Recurrent membranous nephropathy with a possible alteration in the etiology: a case report.


Journal

BMC nephrology
ISSN: 1471-2369
Titre abrégé: BMC Nephrol
Pays: England
ID NLM: 100967793

Informations de publication

Date de publication:
06 07 2021
Historique:
received: 29 01 2021
accepted: 24 06 2021
entrez: 7 7 2021
pubmed: 8 7 2021
medline: 8 2 2022
Statut: epublish

Résumé

Phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type-1 domain-containing 7A (THSD7A) are the two major pathogenic antigens for membranous nephropathy (MN). It has been reported that THSD7A-associated MN has a higher prevalence of comorbid malignancy than PLA2R1-associated MN. Here we present a case of MN whose etiology might change from idiopathic to malignancy-associated MN during the patient's clinical course. A 68-year-old man with nephrotic syndrome was diagnosed with MN by renal biopsy. Immunohistochemistry showed that the kidney specimen was negative for THSD7A. The first course of corticosteroid therapy achieved partial remission; however, nephrotic syndrome recurred 1 year later. Two years later, his abdominal echography revealed a urinary bladder tumor, but he did not wish to undergo additional diagnostic examinations. Because his proteinuria increased consecutively, corticosteroid therapy was resumed, but it failed to achieve remission. Another kidney biopsy was performed and revealed MN with positive staining for THSD7A. PLA2R1 staining levels were negative for both first and second biopsies. Because his bladder tumor had gradually enlarged, he agreed to undergo bladder tumor resection. Pathological examination indicated that the tumor was THDS7A-positive bladder cancer. Subsequently, his proteinuria decreased and remained in remission. This case suggests that the etiology of MN might be altered during the therapeutic course. Intensive screening for malignancy may be preferable in patients with unexpected recurrence of proteinuria and/or change in therapy response.

Sections du résumé

BACKGROUND
Phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type-1 domain-containing 7A (THSD7A) are the two major pathogenic antigens for membranous nephropathy (MN). It has been reported that THSD7A-associated MN has a higher prevalence of comorbid malignancy than PLA2R1-associated MN. Here we present a case of MN whose etiology might change from idiopathic to malignancy-associated MN during the patient's clinical course.
CASE PRESENTATION
A 68-year-old man with nephrotic syndrome was diagnosed with MN by renal biopsy. Immunohistochemistry showed that the kidney specimen was negative for THSD7A. The first course of corticosteroid therapy achieved partial remission; however, nephrotic syndrome recurred 1 year later. Two years later, his abdominal echography revealed a urinary bladder tumor, but he did not wish to undergo additional diagnostic examinations. Because his proteinuria increased consecutively, corticosteroid therapy was resumed, but it failed to achieve remission. Another kidney biopsy was performed and revealed MN with positive staining for THSD7A. PLA2R1 staining levels were negative for both first and second biopsies. Because his bladder tumor had gradually enlarged, he agreed to undergo bladder tumor resection. Pathological examination indicated that the tumor was THDS7A-positive bladder cancer. Subsequently, his proteinuria decreased and remained in remission.
CONCLUSIONS
This case suggests that the etiology of MN might be altered during the therapeutic course. Intensive screening for malignancy may be preferable in patients with unexpected recurrence of proteinuria and/or change in therapy response.

Identifiants

pubmed: 34229600
doi: 10.1186/s12882-021-02457-0
pii: 10.1186/s12882-021-02457-0
pmc: PMC8258946
doi:

Substances chimiques

Adrenal Cortex Hormones 0
Autoantibodies 0
PLA2R1 protein, human 0
Receptors, Phospholipase A2 0
THSD7A protein, human 0
Thrombospondins 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

253

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Auteurs

Ayumi Matsumoto (A)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

Isao Matsui (I)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan. matsui@kid.med.osaka-u.ac.jp.

Keiji Mano (K)

Department of Nephrology, Daini Osaka Police Hospital, 2-6-40, Karasuga-tsuji, Tennoji, Osaka, 543-8922, Japan.

Hitoshi Mizuno (H)

Department of Nephrology, Daini Osaka Police Hospital, 2-6-40, Karasuga-tsuji, Tennoji, Osaka, 543-8922, Japan.

Yusuke Katsuma (Y)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

Seiichi Yasuda (S)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

Karin Shimada (K)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

Kazunori Inoue (K)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

Takashi Oki (T)

Department of Urology, Mimihara General Hospital, 4-465, kyowacho, Sakai-ku, Sakai, Osaka, 590-8505, Japan.

Tadashi Hanai (T)

Department of Urology, Daini Osaka Police Hospital, 2-6-40, Karasuga-tsuji, Tennoji, Osaka, 543-8922, Japan.

Keiko Kojima (K)

Department of Pathology, Daini Osaka Police Hospital, 2-6-40, Karasuga-tsuji, Tennoji, Osaka, 543-8922, Japan.

Tetsuya Kaneko (T)

Department of Nephrology, Daini Osaka Police Hospital, 2-6-40, Karasuga-tsuji, Tennoji, Osaka, 543-8922, Japan.

Yoshitaka Isaka (Y)

Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

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Classifications MeSH