Introduction

Membranous nephropathy (MN) is the most common cause of the nephrotic syndrome in Europe, with an incidence of 5–10/million/year in adults [1]. Although MN can occur secondary to infections, systemic diseases, use of drugs or malignancies, in most patients no underlying cause is identified [idiopathic membranous nephropathy (iMN)]. Recent studies have identified antibodies against the M-type PLA2-receptor, an antigen present on podocytes, in 70% of patients with iMN, thus establishing iMN as an autoimmune disease [2]. These findings were supported by a genome wide association study that found an association between PLA2R and iMN [3].

In this comment, we describe the management of patients with MN (Figure 1).

Fig. 1.

Flow chart: strategy for the management of patients with MN. D + M, duration and magnitude; CYP, cyclophosphamide; CNI, calcineurin inhibitor; MMF, mycophenolate mofetil.

Exclude secondary causes of MN

Secondary causes of MN are listed in Table 1. Most causes can be excluded by detailed medical history, a review of the patient’s drug history, physical examination and laboratory studies (Table 1). Awareness of a malignancy is particularly important in the elderly [1, 4]. The prevalence of a malignancy was 4.1% in patients <60 years and 19.4% in patients >60 years of age [5]. Studies have suggested that iMN can be differentiated from malignancy-related MN. Japanese investigators reported that glomerular staining for IgG1 was significantly stronger in malignancy-related MN, and equal to IgG4, whereas in iMN, there was predominant staining for IgG4 [6]. The French group reported an increased number of inflammatory cells in the glomerulus of patients with a malignancy [4]. Using a cutoff value of eight cells per glomerulus, specificity and sensitivity were 75 and 92%, respectively. Although promising, these data need validation. Preliminary data indicate that antibodies against …

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