2023
DOI: 10.1053/j.akdh.2022.12.005
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An Update on Kidney Ammonium Transport Along the Nephron

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Cited by 10 publications
(8 citation statements)
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“…Glutamine is the primary substrate for ammoniagenesis in the proximal tubule. At this stage, bicarbonate reabsorption is mediated by a specific transporter (electrogenic sodium bicarbonate cotransporter isoform 1A; NBCe-1 A) [ 8 ]. These receptors are present exclusively in the proximal tubule, and they play a key role in bicarbonate reabsorption.…”
Section: Discussionmentioning
confidence: 99%
“…Glutamine is the primary substrate for ammoniagenesis in the proximal tubule. At this stage, bicarbonate reabsorption is mediated by a specific transporter (electrogenic sodium bicarbonate cotransporter isoform 1A; NBCe-1 A) [ 8 ]. These receptors are present exclusively in the proximal tubule, and they play a key role in bicarbonate reabsorption.…”
Section: Discussionmentioning
confidence: 99%
“…The total amount of amino acids in the renal filtrate is reabsorbed in PCT and partially metabolized (mainly glutamine) producing ammonia and bicarbonate. Glutamine transport and metabolism are coupled to proton excretion ( Harris et al, 2023 ). The glutamine transfer by apical Na + -dependent neutral amino acid transporter 1 and basolateral Na + -coupled neutral amino acid transporter 3 is complemented by glutaminase activity.…”
Section: Survey Methodologymentioning
confidence: 99%
“…The epithelial collecting system also implements NH 3 /NH 4 + transport regulated by a complex process that involves at least two Rhesus glycoproteins: RhB (SLC42A2) and RhC (SLC42A3) ( Harris et al, 2023 ; Takvam et al, 2023 ). Rhbg expressed in IC-α and non-α, non-β intercalated cells, principal cells in the basolateral plasma membrane.…”
Section: Survey Methodologymentioning
confidence: 99%
“…Ammonium excretion is particularly important because it can increase considerably under conditions of metabolic acidosis as a compensatory response. 1,2 Disorders of acid-base homeostasis can result in a number of clinical problems such as electrolyte abnormalities, bone disorders, muscle weakness, and cardiac arrhythmias. In humans with progressive chronic kidney disease (CKD), a substantial proportion of individuals (up to 40%) develop metabolic acidosis, where inadequate capacity for ammonia excretion appears to be the driving force.…”
Section: Introductionmentioning
confidence: 99%
“…The 2 normal components of daily acid excretion are titratable acidity and ammonium excretion, which lead to the formation of new bicarbonate. Ammonium excretion is particularly important because it can increase considerably under conditions of metabolic acidosis as a compensatory response 1,2 …”
Section: Introductionmentioning
confidence: 99%