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There is evidence to suggest that M‐type phospholipase A2 (PLA2R) antibodies activate the mannose‐binding lectin (MBL) cascade, resulting in glomerular damage and proteinuria in patients with primary membranous nephropathy (PMN). Furthermore, there are few reports indicating that aberrant MBL activation is associated with endothelial dysfunction and accelerated atherosclerosis. While PMN is a common cause of adult nephrotic syndrome, and patients are at increased risk of cardiovascular disease (CVD), there is a lack of research that explores the factors that contribute to this condition. This study aims to determine the MBL levels in PMN and their relation to the clinical activity and endothelial dysfunction in PMN. The MBL levels of 22 biopsy‐confirmed PMN patients were assessed at baseline and after 6 months of immunosuppressive therapy. In order to evaluate endothelial dysfunction in PMN patients, flow‐mediated vasodilation (FMD) was measured at baseline and after treatment. A total of 22 healthy controls were included in this study to measure MBL levels and FMD. A significant difference was observed between MBL levels in PMN patients and healthy controls (p <.01). MBL levels decreased significantly after immunosuppressive therapy (p =.04). The baseline MBL levels and FMD levels exhibited a strong correlation (Spearman correlation coefficient [ρ] = 0.51: p =.01). In conclusion, the study signals the activation of the MBL cascade and its association with endothelial dysfunction in PMN patients. [ABSTRACT FROM AUTHOR]

Background: Collapsing focal segmental glomerulosclerosis (cFSGS) is an aggressive glomerular disease presenting as a nephrotic syndrome that has lower rates of remission with conventional immunosuppressive therapy and rapidly progresses to end‐stage‐renal‐disease (ESRD). We report eight cases of HIV‐negative cFSGS treated with rituximab. Methods: The current report is a retrospective case series of cFSGS treated with rituximab from January 2011 to March 2020, at varying phases of the disease. Results: Eight out of the 70 cFSGS patients received rituximab. The median age of patients was 30 years (IQR 24.25‐37.5); five patients were males. The median serum creatinine, mean serum albumin and median 24 hours urinary protein at presentation was 0.9 (IQR 0.66‐1.27) mg/dL, 2.95 ± 1.15 g/dL, 4.87 (IQR 1.64‐5.75) g/day, respectively. Two patients were steroid‐resistant, one steroid and tacrolimus dependent, one steroid and cyclosporine dependent, two steroids and tacrolimus resistant, one steroid, tacrolimus, cyclophosphamide, mycophenolate mofetil resistant and one steroid‐resistant and tacrolimus dependent before rituximab therapy. Rituximab was given either as targeted therapy (after an initial dose of 375 mg/m2; patients having CD‐19 levels >5/μL or >1% at 1 month received additional low‐dose [100 mg] of rituximab), or weekly regimen. Five patients received CD‐19 targeted rituximab; three received weekly doses of 375 mg/m2, cumulative doses being 820 ± 228.03 mg, and 1800 ± 721.11 mg, respectively. At the end of median follow‐up of 15 months, five (62.5%) patients were in remission (three partial, two complete remissions), two (25%) were resistant to therapy; one (12.5%) progressed to ESRD. Conclusion: Rituximab is reasonably safe and achieves/maintains remission in 60% of cFSGS cases. SUMMARY AT A GLANCE: This is a retrospective study reporting the effects of Rituximab on 8 patients with the collapsing form of focal segmental glomerulosclerosis. Whilst retrospective in nature, the study suggested that rituximab might be a promising form of treatment for this condition, which is traditionally resistant to immunosuppression therapy, resulting in a remission rate of 60% with a reasonable safety profile. [ABSTRACT FROM AUTHOR]