Immune-mediated membranous nephropathy: Long term fluconazole usage caused podocyte autophagy.

The primary consequences of membranous nephropathy (MN) are the development of nephrotic syndrome including hypogammaglobulinemia, the increased infectious risk, the loss of protein-bound vitamin D, and, above all, an elevated thromboembolic incidence of up to 50% in severe proteinuria patients. Membrane nephropathy may be either idiopathic or primary, not recognized (70%-80%) or secondary (20%-30%) to pathological sicknesses such as hepatitis B, systemic lupus erythematosus, malignancies, and side-effects of medicines. The immunological responses in MN involve multiple components: immunoglobulin G (IgG), long-escaped antigens, and the membrane attachment complex, formed by the supplement to form C5b-9.

A study of altered calcium sensing system caused primary membranous nephropathy to end-stage renal failure.

PMN (primary membranous nephropathy) is the most prevalent source of idiopathic nephrotic syndrome, which further progressed to ESRD (end-stage renal disease) in non-diabetic adults worldwide. Autoantibodies circulating against podocyte membrane proteins PLA2R1 and THSD7A are present in approximately 75-80% of incidents. Furthermore, a research presented an unusual case of IgG4-RD correlated with elevated serum levels of calcium concluded that renal irregularities have been preceded and triggered by hypercalcemia.

Rituximab for the management of idiopathic membranous nephropathy: a meta-analysis.

Purpose: The aim of this study was to evaluate the efficacy of rituximab therapy in the management of idiopathic membranous nephropathy (IMN).

Methods: After literature search, data from eligible studies were used to perform random-effects meta-analyses to estimate remission rates and changes in proteinuria at the latest follow-up after rituximab therapy. The outcomes were used for metaregression to identify the factors affecting the efficacy of rituximab.