ReviewPflugers Archiv : European journal of physiology2009
Regulated acid-base transport in the collecting duct.
Review in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 162 citations in OpenAlex.
- Uncoupling proximal tubule ammoniagenesis from bicarbonate generation byAmerican journal of physiology. Renal physiology · 2026Article
- ATP6V1B1-Associated Inherited Distal Renal Tubular Acidosis in Children: Insights from a Literature Review.Children (Basel, Switzerland) · 2026Review
- WDR72 Is Required for Urinary Acidification and Normal HActa physiologica (Oxford, England) · 2026Article
- Chloremia Disturbances in Critical Care: A Narrative Review of Pathophysiology, Clinical Impact and Management Strategies.Life (Basel, Switzerland) · 2026Review
- Primary Distal Renal Tubular Acidosis: Toward an Optimal Correction of Metabolic Acidosis.Clinical journal of the American Society of Nephrology : CJASN · 2024Review
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosis.American journal of physiology. Renal physiology · 2023Article
- Transcriptomic response ofFrontiers in physiology · 2023Article
- Gallic and Hesperidin Ameliorate Electrolyte Imbalances in AlClBiochemistry research international · 2022Article
- Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021Article
- Kidney intercalated cells and the transcription factor FOXi1 drive cystogenesis in tuberous sclerosis complex.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Metabolic acidosis and hyperkalemia differentially regulate cation HCN3 channel in the rat nephron.Journal of molecular histology · 2020Article
- Renal Tubular Acidosis.Indian journal of pediatrics · 2020Review
- Adaptive response of the murine collecting duct to alkali loading.Pflugers Archiv : European journal of physiology · 2020Article
- NBCe1-A is required for the renal ammonia and KAmerican journal of physiology. Renal physiology · 2020Article
- Distal renal tubular acidosis: genetic causes and management.World journal of pediatrics : WJP · 2019Review
- Article
- Intercalated Cells of the Kidney Collecting Duct in Kidney Physiology.Seminars in nephrology · 2019Review
- Xenobiotic transporter activity in zebrafish embryo ionocytes.Aquatic toxicology (Amsterdam, Netherlands) · 2019Article
- Pathophysiology, diagnosis and treatment of inherited distal renal tubular acidosis.Journal of nephrology · 2018Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renal collecting system serves the fine-tuning of renal acid-base secretion. Acid-secretory type-A intercalated cells secrete protons via a luminally expressed V-type H(+)-ATPase and generate new bicarbonate released by basolateral chloride/bicarbonate exchangers including the AE1 anion exchanger. Efficient proton secretion depends both on the presence of titratable acids (mainly phosphate) and the concomitant secretion of ammonia being titrated to ammonium. Collecting duct ammonium excretion requires the Rhesus protein RhCG as indicated by recent KO studies. Urinary acid secretion by type-A intercalated cells is strongly regulated by various factors among them acid-base status, angiotensin II and aldosterone, and the Calcium-sensing receptor. Moreover, urinary acidification by H(+)-ATPases is modulated indirectly by the activity of the epithelial sodium channel ENaC. Bicarbonate secretion is achieved by non-type-A intercalated cells characterized by the luminal expression of the chloride/bicarbonate exchanger pendrin. Pendrin activity is driven by H(+)-ATPases and may serve both bicarbonate excretion and chloride reabsorption. The activity and expression of pendrin is regulated by different factors including acid-base status, chloride delivery, and angiotensin II and may play a role in NaCl retention and blood pressure regulation. Finally, the relative abundance of type-A and non-type-A intercalated cells may be tightly regulated. Dysregulation of intercalated cell function or abundance causes various syndromes of distal renal tubular acidosis underlining the importance of these processes for acid-base homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.