Abstract
Since urine samples more directly reflect kidney alterations and damage than blood samples, we investigated whether urine anti-PLA2R antibody (uPLA2R-Ab) could be utilized similarly to serum anti-PLA2R antibody (sPLA2R-Ab) as a noninvasive biomarker of idiopathic membranous nephropathy (IMN). In this study, we performed a qualitative analysis using an indirect immunofluorescence test (IIFT) and measured uPLA2R-Ab and sPLA2R-Ab concentrations using an enzyme-linked immunosorbent assay (ELISA) in 28 patients with biopsy-proven IMN and 12 patients with secondary membranous nephropathy (SMN). Overall, 64.3% (n=18) of patients with IMN had IIFT-positive sPLA2R-Ab, 67.9% (n=19) of patients with IMN had IIFT-positive uPLA2R-Ab, and none of the SMN patients had IIFT-positive sPLA2R-Ab or uPLA2R-Ab. The titers of the anti-PLA2R antibody from the IMN patients in the urine (10.72±22.24 RU/μmol, presented as uPLA2R-Ab/urine creatinine) and serum (107.36±140.93 RU/ml) were higher than those from the SMN patients (0.51±0.46 RU/μmol, 0.008±0.029 RU/ml, respectively, p<0.05). Statistical analyses indicated that there were positive correlations between uPLA2R-Ab and gPLA2R, sPLA2R-Ab or urinary protein and negative correlations between uPLA2R-Ab and serum albumin in patients with IMN. In conclusion, uPLA2R-Ab is a novel biomarker of IMN. sPLA2R-Ab combined with uPLA2R-Ab might be more helpful for diagnosis and activity in PLA2R associated MN.
Highlights
Membranous nephropathy (MN) is a major cause of nephrotic syndrome in adults [1,2,3], a leading cause of end-stage renal disease in patients with primary glomerulonephritis and the primary glomerulonephritis that recurs after kidney transplantation [4]
Among the 12 secondary membranous nephropathy (SMN) patients, 7 patients were diagnosed with systemic lupus erythematosus, 3 with connective tissue disease, and 2 with hepatitis B virus (HBV)-associated nephritis
No significant differences in weight, age, proteinuria, serum albumin, serum creatinine or estimated glomerular filtration rate were found between idiopathic membranous nephropathy (IMN) and SMN patients
Summary
Membranous nephropathy (MN) is a major cause of nephrotic syndrome in adults [1,2,3], a leading cause of end-stage renal disease in patients with primary glomerulonephritis and the primary glomerulonephritis that recurs after kidney transplantation [4]. An accurate pathological diagnosis can be made using immunofluorescence, light microscopy and electron microscopy [5], the definitive pathophysiology of idiopathic membranous nephropathy remains unclear. IMN is considered an autoimmune disease due to the landmark discovery of the phospholipase A2 receptor (PLA2R), which was found to be targeted by circulating antibodies in 70%-80% of adult patients with. In addition to PLA2R, thrombospondin type-1 domain-containing 7A (THSD7A) is another relevant autoantigen, and circulating autoantibodies against this protein have been detected in 5-10% of patients who are negative for anti-PLA2R [8].
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