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Article ; Online: Magnesium reabsorption in the kidney.

de Baaij, Jeroen H F

American journal of physiology. Renal physiology

2023 Volume 324, Issue 3, Page(s) F227–F244

Abstract: ... ...

Abstract	Mg
MeSH term(s)	Animals ; Mice ; Humans ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism ; Magnesium/metabolism ; Kidney Tubules, Distal/metabolism ; Kidney Tubules, Proximal/metabolism ; Signal Transduction ; Protein Serine-Threonine Kinases/metabolism
Chemical Substances	TRPM Cation Channels ; Magnesium (I38ZP9992A) ; TRPM7 protein, human (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Trpm7 protein, mouse (EC 2.7.1.-)
Language	English
Publishing date	2023-01-12
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00298.2022
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Article ; Online: mTOR signaling in renal ion transport.

Adella, Anastasia / de Baaij, Jeroen H F

Acta physiologica (Oxford, England)

2023 Volume 238, Issue 1, Page(s) e13960

Abstract: The mammalian target of rapamycin (mTOR) signaling pathway is crucial in maintaining cell growth and metabolism. The mTOR protein kinase constitutes the catalytic subunit of two multimeric protein complexes called mTOR complex 1 (mTORC1) and mTOR complex ...

Abstract	The mammalian target of rapamycin (mTOR) signaling pathway is crucial in maintaining cell growth and metabolism. The mTOR protein kinase constitutes the catalytic subunit of two multimeric protein complexes called mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). As such, this pathway is indispensable for many organs, including the kidney. Since its discovery, mTOR has been associated with major renal disorders such as acute kidney injury, chronic kidney disease, and polycystic kidney disease. On top of that, emerging studies using pharmacological interventions and genetic disease models have unveiled mTOR role in renal tubular ion handling. Along the tubule, mTORC1 and mTORC2 subunits are ubiquitously expressed at mRNA level. Nevertheless, at the protein level, current studies suggest that a tubular segment-specific balance between mTORC1 and mTORC2 exists. In the proximal tubule, mTORC1 regulates nutrients transports through various transporters located in this segment. On the other hand, in the thick ascending limb of the loop of Henle, both complexes play a role in regulating NKCC2 expression and activity. Lastly, in the principal cells of the collecting duct, mTORC2 determines Na
MeSH term(s)	Humans ; Acute Kidney Injury/metabolism ; Kidney/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mechanistic Target of Rapamycin Complex 2/metabolism ; Signal Transduction/physiology ; Sirolimus/metabolism ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases/metabolism ; Biological Transport
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 2 (EC 2.7.11.1) ; MTOR protein, human (EC 2.7.1.1) ; Sirolimus (W36ZG6FT64) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-04-13
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.13960
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Article ; Online: Mitochondrial Dysfunction in Kidney Tubulopathies.

Hoogstraten, Charlotte A / Hoenderop, Joost G / de Baaij, Jeroen H F

Annual review of physiology

2023 Volume 86, Page(s) 379–403

Abstract: Mitochondria play a key role in kidney physiology and pathology. They produce ATP to fuel energy-demanding water and solute reabsorption processes along the nephron. Moreover, mitochondria contribute to cellular health by the regulation of autophagy, ( ... ...

Abstract	Mitochondria play a key role in kidney physiology and pathology. They produce ATP to fuel energy-demanding water and solute reabsorption processes along the nephron. Moreover, mitochondria contribute to cellular health by the regulation of autophagy, (oxidative) stress responses, and apoptosis. Mitochondrial abundance is particularly high in cortical segments, including proximal and distal convoluted tubules. Dysfunction of the mitochondria has been described for tubulopathies such as Fanconi, Gitelman, and Bartter-like syndromes and renal tubular acidosis. In addition, mitochondrial cytopathies often affect renal (tubular) tissues, such as in Kearns-Sayre and Leigh syndromes. Nevertheless, the mechanisms by which mitochondrial dysfunction results in renal tubular diseases are only scarcely being explored. This review provides an overview of mitochondrial dysfunction in the development and progression of kidney tubulopathies. Furthermore, it emphasizes the need for further mechanistic investigations to identify links between mitochondrial function and renal electrolyte reabsorption.
MeSH term(s)	Humans ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Bartter Syndrome/metabolism ; Bartter Syndrome/pathology ; Kearns-Sayre Syndrome/metabolism ; Kearns-Sayre Syndrome/pathology ; Kidney Diseases/pathology ; Mitochondria
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-042222-025000
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Article ; Online: Chloride-sensitive signaling turns the potassium switch on.

Hoorn, Ewout J / de Baaij, Jeroen H F

Kidney international

2022 Volume 102, Issue 5, Page(s) 956–958

Abstract: The potassium switch refers to plasma potassium regulation of the sodium-chloride cotransporter (NCC), which controls distal sodium delivery and therefore potassium secretion. Low extracellular potassium activates NCC by relieving chloride inhibition of ... ...

Abstract	The potassium switch refers to plasma potassium regulation of the sodium-chloride cotransporter (NCC), which controls distal sodium delivery and therefore potassium secretion. Low extracellular potassium activates NCC by relieving chloride inhibition of With-No-Lysine 4 (WNK4). A new mouse model carrying a chloride-insensitive WNK4 mutant still shows NCC activation on low potassium diet. These effects are mediated by WNK4 activation and kelch-like 3 (KLHL3) inhibition and reveal additional chloride-sensitive pathways for NCC activation.
MeSH term(s)	Mice ; Animals ; Potassium/metabolism ; Chlorides/metabolism ; Protein Serine-Threonine Kinases/genetics ; Sodium Chloride Symporters/metabolism ; Sodium/metabolism ; Solute Carrier Family 12, Member 3/metabolism
Chemical Substances	Potassium (RWP5GA015D) ; Chlorides ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Sodium Chloride Symporters ; Sodium (9NEZ333N27) ; Solute Carrier Family 12, Member 3
Language	English
Publishing date	2022-10-22
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.2022.08.023
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Article ; Online: The genetic spectrum of Gitelman(-like) syndromes.

Schlingmann, Karl P / de Baaij, Jeroen H F

Current opinion in nephrology and hypertension

2022 Volume 31, Issue 5, Page(s) 508–515

Abstract: Purpose of review: Gitelman syndrome is a recessive salt-wasting disorder characterized by hypomagnesemia, hypokalemia, metabolic alkalosis and hypocalciuria. The majority of patients are explained by mutations and deletions in the SLC12A3 gene, ... ...

Abstract	Purpose of review: Gitelman syndrome is a recessive salt-wasting disorder characterized by hypomagnesemia, hypokalemia, metabolic alkalosis and hypocalciuria. The majority of patients are explained by mutations and deletions in the SLC12A3 gene, encoding the Na+-Cl--co-transporter (NCC). Recently, additional genetic causes of Gitelman-like syndromes have been identified that should be considered in genetic screening. This review aims to provide a comprehensive overview of the clinical, genetic and mechanistic aspects of Gitelman(-like) syndromes. Recent findings: Disturbed Na+ reabsorption in the distal convoluted tubule (DCT) is associated with hypomagnesemia and hypokalemic alkalosis. In Gitelman syndrome, loss-of-function mutations in SLC12A3 cause impaired NCC-mediated Na+ reabsorption. In addition, patients with mutations in CLCKNB, KCNJ10, FXYD2 or HNF1B may present with a similar phenotype, as these mutations indirectly reduce NCC activity. Furthermore, genetic investigations of patients with Na+-wasting tubulopathy have resulted in the identification of pathogenic variants in MT-TI, MT-TF, KCNJ16 and ATP1A1. These novel findings highlight the importance of cell metabolism and basolateral membrane potential for Na+ reabsorption in the DCT. Summary: Altogether, these findings extend the genetic spectrum of Gitelman-like electrolyte alterations. Genetic testing of patients with hypomagnesemia and hypokalemia should cover a panel of genes involved in Gitelman-like syndromes, including the mitochondrial genome.
MeSH term(s)	Alkalosis/complications ; Alkalosis/genetics ; Bartter Syndrome/genetics ; Gitelman Syndrome/complications ; Gitelman Syndrome/genetics ; Humans ; Hypokalemia/genetics ; Magnesium/metabolism ; Sodium/metabolism ; Solute Carrier Family 12, Member 3/genetics
Chemical Substances	SLC12A3 protein, human ; Solute Carrier Family 12, Member 3 ; Sodium (9NEZ333N27) ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2022-07-11
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000818
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Article ; Online: Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes.

Oost, Lynette J / Tack, Cees J / de Baaij, Jeroen H F

Endocrine reviews

2022 Volume 44, Issue 3, Page(s) 357–378

Abstract: Hypomagnesemia is 10-fold more common in individuals with type 2 diabetes (T2D) than in the healthy population. Factors that are involved in this high prevalence are low Mg2+ intake, gut microbiome composition, medication use, and presumably genetics. ... ...

Abstract	Hypomagnesemia is 10-fold more common in individuals with type 2 diabetes (T2D) than in the healthy population. Factors that are involved in this high prevalence are low Mg2+ intake, gut microbiome composition, medication use, and presumably genetics. Hypomagnesemia is associated with insulin resistance, which subsequently increases the risk to develop T2D or deteriorates glycemic control in existing diabetes. Mg2+ supplementation decreases T2D-associated features like dyslipidemia and inflammation, which are important risk factors for cardiovascular disease (CVD). Epidemiological studies have shown an inverse association between serum Mg2+ and the risk of developing heart failure (HF), atrial fibrillation (AF), and microvascular disease in T2D. The potential protective effect of Mg2+ on HF and AF may be explained by reduced oxidative stress, fibrosis, and electrical remodeling in the heart. In microvascular disease, Mg2+ reduces the detrimental effects of hyperglycemia and improves endothelial dysfunction; however, clinical studies assessing the effect of long-term Mg2+ supplementation on CVD incidents are lacking, and gaps remain on how Mg2+ may reduce CVD risk in T2D. Despite the high prevalence of hypomagnesemia in people with T2D, routine screening of Mg2+ deficiency to provide Mg2+ supplementation when needed is not implemented in clinical care as sufficient clinical evidence is lacking. In conclusion, hypomagnesemia is common in people with T2D and is involved both as cause, probably through molecular mechanisms leading to insulin resistance, and as consequence and is prospectively associated with development of HF, AF, and microvascular complications. Whether long-term supplementation of Mg2+ is beneficial, however, remains to be determined.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Risk Factors ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/complications ; Magnesium/therapeutic use ; Insulin Resistance ; Heart Disease Risk Factors
Chemical Substances	Magnesium (I38ZP9992A)
Language	English
Publishing date	2022-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/endrev/bnac028
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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: 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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