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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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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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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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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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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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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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Article ; Online: Genetic and drug-induced hypomagnesemia: different cause, same mechanism.

Bosman, Willem / Hoenderop, Joost G J / de Baaij, Jeroen H F

The Proceedings of the Nutrition Society

2021 Volume 80, Issue 3, Page(s) 327–338

Abstract: Magnesium (Mg2+) plays an essential role in many biological processes. Mg2+ deficiency is therefore associated with a wide range of clinical effects including muscle cramps, fatigue, seizures and arrhythmias. To maintain sufficient Mg2+ levels, (re) ... ...

Abstract	Magnesium (Mg2+) plays an essential role in many biological processes. Mg2+ deficiency is therefore associated with a wide range of clinical effects including muscle cramps, fatigue, seizures and arrhythmias. To maintain sufficient Mg2+ levels, (re)absorption of Mg2+ in the intestine and kidney is tightly regulated. Genetic defects that disturb Mg2+ uptake pathways, as well as drugs interfering with Mg2+ (re)absorption cause hypomagnesemia. The aim of this review is to provide an overview of the molecular mechanisms underlying genetic and drug-induced Mg2+ deficiencies. This leads to the identification of four main mechanisms that are affected by hypomagnesemia-causing mutations or drugs: luminal transient receptor potential melastatin type 6/7-mediated Mg2+ uptake, paracellular Mg2+ reabsorption in the thick ascending limb of Henle's loop, structural integrity of the distal convoluted tubule and Na+-dependent Mg2+ extrusion driven by the Na+/K+-ATPase. Our analysis demonstrates that genetic and drug-induced causes of hypomagnesemia share common molecular mechanisms. Targeting these shared pathways can lead to novel treatment options for patients with hypomagnesemia.
MeSH term(s)	Biological Transport ; Humans ; Kidney Tubules, Distal/metabolism ; Magnesium/metabolism ; Metabolic Diseases/metabolism ; Pharmaceutical Preparations/metabolism
Chemical Substances	Pharmaceutical Preparations ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2021-04-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391142-1
ISSN	1475-2719 ; 0029-6651
ISSN (online)	1475-2719
ISSN	0029-6651
DOI	10.1017/S0029665121000926
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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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Article ; Online: Interplay between purinergic signalling and extracellular vesicles in health and disease.

Carotti, Valentina / Rigalli, Juan P / van Asbeck-van der Wijst, Jenny / Hoenderop, Joost G J

Biochemical pharmacology

2022 Volume 203, Page(s) 115192

Abstract: Purinergic signalling is a receptor-mediated process characterized by the binding of extracellular nucleotides and nucleosides to purinergic receptors, which results in the activation intracellular signalling pathways, and, ultimately, leads to changes ... ...

Abstract	Purinergic signalling is a receptor-mediated process characterized by the binding of extracellular nucleotides and nucleosides to purinergic receptors, which results in the activation intracellular signalling pathways, and, ultimately, leads to changes in cell physiology. Purinergic signalling has been related to the regulation of important physiological processes (e.g., renal electrolyte reabsorption; platelet aggregation; immune response). In addition, it has been associated with pathophysiological situations such as cancer and inflammation. Extracellular vesicles (EVs) are nanoparticles released by all cells of the organism, which play a key role in cell-cell communication. In this regard, EVs can mediate effects on target cells located at distant locations. Within their cargo, EVs contain molecules with the potential to affect purinergic signalling at the target cells and tissues. Here, we review the studies addressing the regulation of purinergic signalling by EVs based on the cell type or tissue where the regulation takes place. In this regard, EVs are found to play a major role in modulating the extracellular ATP levels and, specially, adenosine. This has a clear impact on, for instance, the inflammatory and immune response against cancer cells. Furthermore, we discuss the data available on the regulation of EV secretion and its cargo by purinergic signalling. Here, a major role of the purinergic receptor P2X7 and again, an impact on processes such as inflammation, immune response and cancer pathogenesis has been established. Finally, we highlight uninvestigated aspects of these two regulatory networks and address their potential as therapeutic targets.
MeSH term(s)	Cell Communication ; Extracellular Vesicles/metabolism ; Humans ; Inflammation/metabolism ; Neoplasms/metabolism ; Receptors, Purinergic/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, Purinergic
Language	English
Publishing date	2022-07-26
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115192
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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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