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Article ; Online: State of knowledge on ammonia handling by the kidney.

Bourgeois, Soline / Houillier, Pascal

Pflugers Archiv : European journal of physiology

2024 Volume 476, Issue 4, Page(s) 517–531

Abstract: The disposal of ammonia, the main proton buffer in the urine, is important for acid-base homeostasis. Renal ammonia excretion is the predominant contributor to renal net acid excretion, both under basal condition and in response to acidosis. New insights ...

Abstract	The disposal of ammonia, the main proton buffer in the urine, is important for acid-base homeostasis. Renal ammonia excretion is the predominant contributor to renal net acid excretion, both under basal condition and in response to acidosis. New insights into the mechanisms of renal ammonia production and transport have been gained in the past decades. Ammonia is the only urinary solute known to be produced in the kidney and selectively transported through the different parts of the nephron. Both molecular forms of total ammonia, NH
MeSH term(s)	Humans ; Ammonia/metabolism ; Acid-Base Equilibrium/physiology ; Kidney/metabolism ; Homeostasis/physiology ; Acidosis/metabolism
Chemical Substances	Ammonia (7664-41-7)
Language	English
Publishing date	2024-03-07
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-024-02940-1
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Article ; Online: Regulation of renal pendrin activity by aldosterone.

Bourgeois, Soline / Wagner, Carsten A

Current opinion in nephrology and hypertension

2020 Volume 30, Issue 1, Page(s) 131–137

Abstract: Purpose of review: Pendrin resides on the luminal membrane of type B intercalated cells in the renal collecting tubule system mediating the absorption of chloride in exchange for bicarbonate. In mice or humans lacking pendrin, blood pressure is lower, ... ...

Abstract	Purpose of review: Pendrin resides on the luminal membrane of type B intercalated cells in the renal collecting tubule system mediating the absorption of chloride in exchange for bicarbonate. In mice or humans lacking pendrin, blood pressure is lower, and pendrin knockout mice are resistant to aldosterone-induced hypertension. Here we discuss recent findings on the regulation of pendrin. Recent findings: Pendrin activity is stimulated during alkalosis partly mediated by secretin. Also, angiotensin II and aldosterone stimulate pendrin activity requiring the mineralocorticoid receptor in intercalated cells. Angiotensin II induces dephosphorylation of the mineralocorticoid receptor rendering the receptor susceptible for aldosterone binding. In the absence of the mineralocorticoid receptor in intercalated cells, angiotensin II does not stimulate pendrin. The effect of aldosterone on pendrin expression is in part mediated by the development of hypokalemic alkalosis and blunted by K-supplements or amiloride. Part of the blood pressure-increasing effect of pendrin is also mediated by its stimulatory effect on the epithelial Na-channel in neighbouring principal cells. Summary: These findings identify pendrin as a critical regulator of renal salt handling and blood pressure along with acid--base balance. A regulatory network of hormones fine-tuning activity is emerging. Drugs blocking pendrin are being developed.
MeSH term(s)	Aldosterone/metabolism ; Angiotensin II/metabolism ; Animals ; Bicarbonates/metabolism ; Blood Pressure/physiology ; Chlorides/metabolism ; Humans ; Kidney/cytology ; Kidney/metabolism ; Kidney Tubules, Collecting/cytology ; Kidney Tubules, Collecting/metabolism ; Mice ; Phosphorylation ; Receptors, Mineralocorticoid/metabolism ; Sulfate Transporters/biosynthesis ; Sulfate Transporters/genetics ; Sulfate Transporters/metabolism
Chemical Substances	Bicarbonates ; Chlorides ; Receptors, Mineralocorticoid ; SLC26A4 protein, human ; Sulfate Transporters ; Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB)
Language	English
Publishing date	2020-11-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
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.0000000000000669
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Article ; Online: The B1 H + -ATPase ( Atp6v1b1 ) Subunit in Non-Type A Intercalated Cells is Required for Driving Pendrin Activity and the Renal Defense Against Alkalosis.

Bourgeois, Soline / Kovacikova, Jana / Bugarski, Milica / Bettoni, Carla / Gehring, Nicole / Hall, Andrew / Wagner, Carsten A

Journal of the American Society of Nephrology : JASN

2023 Volume 35, Issue 1, Page(s) 7–21

Abstract: Significance statement: In the kidney, the B1 H + -ATPase subunit is mostly expressed in intercalated cells (IC). Its importance in acid-secreting type A ICs is evident in patients with inborn distal renal tubular acidosis and ATP6V1B1 mutations. ... ...

Abstract	Significance statement: In the kidney, the B1 H + -ATPase subunit is mostly expressed in intercalated cells (IC). Its importance in acid-secreting type A ICs is evident in patients with inborn distal renal tubular acidosis and ATP6V1B1 mutations. However, the protein is also highly expressed in alkali-secreting non-type A ICs where its function is incompletely understood. We demonstrate in Atp6v1b1 knock out mice that the B1 subunit is critical for the renal response to defend against alkalosis during an alkali load or chronic furosemide treatment. These findings highlight the importance of non-type A ICs in maintaining acid-base balance in response to metabolic challenges or commonly used diuretics. Background: Non-type A ICs in the collecting duct system express the luminal Cl - /HCO 3- exchanger pendrin and apical and/or basolateral H + -ATPases containing the B1 subunit isoform. Non-type A ICs excrete bicarbonate during metabolic alkalosis. Mutations in the B1 subunit (ATP6V1B1) cause distal renal tubular acidosis due to its role in acid secretory type A ICs. The function of B1 in non-type A ICs has remained elusive. Methods: We examined the responses of Atp6v1b1-/- and Atp6v1b1+/+ mice to an alkali load and to chronic treatment with furosemide. Results: An alkali load or 1 week of furosemide resulted in a more pronounced hypokalemic alkalosis in male ATP6v1b1-/- versus Atp6v1b1+/+ mice that could not be compensated by respiration. Total pendrin expression and activity in non-type A ICs of ex vivo microperfused cortical collecting ducts were reduced, and β2 -adrenergic stimulation of pendrin activity was blunted in ATP6v1b1-/- mice. Basolateral H + -ATPase activity was strongly reduced, although the basolateral expression of the B2 isoform was increased. Ligation assays for H + -ATPase subunits indicated impaired assembly of V 0 and V 1 H + -ATPase domains. During chronic furosemide treatment, ATP6v1b1-/- mice also showed polyuria and hyperchloremia versus Atp6v1b1+/+ . The expression of pendrin, the water channel AQP2, and subunits of the epithelial sodium channel ENaC were reduced. Conclusions: Our data demonstrate a critical role of H + -ATPases in non-type A ICs function protecting against alkalosis and reveal a hitherto unrecognized need of basolateral B1 isoform for a proper H + -ATPase complexes assembly and ability to be stimulated.
MeSH term(s)	Humans ; Male ; Mice ; Animals ; Acidosis, Renal Tubular/genetics ; Furosemide/pharmacology ; Aquaporin 2/metabolism ; Vacuolar Proton-Translocating ATPases/metabolism ; Kidney/metabolism ; Alkalosis/metabolism ; Sulfate Transporters/metabolism ; Protein Isoforms ; Alkalies ; Kidney Tubules, Collecting/metabolism
Chemical Substances	Furosemide (7LXU5N7ZO5) ; Aquaporin 2 ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-) ; Sulfate Transporters ; Protein Isoforms ; Alkalies ; ATP6V1B1 protein, human ; Atp6v1b1 protein, mouse (EC 3.6.1.-)
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.0000000000000259
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Article ; Online: Molecular Pathophysiology of Acid-Base Disorders.

Wagner, Carsten A / Imenez Silva, Pedro H / Bourgeois, Soline

Seminars in nephrology

2019 Volume 39, Issue 4, Page(s) 340–352

Abstract: Acid-base balance is critical for normal life. Acute and chronic disturbances impact cellular energy metabolism, endocrine signaling, ion channel activity, neuronal activity, and cardiovascular functions such as cardiac contractility and vascular blood ... ...

Abstract	Acid-base balance is critical for normal life. Acute and chronic disturbances impact cellular energy metabolism, endocrine signaling, ion channel activity, neuronal activity, and cardiovascular functions such as cardiac contractility and vascular blood flow. Maintenance and adaptation of acid-base homeostasis are mostly controlled by respiration and kidney. The kidney contributes to acid-base balance by reabsorbing filtered bicarbonate, regenerating bicarbonate through ammoniagenesis and generation of protons, and by excreting acid. This review focuses on acid-base disorders caused by renal processes, both inherited and acquired. Distinct rare inherited monogenic diseases affecting acid-base handling in the proximal tubule and collecting duct have been identified. In the proximal tubule, mutations of solute carrier 4A4 (SLC4A4) (electrogenic Na
MeSH term(s)	Acid-Base Equilibrium/genetics ; Acid-Base Equilibrium/physiology ; Acidosis, Renal Tubular/complications ; Acidosis, Renal Tubular/genetics ; Acidosis, Renal Tubular/physiopathology ; Ammonia/metabolism ; Animals ; Bicarbonates/metabolism ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Kidney/metabolism
Chemical Substances	Bicarbonates ; Ammonia (7664-41-7)
Language	English
Publishing date	2019-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2019.04.004
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Article ; Online: Two Rhesus protein ammonia transporters team up to eliminate ammonium into urine.

Wagner, Carsten A / Bourgeois, Soline

American journal of physiology. Renal physiology

2014 Volume 306, Issue 7, Page(s) F721–3

MeSH term(s)	Acidosis/metabolism ; Animals ; Cation Transport Proteins/metabolism ; Glycoproteins/metabolism ; Kidney/metabolism ; Kidney Tubules, Collecting/metabolism ; Membrane Glycoproteins/metabolism ; Membrane Transport Proteins/metabolism
Chemical Substances	Cation Transport Proteins ; Glycoproteins ; Membrane Glycoproteins ; Membrane Transport Proteins
Language	English
Publishing date	2014-04-01
Publishing country	United States
Document type	Comment ; Editorial ; 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.00681.2013
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Article ; Online: PCK1 is a key regulator of metabolic and mitochondrial functions in renal tubular cells.

Verissimo, Thomas / Dalga, Delal / Arnoux, Grégoire / Sakhi, Imene / Faivre, Anna / Auwerx, Hannah / Bourgeois, Soline / Paolucci, Deborah / Gex, Quentin / Rutkowski, Joseph M / Legouis, David / Wagner, Carsten A / Hall, Andrew M / de Seigneux, Sophie

American journal of physiology. Renal physiology

2023 Volume 324, Issue 6, Page(s) F532–F543

Abstract: Phosphoenolpyruvate carboxykinase 1 (PCK1 or PEPCK-C) is a cytosolic enzyme converting oxaloacetate to phosphoenolpyruvate, with a potential role in gluconeogenesis, ammoniagenesis, and cataplerosis in the liver. Kidney proximal tubule cells display high ...

Abstract	Phosphoenolpyruvate carboxykinase 1 (PCK1 or PEPCK-C) is a cytosolic enzyme converting oxaloacetate to phosphoenolpyruvate, with a potential role in gluconeogenesis, ammoniagenesis, and cataplerosis in the liver. Kidney proximal tubule cells display high expression of this enzyme, whose importance is currently not well defined. We generated PCK1 kidney-specific knockout and knockin mice under the tubular cell-specific PAX8 promoter. We studied the effect of PCK1 deletion and overexpression at the renal level on tubular physiology under normal conditions and during metabolic acidosis and proteinuric renal disease. PCK1 deletion led to hyperchloremic metabolic acidosis characterized by reduced but not abolished ammoniagenesis. PCK1 deletion also resulted in glycosuria, lactaturia, and altered systemic glucose and lactate metabolism at baseline and during metabolic acidosis. Metabolic acidosis resulted in kidney injury in PCK1-deficient animals with decreased creatinine clearance and albuminuria. PCK1 further regulated energy production by the proximal tubule, and PCK1 deletion decreased ATP generation. In proteinuric chronic kidney disease, mitigation of PCK1 downregulation led to better renal function preservation. PCK1 is essential for kidney tubular cell acid-base control, mitochondrial function, and glucose/lactate homeostasis. Loss of PCK1 increases tubular injury during acidosis. Mitigating kidney tubular PCK1 downregulation during proteinuric renal disease improves renal function.
MeSH term(s)	Animals ; Mice ; Acidosis/metabolism ; Glucose/metabolism ; Kidney/metabolism ; Lactates/metabolism ; Mitochondria/metabolism ; Phosphoenolpyruvate/metabolism ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; Phosphoenolpyruvate Carboxykinase (GTP)/metabolism
Chemical Substances	Glucose (IY9XDZ35W2) ; Lactates ; Phosphoenolpyruvate (73-89-2) ; Phosphoenolpyruvate Carboxykinase (GTP) (EC 4.1.1.32) ; Pck1 protein, mouse (EC 4.1.1.32)
Language	English
Publishing date	2023-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.00038.2023
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Article ; Online: Haploinsufficiency of the Mouse Atp6v1b1 Gene Leads to a Mild Acid-Base Disturbance with Implications for Kidney Stone Disease.

Bourgeois, Soline / Bettoni, Carla / Baron, Stéphanie / Wagner, Carsten A

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2018 Volume 47, Issue 3, Page(s) 1095–1107

Abstract: Background/aims: Homozygous mutations or deletion of the ATP6V1B1 gene encoding for the B1 subunit of the vacuolar H+-ATPase leads to distal renal tubular acidosis in man and mice. In humans, heterozygous carriers of B1 mutations can develop incomplete ... ...

Abstract	Background/aims: Homozygous mutations or deletion of the ATP6V1B1 gene encoding for the B1 subunit of the vacuolar H+-ATPase leads to distal renal tubular acidosis in man and mice. In humans, heterozygous carriers of B1 mutations can develop incomplete dRTA with nephroclacinosis. Here, we investigated whether Atp6v1b1+/- mice also develop acid-base disturbances during an HCl acid load. Methods: We subjected Atp6v1b1+/+, Atp6v1b1+/-, Atp6v1b1-/- to an HCl-load for 7 days and investigated acid-base status, kidney function, and expression of renal acid-base transport proteins. Results: Atp6v1b1-/- mice had more alkaline urine and low ammoniuria, whereas Atp6v1b1+/- mice showed no difference in their urine parameters but higher blood chloride and lower blood pCO2 compared to controls. Subcellular localization of a4 and B2 subunits of H+-ATPase were unchanged within the 3 genotypes and Atp6v1b1+/+ and Atp6v1b1+/- mice exhibited a similar luminal localization of B1 subunit in intercalated cells. However, B1, B2 and a4 expression were decreased in renal membrane fractions from Atp6v1b1+/- mice compared to Atp6v1b1+/+ while B2 and a4 were unchanged and B1 protein was reduced in Atp6v1b+-/- kidneys. Compensatory mechanisms of B1 ablation were found only in the collecting duct with a down-regulation of pendrin in Atp6v1b1-/- mice. Conclusions: In conclusion, 1) Atp6v1b1+/- mice developed a mild incomplete dRTA. dRTA is partly compensated by respiration. 2) Compensatory mechanisms for the absence of B1 take place only in the collecting duct of Atp6v1b1-/- kidneys.
MeSH term(s)	Animals ; Haploinsufficiency ; Kidney/metabolism ; Kidney/pathology ; Kidney Calculi/genetics ; Kidney Calculi/metabolism ; Mice ; Mice, Knockout ; Vacuolar Proton-Translocating ATPases/genetics ; Vacuolar Proton-Translocating ATPases/metabolism ; Water-Electrolyte Balance
Chemical Substances	Atp6v1b1 protein, mouse (EC 3.6.1.-) ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
Language	English
Publishing date	2018-05-25
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000490186
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Article ; Online: More actors in ammonia absorption by the thick ascending limb.

Houillier, Pascal / Bourgeois, Soline

American journal of physiology. Renal physiology

2012 Volume 302, Issue 3, Page(s) F293–7

Abstract: This review will briefly summarize current knowledge on the basolateral ammonia transport mechanisms in the thick ascending limb (TAL) of the loop of Henle. This segment transports ammonia against a concentration gradient and is responsible for the ... ...

Abstract	This review will briefly summarize current knowledge on the basolateral ammonia transport mechanisms in the thick ascending limb (TAL) of the loop of Henle. This segment transports ammonia against a concentration gradient and is responsible for the accumulation of ammonia in the medullary interstitium, which, in turn, favors ammonia secretion across the collecting duct. Experimental data indicate that the sodium/hydrogen ion exchanger isoform 4 (NHE4; Scl9a4) is a sodium/ammonia exchanger and plays a major role in this process. Disruption of murine NHE4 leads to metabolic acidosis with inappropriate urinary ammonia excretion and decreases the ability of the TAL to absorb ammonia and to build the corticopapillary ammonia gradient. However, NHE4 does not account for the entirety of ammonia absorption by the TAL, indicating that, at least, one more transporter is involved.
MeSH term(s)	Acidosis/metabolism ; Ammonia/metabolism ; Animals ; Biological Transport/physiology ; Humans ; Kidney Cortex/metabolism ; Loop of Henle/metabolism ; Mice ; Sodium-Hydrogen Exchangers/metabolism
Chemical Substances	Slc9a4 protein, mouse ; Sodium-Hydrogen Exchangers ; Ammonia (7664-41-7)
Language	English
Publishing date	2012-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00307.2011
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Article ; Online: The ugly duckling of urinary acidification: what is the contribution of the thick ascending limb of the loop of Henle to urinary acidification?

Wagner, Carsten A / Mohebbi, Nilufar / Bourgeois, Soline

American journal of physiology. Renal physiology

2015 Volume 309, Issue 5, Page(s) F431–3

MeSH term(s)	Animals ; Bicarbonates/metabolism ; Loop of Henle/metabolism ; Macrolides ; Male
Chemical Substances	Bicarbonates ; Macrolides
Language	English
Publishing date	2015-09-01
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00296.2015
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Article ; Online: Alkali therapy protects renal function, suppresses inflammation, and improves cellular metabolism in kidney disease.

Pastor Arroyo, Eva Maria / Yassini, Nima / Sakiri, Elif / Russo, Giancarlo / Bourgeois, Soline / Mohebbi, Nilufar / Amann, Kerstin / Joller, Nicole / Wagner, Carsten A / Imenez Silva, Pedro Henrique

Clinical science (London, England : 1979)

2022 Volume 136, Issue 8, Page(s) 557–577

Abstract: Chronic kidney disease (CKD) affects approximately 10-13% of the population worldwide and halting its progression is a major clinical challenge. Metabolic acidosis is both a consequence and a possible driver of CKD progression. Alkali therapy counteracts ...

Abstract	Chronic kidney disease (CKD) affects approximately 10-13% of the population worldwide and halting its progression is a major clinical challenge. Metabolic acidosis is both a consequence and a possible driver of CKD progression. Alkali therapy counteracts these effects in CKD patients, but underlying mechanisms remain incompletely understood. Here we show that bicarbonate supplementation protected renal function in a murine CKD model induced by an oxalate-rich diet. Alkali therapy had no effect on the aldosterone-endothelin axis but promoted levels of the anti-aging protein klotho; moreover, it suppressed adhesion molecules required for immune cell invasion along with reducing T-helper cell and inflammatory monocyte invasion. Comparing transcriptomes from the murine crystallopathy model and from human biopsies of kidney transplant recipients (KTRs) suffering from acidosis with or without alkali therapy unveils parallel transcriptome responses mainly associated with lipid metabolism and oxidoreductase activity. Our data reveal novel pathways associated with acidosis in kidney disease and sensitive to alkali therapy and identifies potential targets through which alkali therapy may act on CKD and that may be amenable for more targeted therapies.
MeSH term(s)	Acidosis/complications ; Acidosis/drug therapy ; Alkalies/therapeutic use ; Animals ; Female ; Humans ; Inflammation ; Kidney/metabolism ; Male ; Mice ; Renal Insufficiency, Chronic
Chemical Substances	Alkalies
Language	English
Publishing date	2022-05-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	206835-7
ISSN	1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
ISSN (online)	1470-8736
ISSN	0301-0538 ; 0009-0360 ; 0143-5221
DOI	10.1042/CS20220095
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