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. In-addition, previous research also indicates an elevated amount of calcium in the blood of PMN patients. However, we also found conflicting evidence from previous studies showing that autoantibodies that suppress the calcium-sensing receptor (CaSR) induce a high level of calcium in some cases of IgG4RD. Notably, the calcium ion plays a critical function not only as intracellular signaling molecule but binds extracellular receptor activity to intracellular events. Moreover, the raise in intracellular calcium levels during PMN is known as a crucial event involved in the activation of numerous nucleases, proteases and implicitly facilitates the release of prostaglandins, cytokines and superoxide radicals capable of causing cell damage and death. Thus, the precise mechanism of the PMN disease to renal failure is not fully clear and the disease incidence differs among patients. Therefore, we are hypothesizing the role of disrupted calcium signaling in PMN that progress to ESRD.