MEmbranous nePHropathy
Classify subtype, guide therapy, and monitor responses
Membranous nephropathy (MN) is one of the leading causes of nephrotic syndrome in adults. Our comprehensive menu of clinically validated pathology- and serum-based assays assists with diagnosis, monitors disease progression, and guides clinical outcomes.
Membranous nePHropathy test menu
Serum-based testing
We offer a comprehensive menu of clinically validated serum-based assays to assist with the diagnosis of MN, monitor disease progression, and guide clinical outcomes.
Key testing
- PMND1 | Primary Membranous Nephropathy Diagnostic Cascade, Serum
- Detects low levels of anti-PLA2R antibodies in patients with borderline or negative PLA2R ELISA results.
- Distinguishes PLA2R-associated MN from other antigen-associated MN in patients with biopsy-proven MN.
- Determines levels of anti-PLA2R antibodies to predict remission or disease relapse status.
- Determines relapse or presence of untreated disease in chronic kidney disease patients awaiting a transplant.
- Provides an alternative diagnostic option for some patients who cannot undergo a kidney biopsy due to contraindications.
- PLA2M | Phospholipase A2 Receptor, Monitoring, Enzyme-Linked Immunosorbent Assay, Serum
- PLA2I | Phospholipase A2 Receptor, Immunofluorescence, Serum
Highlights
John Lieske, M.D., describes Mayo Clinic Laboratories' new test for primary membranous nephropathy. PMND1 is a diagnostic cascade that provides a cost-effective approach to detecting antigens known to cause membranous nephropathy — a condition that can lead to kidney failure.
Tissue-based testing
Our new, one-of-a-kind mass spectrometry membranous nephropathy panel can identify 13 different antigens, which can help a physician diagnose, treat, or assess prognosis for their patients.
Key testing
- MSMN | Membranous Nephropathy Target Antigen Identification, Mass Spectrometry, Tissue
- This panel uses laser microdissection of the kidney tissue followed by tandem mass spectrometry, which can determine the underlying target antigen in 70%–80% of MN cases.
- Provides physicians with more answers than are currently available using traditional IF/IHC stains.
- This method requires significantly less kidney tissue to complete vs. individual IF/IHC stained slides, which can be helpful in cases where limited tissue is available.
Additional testing
- RPCWT | Renal Pathology Consultation, Wet Tissue
- Note: RPCWT automatically performs IF staining for PLA2R if MN is present (based on LM and IF). If PLA2R IF is negative, MSMN will be performed.
- SEMA3 | Semaphorin 3B (SEMA3B) Immunostain, Technical Component Only
- EXT2 | Exostosin 2 (EXT2) Immunostain, Technical Component Only
- PLAIF | Phospholipase A2 Receptor (PLA2R), Renal Biopsy
- THSIF | Thrombospondin Type 1 Domain Containing 7A (THSD7A), Immunofluorescence
- NELL1 | Neural Epidermal Growth Factor-Like 1 Protein Immunostain, Technical Component Only
Highlights
Sanjeev Sethi, M.D., Ph.D., explains how Mayo Clinic Laboratories' new mass spectrometry test (Mayo ID: MSMN) identifies most antigens now known to cause membranous nephropathy. Precise identification of antigens is important for optimal management of this serious kidney disease.
Mayo Clinic renal pathologist Dr. Sanjeev Sethi identified NELL-1 as a biomarker for membranous nephropathy (MN) in 2019. Two years later, Dr. Sethi helped implement the first ever IHC test to detect NELL-1 antigen, which appears in about 10% of MN patients and is linked to underlying malignancy.
Sanjeev Sethi, M.D., Ph.D., discusses how Mayo Clinic Laboratories’ new immunohistochemistry test for the detection of NELL-1 antigen, a biomarker for membranous nephropathy found in 10% to 15% of patients, provides diagnostic certainty and insight on disease expression.
References
- Sethi S, Beck LH, Glassock RJ, et all. Mayo Clinic consensus report on membranous nephropathy: proposal for a novel classification. Kidney Int. December 2023;104(6):1092-1102.
- Sethi S, Madden B. Mapping antigens of membranous nephropathy: almost there. Kidney Int. March 2023; 103(3):469-472.