Evidence map›Paper›PMID 29344504›Full record

ReviewKidney diseases (Basel, Switzerland)2017

New Findings on the Pathogenesis of Distal Renal Tubular Acidosis.

Francesco Trepiccione, Federica Prosperi, Luigi Regenburgh de la Motte, Christian A Hübner, Regine Chambrey, Dominique Eladari, Giovambattista Capasso

Open access · goldAbstract readReview
In one paragraph

Review in Kidney diseases (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 39 citations in OpenAlex.

  1. Molecular genetics and long-term outcomes of primary distal renal tubular acidosis in Asia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Observational
  2. Review
  3. Article
  4. UtilizingJournal of developmental biology · 2025
    Review
  5. Distal Renal Tubular Acidosis Secondary to Hyperbilirubinemia.European journal of case reports in internal medicine · 2025
    Article
  6. ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024
    Article
  7. Review
  8. Organs-on-chip technology: a tool to tackle genetic kidney diseases.Pediatric nephrology (Berlin, Germany) · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Renal Tubular Acidosis.Indian journal of pediatrics · 2020
    Review
  13. Article
  14. Distal renal tubular acidosis: genetic causes and management.World journal of pediatrics : WJP · 2019
    Review
  15. Review
  16. Approach to Renal Tubular Acidosis - A Review.Indian journal of endocrinology and metabolism
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 4 countries.

Francesco TrepiccioneDepartment of Cardiothoracic and Respiratory Science, University of Campania "Luigi Vanvitelli," Naples, Italy.
Federica ProsperiDepartment of Cardiothoracic and Respiratory Science, University of Campania "Luigi Vanvitelli," Naples, Italy.
Luigi Regenburgh de la MotteDepartment of Cardiothoracic and Respiratory Science, University of Campania "Luigi Vanvitelli," Naples, Italy.
Christian A HübnerInstitute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany.
Regine ChambreyInserm U1188, Diabète athérothrombose Thérapies Réunion Océan Indien (DéTROI), Université de La Réunion, France.
Dominique EladariService d'Explorations Fonctionnelles Rénales, Hôpital Felix Guyon, CHU de la Réunion, Saint-Denis, Ile de la Réunion, France.
Giovambattista CapassoDepartment of Cardiothoracic and Respiratory Science, University of Campania "Luigi Vanvitelli," Naples, Italy.
University of Campania "Luigi Vanvitelli" · ITCentre Hospitalier Universitaire de La Réunion · FRInserm · FRJena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDistal renal tubular acidosis (dRTA) is characterized by an impairment of the urinary acidification process in the distal nephron. Complete or incomplete metabolic acidosis coupled with inappropriately alkaline urine are the hallmarks of this condition. Genetic forms of dRTA are caused by loss of function mutations of either SUMMARY: Alterations of acid-base homeostasis are variably associated with hypokalemia, hypercalciuria, nephrocalcinosis or nephrolithiasis, and a salt-losing phenotype. Here we report the diagnostic test and the underlying physiopathological mechanisms. The molecular mechanisms identified so far can explain the defect in acid secretion, but do not explain all clinical features. We review the latest experimental findings on the pathogenesis of dRTA, reporting mechanisms that are instrumental for the clinician and potentially inspiring a novel therapeutic strategy. KEY MESSAGE: Primary dRTA is usually intended as a single-cell disease because the A-IC are mainly affected. However, novel evidence shows that different cell types of the nephron may contribute to the signs and symptoms, moving the focus from a single-cell towards a renal disease.

Indexed as

AE1Intercalated cellsMetabolic acidosisRenal tubular acidosisvH+ATPase

Identifiers

PMID29344504
PMCPMC5757613
OpenAlexW2747296868

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.