MORL Screening Methodology
Enzyme linked immunosorbent assay (ELISA)
- 1ml frozen EDTA plasma
- EDTA plasma samples must be frozen to below -80°C immediately after separation from cells and shipped on dry ice. These samples remain viable for at least six months when stored at -80°C.
- All EDTA plasma samples MUST be processed and frozen down to -80°C immediately after collection
- Labeled with the sample type AND patient’s name, DOB, MRN and sex
- Cryovials should be put in zip lock bags and completely covered in dry ice to keep the sample frozen until it arrives in the lab
- Shipped overnight on at least 5 lbs of dry ice
- Shipping and receiving dock closed on weekends and holidays
- Deliveries accepted Monday - Friday
If samples arrive thawed they will be REJECTED.
The complement system consists of three initiating pathways - the classical, alternative and lectin - activation of which leads to the generation of C3 and C5 convertases. The latter initiates the sequential activation of the terminal pathway (C5 to C9) resulting in the formation of pore-forming membrane attack complex C5b-9 (MAC), a stable complex that mediates irreversible cell lysis. Fluid-phase C5b-9 complexes (soluble C5b-9) may also form in complex with regulatory proteins like protein S.
C3 Glomerulopathy (C3G): The common pathophysiological basis of both Dense Deposit Disease (DDD) and C3 Glomerulonephritis (C3GN) is dysregulation of the AP. Consumption of AP complement components is dependent on the degree of dysregulation of the C3 and C5 convertases. Soluble C5b-9 is elevated in both DDD and C3GN, but only the difference between C3GN and controls reaches statistical significance (p<0.001 for only C3GN) (see Zhang et al., Defining the complement biomarker profile of C3 glomerulopathy, CJASN 2014).
Atypical Hemolytic Uremic Syndrome: Soluble C5b-9 levels are elevated in the majority of patients with active atypical hemolytic uremic syndrome but less frequently when the disease is in remission. Soluble C5b-9 may be useful as a biomarker to monitor activity of terminal pathway of complement (Bu et al., Soluble C5b-9 as a biomarker for complement activation in atypical hemolytic uremic syndrome, AJKD 2015).
Quick Facts
- CPT code: 83520
- Test code: 06SMAC
- Turnaround time: 2 weeks
- Cost: $352
Background Information
The complement system comprises three primary initiating pathways: the classical, alternative, and lectin pathways. Activation of these pathways culminates in the generation of C3 and C5 convertases. C5 convertase initiates the sequential activation of the terminal pathway (C5 to C9), leading to formation of the pore-forming membrane attack complex C5b–9 (MAC). This stable complex mediates irreversible cell lysis. Additionally, fluid-phase C5b-9 complexes (soluble C5b-9) may form in conjunction with regulatory proteins such as protein S.
The shared pathophysiological mechanism underlying both Dense Deposit Disease and C3 Glomerulonephritis is the dysregulation of the alternative pathway of complement. The extent of consumption of alternative pathway complement components is contingent upon the degree of dysregulation of the C3 and C5 convertases. While soluble C5b-9 levels are elevated in both DDD and C3GN, the difference between C3GN and controls demonstrates statistical significance (p<0.001) for C3GN only (Zhang et al., 2014).
Soluble C5b-9 levels are elevated in many patients with active atypical hemolytic uremic syndrome/complement-mediated TMA but less frequently when the disease is in remission. Soluble C5b-9 may be useful as a biomarker to monitor activity of the terminal pathway of complement (Bu et al., 2015).
The Clinical Diagnostics Service of the Molecular Otolaryngology & Renal Research Laboratories is a CLIA-approved, Joint Commission-accredited diagnostic laboratory.