ELEVATED MBL LEVELS AND ITS ASSOCIATION WITH ENDOTHELIAL DYSFUNCTION IN PMN

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DEEKSHA

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Co-author 1

NEERAJ INAMDAR nainamdar@gmail.com PGIMER NEPHROLOGY CHANDIGARH

Co-author 2

PRABHJOT KAUR prabhjotkaur311090@gmail.com PGIMER NEPHROLOGY CHANDIGARH

Co-author 3

MANPHOOL SINGHAL drmsinghal@yahoo.com PGIMER Radio diagnosis CHANDIGARH

Co-author 4

ANUPAM LAL dralal@rediffmail.com PGIMER Radio diagnosis CHANDIGARH

Co-author 5

UJJWAL GORSI ujjwalgorsi@gmail.com PGIMER Radio diagnosis CHANDIGARH

Co-author 6

Ritambhra Nada ritamduseja@yahoo.com PGIMER HISTOPATHOLOGY CHANDIGARH

Co-author 7

HARBIR SINGH KOHLI kohlihs2009@gmail.com PGIMER NEPHROLOGY CHANDIGARH

Co-author 8

VINOD KUMAR vinsh777@gmail.com PGIMER DERMATOLOGY CHANDIGARH

Co-author 9

RAJA RAMACHANDRAN drraja_1980@yahoo.co.in PGIMER NEPHROLOGY CHANDIGARH

Co-author 10

Co-author 11

Co-author 12

Co-author 13

Co-author 14

Co-author 15

Introduction

Primary membranous nephropathy (PMN) is an autoimmune disorder and a leading cause of nephrotic syndrome in adults. Phospholipase A2 receptor (PLA2R) is the commonest antigen against which circulating antibodies are formed in PMN. It is evident that PLA2R activates the MBL cascade resulting in glomerular damage and proteinuria. However, there are few reports which indicate association of aberrant MBL activation with endothelial dysfunction and accelerated atherosclerosis. Despite PMN being a common cause of adult nephrotic syndrome, there is a lack of studies on cardiovascular outcomes in PMN

Methods

MBL levels and Flow-mediated vasodilatation (FMD), a test for endothelial dysfunctions were assessed in 22 biopsy-confirmed PMN patients at baseline and post six months of immunosuppressive therapy (cyclical cyclophosphamide and glucocorticoid (cCYC/GC) or rituximab). Twenty-two healthy controls were included to measure the MBL levels and FMD.

Results

MBL levels in PMN patients were observed to be significantly higher than the healthy controls (p<0.01). Post immunosuppressive therapy MBL levels significantly went down compared to baseline (p = 0.03). The FMD was significantly lower in PMN patients (p<0.01) compared to healthy controls, further, there was significant improvement in FMD post treatment (p<0.0.1). Significant correlation of baseline MBL levels and baseline percentage of FMD (spearman correlation coefficient (ρ) = 0.605: p<0.01) was observed. In our PMN patient cohort 4 PMN patients out of 22 (18%) were non responder to immunosuppressive therapy. In these patients there was either no change or increase in MBL levels post treatment was observed compared to baseline. Also, no significant improvement in FMD and clinical parameters was observed post therapy. On the contrary, responder group had significant decrease in MBL levels post treatment and improvement in the FMD as well as clinical parameters.

Conclusions

From our study, we anticipate elevated MBL levels could be a risk factor for endothelial dysfunction in PMN patients. However, the findings of the study warranted further investigation in the larger cohort, but the observation opens the new arena for the relevance of MBL in the disease prognostication and its consideration for designing course of treatment for PMN patients.

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