MORL Screening Methodology

Radial immunodiffusion (RID)

  • 1ml frozen EDTA plasma

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  • 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.

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Factor B (MW: 93 kDa) is a complement protein unique to the alternative pathway (AP). In the presence of C3b, FB binds to C3b to form the pre-convertase (C3bB). Factor D cleaves factor B releasing Ba (MW: 33 kDa) to generate the active proteolytic enzyme Bb (MW: 66kDa). The Bb subunit is the catalytically active site of the C3bBb C3 convertase complex and cleaves new C3 to C3a and C3b. If C3bBb recruits additional available C3b, the C5 convertase, C3bBbC3b, forms launching terminal pathway activation. C3 convertase can be dissociated by spontaneous decay or complement regulators (factor H, CR1). It can also be inactivated by factor I-mediated C3b cleavage in presence of cofactors.

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. In both DDD and C3GN, patients often have lower levels of factor B as compared to controls (p<0.001) consistent with dysregulation of the C3 convertase in both diseases (see Zhang et al. Defining the complement biomarker profile of C3 glomerulopathy, CJASN 2014).

Information

Quick Facts

  • CPT code: 86160 
  • Test code: 07FBL
  • Turnaround time: 2 weeks
  • Cost: $165
Requisition Form

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Background Knowledge

Complement factor B (MW: 93 kDa) plays a crucial role in the alternative pathway (AP) of the complement system, which is a key component of the innate immune response. When C3b is present, factor B binds and forms the pre-convertase C3bB. Factor D then cleaves factor B, releasing Ba (MW: 33 kDa) and generating the active proteolytic enzyme Bb (MW: 66 kDa). The Bb subunit of the C3bBb complex serves as the catalytically active site of C3 convertase and cleaves new C3 into C3a and C3b. If additional C3b is recruited by C3bBb, it forms the C5 convertase, C3bBbC3b, thereby initiating terminal pathway activation. The C3 convertase can undergo dissociation through spontaneous decay or interaction with complement regulators (such as factor H and CR1). C3b can also be inactivated by factor I-mediated cleavage in the presence of cofactors. FB levels can be consumed in cases of complement dysregulation (Zhang et al., 2014). 

The Clinical Diagnostics Service of the Molecular Otolaryngology & Renal Research Laboratories is a CLIA-approved, Joint Commission-accredited diagnostic laboratory.