Evidence map›Paper›PMID 32680573›Full record

ArticleBMC nephrology2020

Nephrotic syndrome due to minimal-change disease superimposed on anti-glomerular basement membrane antibody positive glomerulonephritis; a case report.

Yuko Shibata, Kazuhito Fukuoka, Riyo Yokota, Heryon Lee, Hikaru Sayo, Noriko Ikegaya, Kiyotaka Mori, Jin Yamamoto, Aya Isomura, Kiyotaka Nagahama and 4 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in BMC nephrology, 2020. 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
0.1field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
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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 2 institutions in 1 country.

Yuko ShibataDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Kazuhito FukuokaDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan. kfukuoka@ks.kyorin-u.ac.jp.ORCID 0000-0003-3974-3082
Riyo YokotaDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Heryon LeeDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Hikaru SayoDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Noriko IkegayaDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Kiyotaka MoriDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Jin YamamotoDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Aya IsomuraDepartment of Pathology, Kyorin University Hospital, Tokyo, Japan.
Kiyotaka NagahamaDepartment of Pathology, Kyorin University Hospital, Tokyo, Japan.
Hiroaki ShimoyamadaDepartment of Pathology, Kyorin University Hospital, Tokyo, Japan.
Takahisa KawakamiDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Yoshinori KomagataDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Shinya KanameDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, 6-20-2, Mitaka-shi, Tokyo, 181-8611, Japan.
Kyorin University · JPKyorin University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe prognosis for renal function in anti-GBM glomerulonephritis (anti-GBM GN) is extremely poor, and when renal impairment progresses severely, it is difficult to expect improvement. In addition, it is also known that once the disease activity can be controlled by aggressive treatment, its recurrence is rare. We experienced an anti-GBM GN that improved from severe renal dysfunction and relapsed. A possible cause was the superimpose of nephrotic syndrome due to minimal change disease (MCD). CASE PRESENTATION: A 30-year-old man was admitted to our hospital because of general malaise, fever, oliguria and renal dysfunction. The patient's laboratory data showed serum creatinine as high as 6.6 mg/dl, and severe inflammation (C-reactive protein 20.6 mg/dl). Anti-glomerular basement membrane antibody (anti-GBM Ab) was detected in his serum, which led to the diagnosis of anti-GBM GN. Treatment was initiated with high-dose glucocorticoid (GC) and plasma exchange therapy (PE), and the patient's renal function and oliguria improved rapidly and he was discharged 40 days after admission. Renal biopsy findings showed cellular crescents associated with linear IgG depositions along the glomerular tufts compatible with anti-GBM GN, but only about one-third of the glomeruli was involved, suggesting that it still remains an early stage of the disease. However, 2 months after discharge, he had a relapse and was readmitted due to severe proteinuria with positive anti-GBM Ab. On the second admission, after high-dose GC and PE combined with intravenous cyclophosphamide, and remission was achieved. Despite the relatively minor renal biopsy findings, the patient showed rapid renal dysfunction and relatively rapid improvement with our treatment. Electron microscopy of the renal biopsy tissue showed significant foot process effacement on podocytes in the apparently normal glomeruli, without electron dense deposits.

conclusionOn the basis of clinical course and renal pathology, it is suggested that the present case was a rare complication of an early stage of anti-GBM GN and minimal change nephrotic syndrome. Although the simultaneous development of anti-GBM GN and MCD with anti-GBM antibody is unclear, it might have been precipitated by influenza infection or some unknown factor.

Indexed as

AdultAnti-Glomerular Basement Membrane DiseaseAutoantibodiesCyclophosphamideGlucocorticoidsHumansImmunosuppressive AgentsKidney GlomerulusMaleMicroscopy, ElectronNephrosis, LipoidNephrotic SyndromePlasma ExchangePodocytesRecurrenceantiglomerular basement membrane antibodyAutoantibodiesCyclophosphamideGlucocorticoidsImmunosuppressive AgentsAnt-glomerular basement antibody glomerulonephritis (anti-GBM GN)Anti-glomerular basement antibody disease (anti-GBM disease)Atypical-anti-GBM glomerulonephritisIntravenous cyclophosphamideMinimal change nephrotic syndrome (MCNS)Plasma exchange

Identifiers

PMID32680573
PMCPMC7368767
OpenAlexW3042734716

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Registered trials

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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.