Evidence map›Paper›PMID 19937361›Full record

ArticleClinical and experimental nephrology2010

Genetical, histological, and clinical characteristics of IgA-negative mesangioproliferative glomerulopathy.

Kazunori Owada, Hodaka Suzuki, Tetsuo Katoh, Tsuyoshi Watanabe

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Article in Clinical and experimental nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 6 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Kazunori OwadaDepartment of Internal Medicine III, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima, 960-1295, Japan.
Hodaka Suzuki
Tetsuo Katoh
Tsuyoshi Watanabe
Fukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesangioproliferative glomerulopathy (MesPGN) is a well-defined pathohistological entity. However, the clinical characteristics and prognosis have not been fully established in patients without immunoglobulin (Ig)A (N-IgAN) in contrast to patients with IgA nephropathy (IgAN).

methodsA total of 837 consecutive patients underwent renal biopsies. Among them, 465 patients were diagnosed with MesPGN by light microscopy. With immunofluorescent study and electron microscopy (EM), 344 were diagnosed as having IgAN. Among the rest, 84 patients who had no immunofluorescence evidence of IgA and no deposits in EM were defined as N-IgAN. We compared the clinical characteristics, histological findings, and genotypes of the angiotensin-converting enzyme (ACE) gene and plasminogen activator inhibitor-1 gene between IgAN and N-IgAN patients.

resultsUrinary protein excretion and the degree of hematuria were significantly lower in N-IgAN than IgAN patients (0.50 vs. 0.82 g/day; P = 0.01), (1.33 vs. 2.50; P < 0.001, respectively). Creatinine clearance was higher in N-IgAN than IgAN patients (89.4 vs. 74.4 ml/min; P < 0.001). Histopathologically, N-IgAN patients had significantly less advanced glomerular and tubulointerstitial lesions than IgAN patients. Pathological grades in patients with untreated IgAN were more advanced in a time-dependent manner, whereas there was no relationship between histological grades and time of illness in N-IgAN patients. Frequency of the DD genotype of the ACE gene was significantly lower in N-IgAN (DD/ID+II = 8/76) than IgAN (24/90) patients.

conclusionsIgA-negative MesPGN is a distinct type of glomerulopathy with a benign renal prognosis. Insertion/deletion polymorphisms of the ACE gene may play some role in the genesis and progression of MesPGN.

Indexed as

AdultFemaleGlomerulonephritisGlomerulonephritis, IGAHumansKidney GlomerulusMaleMiddle AgedPeptidyl-Dipeptidase APlasminogen Activator Inhibitor 1ProteinuriaPeptidyl-Dipeptidase APlasminogen Activator Inhibitor 1

Identifiers

PMID19937361
OpenAlexW2021944402

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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.