnesium may be a new modifiable risk factor and an increase of dialysate magnesium concentration may be an easy, safe and effective way to increase plasma magnesium concentrations. Detailed information on modulating dialysate magnesium concentrations is limited in literature. Primary objective of this study is to determine the safety and feasibility to increase plasma magnesium concentrations in people treated with haemodialysis by means of sequentially increasing concentration of magnesium in the dialysate.
    Methods and analysis: In this randomised double-blinded standard of care controlled trial, 53 persons treated with haemodialysis will be randomly allocated 2:1 to either a stepwise individually titrated increase of dialysate magnesium concentration from 0.50 to 0.75 to 1.00 mmol/L during 8 weeks, or a standard dialysate magnesium concentration of 0.50 mmol/L. Other study measurements include dietary records, questionnaires, ECG, Holter registration and pulse wave velocity. The primary endpoint is predialysis plasma magnesium after the long interdialytic interval at the end of week 8. In addition, the predictive effect of dialysate magnesium concentration and other baseline parameters and dialysis characteristics on plasma magnesium concentration will be explored using linear mixed models. Safety endpoint is defined by the occurrence of hypermagnesemia above 1.25 mmol/L, or bradycardia or prolonged QTc interval detected on the ECG.
    Ethics and dissemination: The study is conducted in accordance with the declaration of Helsinki as revised in 2013 and was approved by the Ethical Committee of the VU University Medical Centre. The results of the study will be disseminated by publication in peer-reviewed scientific journals and presentation at national or international conferences in the field of interest.
    Trial registration number: NTR6568/NL6393.
    MeSH term(s) Humans ; Dialysis Solutions ; Renal Dialysis/methods ; Magnesium ; Feasibility Studies ; Pulse Wave Analysis ; Randomized Controlled Trials as Topic
    Chemical Substances Dialysis Solutions ; Magnesium (I38ZP9992A)
    Language English
    Publishing date 2022-11-21
    Publishing country England
    Document type Clinical Trial Protocol ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2599832-8
    ISSN 2044-6055 ; 2044-6055
    ISSN (online) 2044-6055
    ISSN 2044-6055
    DOI 10.1136/bmjopen-2022-063524
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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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