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J Nephropathol. 2013 Oct;2(4):241-8. doi: 10.12860/JNP.2013.38. Epub 2013 Oct 1.

Anti-phospholipase A2 receptor antibody in idiopathic membranous nephropathy: A report from Iranian population.

Author information

1
DrugApplied Research and 2Chronic kidney disease research center, Tabriz University of Medical Sciences.Tabriz, Iran. ;
2
Department of Nephrology, Urmia University of medical sciences, Urmia, Iran.
3
; Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
4
Department of Nephrology, Division of Nephropathology, Isfahan University of Medical Science, Isfahan, Iran.
5
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
6
Immunogenetic research center, Department of Immunology, Tehran University of Medical Science, Tehran, Iran.

Abstract

BACKGROUND:

Idiopathic Membranous Nephropathy (iMN) is the most common cause of nephrotic syndrome in adults. Approximately one third of patients with iMN progress to end-stage renal disease. Anti-phospholipase A2-receptor (anti-PLA2R) antibodies are present in patients with iMN and appear to play a role in the pathogenesis of iMN.

OBJECTIVES:

In this study, we explored the prevalence of anti-PLA2R antibodies in a cohort of patients with iMN in Iran. We also sought to determine circulating levels of anti-secretory PLA2 (anti-sPLA2) antibodies in those with anti-PLA2R antibodies.

PATIENTS AND METHODS:

Using an indirect immunofluorescence assay, we measured anti-PLA2R antibodies in a group of patients with iMN in Iran. The serum levels of anti-sPLA2 antibodies were also measured in those with positive results for anti-PLA2R antibodies.

RESULTS:

We studied 23 patients with iMN (M/F 12/11, 34±9.8 year), two patients with secondary MN and five patients  with the nephrotic syndrome of other causes.Anti-PLA2R antibodies were detected in 17/23 (74%) of patients with iMN, but not in those with secondary MN or other forms of primary glomerular diseases. We found no correlation between anti-PLA2R antibody titer and the degree of proteinuria. We found high titers of anti-sPLA2 antibodies in a subset of patients with high levels of anti-PLA2R antibodies.

CONCLUSIONS:

Anti-PLA2R antibodies are specific for iMN. Proteinuria may also reflect glomerular structural damage rather than immunological activity of the disease. The preliminary idea of any presumptive role of anti-sPLA2antibodies in iMN needs further  investigation.

KEYWORDS:

Anti-phospholipase A2 antibodies nephrotic syndrom; Anti-phospholipase A2-receptor antibodies; End-stage renal disease; Idiopathic membranous nephropathy

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