Evidence map›Paper›PMID 37990184›Full record

ReviewBMC nephrology2023

Diagnosing Fabry nephropathy: the challenge of multiple kidney disease.

Pasquale Esposito, Carmela Caputo, Monica Repetto, Alberto Somaschini, Bellone Pietro, Paolo Colomba, Carmela Zizzo, Angelica Parodi, Valentina Zanetti, Marco Canepa and 4 more

Open access · goldAbstract readCase ReportsReview
In one paragraph

Review in BMC nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Fabry Disease: A Focus on the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
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

14 authors at 5 institutions in 1 country.

Pasquale EspositoDepartment of Internal Medicine, University of Genoa, Genoa, Italy. Pasquale.esposito@unige.it.
Carmela CaputoUnit of Nephrology and Dialysis, Ospedale San Paolo, Savona, Italy.
Monica RepettoUnit of Nephrology and Dialysis, Ospedale San Paolo, Savona, Italy.
Alberto SomaschiniDivision of Cardiology and Cardiac Intensive Care Unit, Ospedale San Paolo, Savona, Italy.
Bellone PietroDivision of Cardiology and Cardiac Intensive Care Unit, Ospedale San Paolo, Savona, Italy.
Paolo ColombaInstitute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), Palermo, Italy.
Carmela ZizzoInstitute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), Palermo, Italy.
Angelica ParodiUnit of Nephrology, Dialysis, and Transplantation, IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
Valentina ZanettiDepartment of Internal Medicine, University of Genoa, Genoa, Italy.
Marco CanepaDepartment of Internal Medicine, University of Genoa, Genoa, Italy.
Virginia EustachiDepartment of Internal Medicine, University of Genoa, Genoa, Italy.
Francesca SanguineriDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetic and Maternal and Infantile Sciences, University of Genoa, Genoa, Italy.
Paola MandichDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetic and Maternal and Infantile Sciences, University of Genoa, Genoa, Italy.
Francesca ViazziDepartment of Internal Medicine, University of Genoa, Genoa, Italy.
University of Genoa · ITOspedale San Paolo · ITOspedale Policlinico San Martino · ITInstitute for Biomedical Research and Innovation · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fabry disease (FD) is an X-linked inherited lysosomal disorder due to a deficiency of the enzyme alpha-galactosidase A (α-gla) due to mutations in the GLA gene. These mutations result in plasma and lysosome accumulation of glycosphingolipids, leading to progressive organ damage and reduced life expectancy. Due to the availability of specific disease-modifying treatments, proper and timely diagnosis and therapy are essential to prevent irreversible complications. However, diagnosis of FD is often delayed because of the wide clinical heterogeneity of the disease and multiple organ involvement developing in variable temporal sequences. This observation is also valid for renal involvement, which may manifest with non-specific signs, such as proteinuria and chronic kidney disease, which are also common in many other nephropathies. Moreover, an additional confounding factor is the possibility of the coexistence of FD with other kidney disorders. Thus, suspecting and diagnosing FD nephropathy in patients with signs of kidney disease may be challenging for the clinical nephrologist. Herein, also through the presentation of a unique case of co-occurrence of autosomal dominant polycystic kidney disease and FD, we review the available literature on cases of coexistence of FD and other renal diseases and discuss the implications of these conditions. Moreover, we highlight the clinical, laboratory, and histological elements that may suggest clinical suspicion and address a proper diagnosis of Fabry nephropathy.

Indexed as

Fabry DiseaseRenal Insufficiency, Chronicalpha-GalactosidaseHumansKidneyMutationalpha-GalactosidaseADPKDAlpha-galactosidase AChronic kidney diseaseFabry diseaseFabry nephropathyGlomerulonephritisKidney biopsy

Identifiers

PMID37990184
PMCPMC10664682
OpenAlexW4388867666

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.