Membranous nephropathy (MN) is a disease with an etiology and pathogenesis that are still not fully understood, and it represents a great challenge. It is characterized by a variable course, spontaneous remissions and relapses. The inability to rely entirely on antibodies and the continuous threat of a malignant disease make the differentiation of MN types extremely difficult. Data of twelve patients with membranous nephropathy, ranging in age between 28 and 67 years, are presented; in total, seven men and five women were observed for a period of 2 to 10 years. In all patients, the diagnosis was confirmed through kidney biopsy and laboratory tests, including immunological, histopathological, and immunohistochemical tests. Histopathological and immunohistochemical tests were applied on available material from the thyroid gland in two patients and the gallbladder in two patients with MN. Data of 102 patients with MN and their comorbidities are evaluated in order to establish correlations. These and other data are used to build a hypothetical pathogenetic model that explains the etiology and the likely pattern of disease occurrence. We found a connection between chronic cholecystitis, thyroiditis, hepatitis, and other diseases in the occurrence of MN and disease course. From our practice and cases, we drew the conclusion that chronic inflammation in sites that express PLA2R leads to the formation of antibodies against PLA2R. These antibodies occur as a preformed immune complex or separately and are deposited in the subepithelial space, leading to MN appearance.

The differentiation between primary and secondary forms of membranous nephropathy (MN) is a cornerstone that is necessary for adequate decision making regarding the treatment options and behavior of each specific case. Kidney biopsy and antibody results can be controversial, and a unique biomarker has still not been found. Background and Objectives: We investigated the lack of mannose-binding lectin (MBL) deposition in patients with secondary MNs (sMNs) with the presence of IgG4 deposition in relation to the presence of MBL deposition in patients with primary MNs (pMNs). We also established a connection between the stage of MN and MBL deposition. Materials and Methods: Materials from 72 renal biopsies with proven MN were used for immunohistochemistry staining (IHC) for the phospholipase A2 receptor (PLA2R), immunoglobulin subtype IgG4, and MBL. Patients were separated into one of the following three groups: primary MN (pMN), idiopathic MN (iMN), and secondary MN (sMN). Serum antibodies for PLA2R and thrombospondin type-I-domain-containing 7A (THSD7A) were also used for the precise evaluation of the type of MN, as well as for detecting positivity for PLA2R using IHC. Which stage of MN was present in relation to the deposition of MBL was evaluated. Results: In total, 50 patients were positive for IgG4, 34 with pMN, 12 with iMN, and 4 with sMN. A total of 20 patients were positive for MBL, 14 with pMN and 6 with iMN; no MBL deposits were found in patients with sMN. MBL positivity was predominantly present in the first two stages of MN, with a gradual reduction in the later stages. Conclusions: The activation of the lectin–complement pathway occurs in the early stages of the disease and is associated with the deposition of IgG4; IgG4 deposition is present in sMN, but there is no MBL deposition. IgG4 cannot be used for the differentiation of primary from secondary MNs, but the lack of MBL can be used as a marker for sMN in the early stages of the disease.

Russell body gastritis (RBG) is an unusual form of chronic inflammation characterized by accumulation of plasma cells containing Russell bodies (RB) in the gastric mucosa. Although its pathogenesis has not been fully evaluated, there is evidence to support a strong association with Helicobacter pylori infection. Only four cases of RBG in association with malignant epithelial gastric tumors were reported. We report the first case of RBG in peritumoral mucosa of a malignant gastrointestinal stromal tumor in association with coccoid form of Helicobacter pylori and a follow-up.

Leiomyosarcoma of the esophagus is a very rare disease, accounting for less than 0.5% of malignant esophageal tumors. Esophageal leiomyosarcoma combined with squamous cell carcinoma is even rarer than solitary leiomyosarcoma. To our knowledge, there are less than ten cases of simultaneously diagnosed leiomyosarcoma and squamous cell carcinoma of the esophagus. A 66-year-old male was admitted to our hospital suffering from epigastric pain, asthenia, weight loss, and difficulties when feeding with solid food which had been present for 2 weeks. A computed tomography scan showed a large tumor tissue mass in the mid-to-distal part of the esophagus. The patient underwent robot-assisted surgery—an esophagectomy with esophagogastrostomy. Histologically, the tumor consisted of highly pleomorphic spindle cells with multiple atypical mitosis and necrotic areas. An immunohistochemical examination was performed to distinguish leiomyosarcoma from spindle cell squamous carcinoma or malignant GIST. Tumor cells stained diffusely positive for smooth muscle actin, but negative for p63, CD117, and CKAE1/AE3. Tumor invasion involved mucosa and submucosa, without tunica muscularis propria. Microinvasive well-differentiated squamous cell carcinoma was also noted in the mucosa at the borders between the tumor and the healthy part of the esophagus. The aim of the manuscript is to present an extremely rare case of combined polypoid leiomyosarcoma and microinvasive squamous cell carcinoma of the esophagus, cured by robot-assisted surgical intervention and to emphasize that such cases should be examined carefully, including additional diagnostic tests such as Immunohistochemistry (IHC) in order to define the correct diagnosis.

Membranous nephropathy is a disease that has been well documented, yet its etiopathogenesis has not been fully clarified and the distinction between its primary and secondary forms has not been completely categorized. The discovery of new antigens and antibodies reveals different percentages of positivity in secondary membranous nephropathy, which is a cause of great confusion and ambiguity not only in diagnosis but also in the choice of a therapeutic approach. The aim of this review is to summarize the literature on newly discovered antigens and antibodies, and to propose a pathogenetic model based on the role of the complement system and its activation pathways. In this model, antigens are categorized based on the type of immunoglobulin deposits and the putative complement pathways that they activate, which can help to differentiate primary from secondary membranous nephropathy. The model also reflects how the deposition of foreign antigens in the basement membrane can activate both the lectin and classical complement pathways, which may explain why positive antibodies are observed in both primary and secondary forms of membranous nephropathy.