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Phospholipase A2 Receptor Autoantibodies, IgG

CPT: 83516
Updated on 08/4/2021
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Synonyms

  • Antibodies to the M-type Phospholipase A2 Receptor

Expected Turnaround Time

2 - 8 days

3 - 8 days

2 - 8 days


Related Documents


Specimen Requirements


Specimen

Serum


Volume

0.5 mL


Minimum Volume

0.2 mL (Note: This volume does not allow for repeat testing.)


Container

Red-top tube or gel-barrier tube


Collection

If a red-top tube is used, transfer separated serum to a plastic transport tube.


Storage Instructions

Room temperature


Stability Requirements

Temperature

Period

Room temperature

14 days

Refrigerated

14 days

Frozen

14 days

Freeze/thaw cycles

Stable x3


Test Details


Use

The anti-PLA2R ELISA (IgG) test kit is intended for the qualitative or semiquantitative determination of IgG class autoantibodies against phospholipase A2 receptor (PLA2R) in human serum.1 It is used as an aid in the diagnosis of primary membranous glomerulonephritis (pMGN), in conjunction with other laboratory and clinical findings.


Limitations

The test is not a standalone test but an adjunct to other clinical information. A diagnosis of membranous nephropathy (MN) should not be made on a single test result. The clinical symptoms, results on physical examination, and laboratory tests (eg, serological tests), when appropriate, should always be taken into account when considering the diagnosis of primary versus secondary MN.

Absence of circulating PLA2R autoantibodies does not rule out a diagnosis of PLA2R-related membranous nephropathy. Clinical evidence must not be overruled in favor of a numerical value.

The assay has not been demonstrated to be effective for monitoring the stage of disease or its response to treatment.

Borderline samples should be considered as potentially positive and retested.


Methodology

Enzyme-linked immunosorbent assay (ELISA)


Additional Information

Membranous nephropathy (MN) belongs to a family of kidney diseases characterized by inflammation and hypersensitivity of the glomeruli (glomerulitis) and/or interstitium (nephritis) of the kidney.2-4 The reported annual incident of MN amounts to 5 to 10 cases per million people in northern Europe.5 MN is an immunologically mediated disease characterized by the deposition of immune complexes at the glomerular basement membrane accompanied by a progressive reduction in kidney function in the majority of patients.2,4 As the disease progresses, thickening of the glomerular basement membrane can be seen by light microscopy, and thus the disease was initially referred to as "membranous glomerulonephritis."2,6 Immune deposits compromise the permeability of the capillary loops, leading to proteinuria and frequently to a nephrotic syndrome characterized by proteinuria, hypoalbuminemia, hyperlipidemia, and edema.7 MN accounts for approximately 20% of cases of nephrotic syndrome in adults.2 Approximately one-third of patients with MN will go on to develop end-stage renal failure within ten years.8 Another third will endure chronic proteinuria and symptoms of nephrotic syndrome while another third will experience spontaneous remission.8

MN can occur secondary to a number of clinical conditions, including infections (ie, hepatitis B and syphilis), systemic lupus erythematosus, cancer, and drug toxicity.2 MN that occurs independent of other known clinical syndromes is referred to as primary membranous nephropathy (pMN). This condition has historically been referred to as "idiopathic" MN because the etiology was unknown. Clinicians now realize that MN is an organ-specific autoimmune disease in which circulating autoantibodies bind to an intrinsic antigen on glomerular podocytes and form deposits of immune complexes on the glomerular capillary walls. Recent clinical studies have revealed that circulating autoantibodies to the podocyte M-type receptor for secretory phospholipase A2 (PLA2R) can be measured in 70% to 80% of patients with pMN.9 While the therapeutic approach to patients with secondary MN focuses on treating the underlying disease, patients with pMN are generally treated with an immunosuppressive strategy.10 It should be noted that a small fraction of individuals with secondary MN can been shown to be positive for anti-PLA2R.1-13 The clinical significance of this finding is unclear. The occurrence of anti-PLA2R autoantibodies in secondary forms of MN may simply be coincidental or may have some role in the development and progression of disease.

Levels of circulating anti-PLA2R have been shown to correlate with clinical disease activity, as measured by level of proteinuria.14 Anti-PLA2R levels have been shown to be of value for predicting the course of the disease in that a correlation was reported between the anti-PLA2R level and the clinical outcome.15,16 Renal failure has been reported to occur less frequently in patients with low anti-PLA2R levels,14 while spontaneous remissions are less common in patients with high levels.12,16 Gunnarsson and coworkers also found that patients with high antibody levels required an immunosuppressive therapy more often than those lower titers.16 This group also observed that antibody correlated with response to immunosuppressive therapy, defined as time from the start of therapy until remission.16 Several studies have reported that patients undergoing immunosuppressive therapy show a decline of anti-PLA2R levels and that autoantibodies levels rise during a relapse.6,10,15,17-20 Recent data suggest that in PLA2R-ab-positive patients, measuring PLA2R-abs at the end of therapy predicts the subsequent course.21

El-Zoghby and coworkers reported that pMN recurs in up to 40% of patients after renal transplantation.22 The risk for recurrence is higher when anti-PLA2R autoantibodies are detected prior to the transplantation.19


Footnotes

1. Dähnrich C, Komorowski L, Probst C, et al. Development of a standardized ELISA for the determination of autoantibodies against human M-type phospholipase A2 receptor membranous nephropathy. Clin Chim Acta. 2013 Jun 5; 421:213-218. 23541686
2. Ronco P, Debiec H. Pathogenesis of membranous nephropathy: Recent advances and future challenges. Nat Rev Nephrol. 2012 Feb 28; 8(4):203-213. 22371247
3. Glassock RJ. Pathogenesis of membranous nephropathy: A new paradigm in evolution. Contrib Nephrol. 2013; 181:131-142. 23689575
4. Debiec H, Ronco P. Immunopathogenesis of membranous nephropathy: An update. Semin Immunopathol. 2014 Jul; 36(4):381-397. 24715030
5. McQuarrie EP, Mackinnon B, Stewart GA, Geddes CC, Scottish Renal Biopsy Registry. Membranous nephropathy remains the commonest primary cause of nephrotic syndrome in a northern European Caucasian population. Nephrol Dial Transplant. 2010 Mar; 25(3):1009-1010. 20037184
6. Beck LH Jr, Salant DJ. Membranous nephropathy: Recent travels and new roads ahead. Kidney Int. 2010 May; 77(9):765-770. 20182413
7. Scheidat S, Stahl RA. Membranous glomerulonephritis. Internist (Berl). 2003 Sep; 44(9):1120-1130. 14566465
8. Steinman TI, Nissenson AR, Glassock RJ, et al. L-carnitine use in dialysis patients: Is national coverage for supplementation justified? What were CMS regulators thinking—or were they? Nephrol News Issues. 2003 Apr; 17(5):28-36. 12715624
9. Beck Jr LH, Bonegio RG, Lambeau G, et al. M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med. 2009 Jul 2; 361(1):11-21. 19571279
10. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis work group. KDIGO clinical practice guideline for glomerulonephritis. Kidney Int Suppl. 2012; 2:186-197.
11. Beck LH Jr, Salant DJ. Membranous nephropathy: From models to man. J Clin Invest. 2014 Jun; 124(6): 23.7-2314. 24892704
12. Gunnarsson I, Schlumberger W, Rönnelid J. Antibodies to M-type phospholipase A2 receptor (PLA2R) and membranous lupus nephritis. Am J Kidney Dis. 2012 Apr; 59(4):585-586. 22177657
13. Qin W, Beck LH Jr, Zeng C, et al. Anti-phospholipase A2 receptor antibody in membranous nephropathy. J Am Soc Nephrol. 2011 Jun; 22(6):1137-1143. 21566055
14. Hofstra JM, Beck Jr LH, Beck DM, Wetzels JF, Salant DJ. Anti-phospholipase A(2) receptor antibodies correlate with clinical status in idiopathic membranous nephropathy. Clin J Am Soc Nephrol. 2011 Jun; 6(6):1286-1291. 21474589
15. Kanigicherla D, Gummadova J, McKenzie EA, et al. Anti-PLA2R antibodies measured by ELISA predict long-term outcome in a prevalent population of patients with idiopathic membranous nephropathy. Kidney Int. 2013 May; 83(5):940-948.23364522
16. Hoxha E, Thiele I, Zahner G, et al. Phospholipase A2 receptor autoantibodies and clinical outcome in patients with primary membranous nephropathy. J Am Soc Nephrol. 2014 Jun; 25(6):1357-1366. 24610926
17. Beck LH Jr, Fervenza FC, Beck DM, et al. Rituximab-induced depletion of anti-PLA2R autoantibodies predicts response in membranous nephropathy. J Am Soc Nephrol. 2011 Aug; 22(8):1543-1550. 21784898
18. Hoxha E, Harendza S, Zahner G, et al. An immunofluorescence test for phospholipase-A2-receptor antibodies and its clinical usefulness in patients with membranous glomerulonephritis. Nephrol Dial Transplant. 2011 Aug; 26(8):2526-2532. 21633097
19. Stahl R, Hoxha E, Fechner K. PLA2R autoantibodies and recurrent membranous nephropathy after transplantation. N Engl J Med. 2010 Jul 29; 363(5):496-498. 20818871
20. Hofstra JM, Fervenza FC, Wetzels JF. Treatment of idiopathic membranous nephropathy. Nat Rev Nephrol. 2013 Aug; 9(8):443-458. 23820815
21. Bech AP, Hofstra JM, Brenchley PE, Wetzels JF. Association of anti-PLA2R antibodies with outcomes after immunosuppressive therapy in idiopathic membranous nephropathy. Clin J Am Soc Nephrol. 2014 Aug 7; 9(8):1386-1392. 25035272
22. El-Zoghby ZM, Grande JP, Fraile MG, Norby SM, Fervenza FC, Cosio FG. Recurrent idiopathic membranous nephropathy: Early diagnosis by protocol biopsies and treatment with anti-CD20 monoclonal antibodies. Am J Transplant. 2009 Dec; 9(12):2800-2807. 19845581

LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
141330 Anti-PLA2R 73737-9 141331 Anti-PLA2R RU/mL 73737-9

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