Background: Crescent formation is rare in primary membranous nephropathy (MN). The mechanism of crescent formation is unknown and the treatments are tentative.
Patient Concerns: A 71-year-old woman presented with nephrotic syndrome, hematuria, and rapidly progressive kidney dysfunction.
Diagnosis: Kidney biopsy was performed, and the diagnosis was MN in combination with crescentic glomerulonephritis. Circulating anti-PLA2R was detected of a high level.
Interventions: The patient received rituximab besides corticosteroids.
Outcomes: The patient achieved complete remission of proteinuria and recovery of kidney function.
Conclusion: Our case suggests that there is a pathologic feature of MN and crescents in the absence of known immunologic factors as well as rituximab could serve as an effective cure and could be considered in serious MN conditions.
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http://dx.doi.org/10.1097/MD.0000000000030663 | DOI Listing |
Medicine (Baltimore)
January 2025
Division of Nephrology, Department of Medicine, National University Hospital, Singapore.
Rationale: We report the efficacy of combination prednisolone and intravenous (IV) rituximab as an immunosuppressive regimen for a young male presenting with extensive venous thromboembolism including a submassive pulmonary embolism secondary to life-threatening nephrotic syndrome from very high risk anti-phospholipase-A2 receptor (PLA2R) positive membranous nephropathy. Initial treatment was with mechanical thrombectomy and anticoagulation. Thereafter, oral prednisolone was initiated to induce remission, during a period of uninterrupted anticoagulation.
View Article and Find Full Text PDFBackground: The recurrence of primary glomerulonephritis (GN) following kidney transplantation poses a significant threat to graft survival. To enhance kidney transplant outcomes, we must lessen the burden of recurrence. In recent years, there has been progress in understanding the incidence, risk factors for recurrence, pathophysiology, biomarkers, and therapeutics, making it worthwhile to conduct an update on primary glomerulonephritis that may recur following kidney transplantation.
View Article and Find Full Text PDFTheranostics
January 2025
Department of Nephrology, China-Japan Friendship Hospital (Institute of Clinical Medical Sciences), Beijing, 100029, China.
The tertiary structure of normal podocytes prevents protein from leaking into the urine. However, observing the complexity of podocytes is challenging because of the scale differences in their three-dimensional structure and the close proximity between neighboring cells in space. In this study, we explored podocyte-secreted angiopoietin-like 4 (ANGPTL4) as a potential morphological marker via super-resolution microscopy (SRM).
View Article and Find Full Text PDFJ Clin Med
December 2024
Clinical Department of Nephrology, Transplantation Medicine and Internal Diseases, Wroclaw Medical University, 50-556 Wroclaw, Poland.
Anti-ETAR (endothelin A receptor) antibodies and anti-CXCR3 (C-X-C motif chemokine receptor 3) antibodies are types of non-HLA (human leukocyte antigens) antibodies that could have some influence on the course of glomerulonephritis. The authors aimed to study the influence of these antibodies' levels on the course of specific glomerulonephritis types. We evaluated the anti-ETAR and anti-CXCR3 antibody levels in the serum of patients with membranous nephropathy (n = 18), focal and segmental glomerulosclerosis (FSGS) (n = 25), systemic lupus erythematosus (n = 17), IgA nephropathy (n = 14), mesangiocapillary glomerulonephritis (n = 6), anti-neutrophil cytoplasmic antibodies (c-ANCA) vasculitis (n = 40), and perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) vasculitis (n = 16), and we compared their levels with the control group (n = 22).
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Unit of Nephrology, Dialysis and Transplantation and Laboratory of Molecular Nephrology, Core Facilities-Proteomics Laboratory, 16147 Genoa, Italy.
Historically, oxidants have been considered mechanisms of glomerulonephritis, but a direct cause-effect correlation has never been demonstrated. Several findings in the experimental model of autoimmune conditions with renal manifestations point to the up-regulation of an oxidant/anti-oxidant system after the initial deposition of autoantibodies in glomeruli. Traces of oxidants in glomeruli cannot be directly measured for their rapid metabolism, while indirect proof of their implications is derived from the observation that Superoxide Oxidase 2 (SOD2) is generated by podocytes after autoimmune stress.
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