Evidence map›Paper›PMID 30155326›Full record

ArticleCase reports in nephrology2018

Mucin-1 Gene Mutation and the Kidney: The Link between Autosomal Dominant Tubulointerstitial Kidney Disease and Focal and Segmental Glomerulosclerosis.

H Trimarchi, M Paulero, T Rengel, I González-Hoyos, M Forrester, F Lombi, V Pomeranz, R Iriarte, A Iotti

Open access · goldAbstract readCase Reports
In one paragraph

Article in Case reports in nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

9 authors at 1 institution in 1 country.

H TrimarchiNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.ORCID 0000-0002-6921-4811
M PauleroNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.ORCID 0000-0002-3630-8993
T RengelNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
I González-HoyosNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
M ForresterNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
F LombiNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
V PomeranzNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
R IriarteNephrology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
A IottiPathology Service, Hospital Británico de Buenos Aires, Buenos Aires, Argentina.
Hospital Británico de Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glomerular diseases are one of the most frequent causes of chronic kidney disease, focal and segmental glomerulosclerosis being one of the commonest glomerulopathies. However, the etiology of this glomerular entity, which merely depicts a morphologic pattern of disease, is often not established and, in most of the patients, remains unknown. Nephrologists tend to assume focal and segmental glomerulosclerosis as a definitive diagnosis. However, despite the increasing knowledge developed in the field, genetic causes of glomerular diseases are currently identified in fewer than 10% of chronic kidney disease subjects. Moreover, unexplained familial clustering among dialysis patients suggests that genetic causes may be underrecognized. Secondary focal and segmental glomerulosclerosis due to genetic mutations mainly located in the podocyte and slit diaphragm can occur from childbirth to adulthood with different clinical presentations, ranging from mild proteinuria and normal renal function to nephrotic syndrome and renal failure. However, this histopathological pattern can also be due to primary defects outside the glomerulus. The present report illustrates an adult case of secondary focal and segmental glomerulosclerosis with a dominant tubulointerstitial damage that led to the pursue of its cause at the tubular level. In this patient with an undiagnosed family history of adult kidney disease, a genetic study unraveled a mutation in the mucin-1 gene and a final diagnosis of adult dominant tubular kidney disease-MUC1 was made.

Identifiers

PMID30155326
PMCPMC6091430
OpenAlexW2885347703

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.