ReviewClinical journal of the American Society of Nephrology : CJASN2024
Primary Distal Renal Tubular Acidosis: Toward an Optimal Correction of Metabolic Acidosis.
Review in Clinical journal of the American Society of Nephrology : CJASN, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Potassium-Rich, Gluten-Free Diets for Patients with Sjögren's Syndrome: A Mini-ReviewEndocrine, metabolic & immune disorders drug targets · 2026Review
- Sjögren's Disease-Associated Renal Tubular Acidosis: An Integrated Immuno-Tubular Model of Tubular Dysfunction.International journal of medical sciences · 2026Review
- Identification of novel pathogenic mutations inRenal failure · 2025Article
- A gain-of-function mutation in ATP6V0A4 drives primary distal renal tubular alkalosis with enhanced V-ATPase activity.The Journal of clinical investigation · 2025Article
- Nephrocalcinosis: unveiling renal tubulopathies in the genomic era.Jornal brasileiro de nefrologiaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The term classic, type 1 renal tubular acidosis or primary distal renal tubular acidosis is used to designate patients with impaired ability to excrete acid normally in the urine as a result of tubular transport defects involving type A intercalated cells in the collecting duct. The clinical phenotype is largely characterized by the complications of chronic metabolic acidosis (MA): stunted growth, bone abnormalities, and nephrocalcinosis and nephrolithiasis that develop as the consequence of hypercalciuria and hypocitraturia. All these manifestations are preventable with early and sustained correction of MA with alkali therapy. The optimal target for plasma bicarbonate should be as close as possible to the range considered normal by current standards (between 23 and 28 mEq/L.). Most of the benefits of alkali therapy are tangible early in the course of the disease in childhood, but life-long treatment is required to prevent the vast array of complications attributable to chronic MA.
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Registered trials
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