A 30-year-old woman on steroid therapy for eosinophilia presented with nephrotic syndrome during steroid tapering. She was diagnosed with membranous nephropathy (MN) stage II-III (positive for IgG1 and IgG4) by renal biopsy. There was no evidence of secondary MN. Her urinary protein level was controlled to 0.5 g/day or less, and her eosinophil count in white blood cell differential was stabilized at less than 10% without increasing the steroid dosage. The renal specimen did not show any enhanced granular expression of PLA2R along the glomerular basement membrane, and PLA2R was not detected in the patient's serum. On retrospective analysis, enhanced granular staining for thrombospondin type-1 domain-containing 7A (THSD7A) in the glomeruli was detected in the biopsy, and anti-THSD7A IgG was detected in the serum using a commercial indirect immunofluorescence test (IFT). Based on these, the case was considered as THSD7A-associated MN with comorbid eosinophilia. The causal relationship between THSD7A-related MN and eosinophilia was unclear. However, a few cases of THSD7A-associated MN with eosinophilia have been reported, and further clarification on the relationship between THSD7A-related MN and eosinophilia is warranted.
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http://dx.doi.org/10.1007/s13730-019-00430-3 | DOI Listing |
Nephrol Dial Transplant
January 2025
Manchester Institute of Nephrology and Transplantation, Manchester University NHS Foundation Trust, Manchester, UK.
Background And Hypothesis: The PLA2R antibody test is a valuable first-line diagnostic tool for primary membranous nephropathy (MN), helping to identify PLA2R-related MN and potentially eliminating the need for a kidney biopsy in some individuals. By reducing the reliance on biopsies, the test streamlines diagnosis and improves patient care. However, determining the optimal PLA2R measurement method and cut-off is critical to maximising the benefits of the test and minimising any harms.
View Article and Find Full Text PDFBackground: With the increasing prevalence of membranous nephropathy (MN), the gut microbiome (GM) is increasingly implicated in its cause, yet the intricate mechanisms remain unclear. Whether changes in the diversity and richness of gut microbial populations among MN patients contribute to disease prevalence is still unanswered, necessitating further exploration into the potential causative link between the GM and MN.
Methods: We conducted a comprehensive bidirectional Mendelian randomization (MR) study.
Am J Physiol Renal Physiol
January 2025
Department of Medicine, Boston Medical Center and Department of Medicine, Boston University. Chobanian & Avedisian School of Medicine.
Transcriptomic analysis of microdissected human glomeruli has suggested novel molecular signatures associated with MN by revealing several genes differentially upregulated in MN compared to other glomerular diseases. We focused on a novel protein, Family with sequence similarity 114 member A1 (FAM114A1) that was identified as the top classifier gene in the dataset. To determine the localization of FAM114A1 within glomeruli, we performed immunofluorescence (IF) staining on normal human kidney specimens.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Shanxi Genetic Engineering Center for Experimental Animal Models, The Fifth Hospital (Shanxi Provincial People's Hospital) of Shanxi Medical University, Taiyuan, Shanxi, China.
Phospholipase A2 receptor 1 (PLA2R1) exists in many animals and plays an important role in membranous nephropathy. In this study, we aimed to evaluate a PLA2R1 knock-in rat model with repaired kidney function to study the molecular mechanisms of membranous nephropathy. We constructed the PLA2R1 knockout [PLA2R1(-)] model and PLA2R1 knock in [PLA2R1(+)] model in rats.
View Article and Find Full Text PDFComb Chem High Throughput Screen
January 2025
Department of Nephrology, the First Affiliated Hospital of Hebei University of Traditional Chinese Medicine, Shijiazhuang 050011,China.
Background: Shengyang Yiwei Decoction showed efficacy in idiopathic membranous nephropathy treatment, and this study aimed to assess the underlying molecular mechanisms.
Methods: Rats with passive Heymann nephritis were divided into the model group, the Shengyang Yiwei Decoction group, the JAK2 inhibitor group, and the STAT3 inhibitor group. Healthy rats served as the normal control.
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