MORL FH Autoantibody
| Label Mnemonic: | FH |
| Epic code: | LAB7432 |
| Downtime form: | Doctor/Provider Orders - Pathology Core and Specialty Care Nursery |
Commercial Mailout Laboratory
6240-8 RCP
356-8593
6240-8 RCP
356-8593
Specimen(s):
Whole Blood (Note: Serum separators with “clot activators” should not be used for the serum samples)
Specimen
Instructions:
Must include the following information:
- Patient identifiers (full name, date of birth, sex and medical record number)
- Pertinent history and clinical findings
- Date of collection & sample type
- Ordering physician
Collection Medium:
 |
| Red top tube 5 mL (Clot Activator) |
Minimum:
Preferred Minimum: 1 mL serum from whole blood
Absolute Minimum: 0.5 mL serum from whole blood
Absolute Minimum: 0.5 mL serum from whole blood
Rejection Criteria:
If samples do not arrive in the reference laboratory labeled (patient name, patient date of birth and sample type) and frozen after processing immediately, they will be rejected for testing.
Delivery Instructions:
Keep on ice and deliver to laboratory immediately. Samples accepted Monday-Friday.Turn Around
Time:
2 weeks upon receipt at reference laboratory
Reference Range:
Normal: <200 AU
Reported as negative, unknown significance, or positive
Reported as negative, unknown significance, or positive
Interpretive Data:
Factor H Autoantibodies
Dense Deposit Disease (DDD, aka Membranoproliferative Glomerulonephritis Type II, MPGNII)
Factor H autoantibodies have been associated with DDD (Meri et al., 1992). In patients with DDD, these autoantibodies bind to and block the N-terminal region of the Factor H protein, which compromises its fluid-phase regulatory function.
Atypical Hemolytic-Uremic Syndrome
Factor H autoantibodies are identified in ~10% patients with aHUS (Dragon-Durey, et al 2005, Moore, et al 2010). Most but not all patients with aHUS who develop Factor H autoantibodies are homozygous for a known polymorphism, del(CFHR3-CFHR1). Homozygosity for this deletion is seen in 15% of patients with aHUS as compared to 5% of controls of northern European ancestry (Zipfel et al 2007, Skerka et al 2009). The Factor H autoantibodies in aHUS patients bind to and block the C-terminal region of the Factor H protein, which interferes with its surface regulatory function (Józsi et al 2007).
Sensitivity >99%
Dense Deposit Disease (DDD, aka Membranoproliferative Glomerulonephritis Type II, MPGNII)
Factor H autoantibodies have been associated with DDD (Meri et al., 1992). In patients with DDD, these autoantibodies bind to and block the N-terminal region of the Factor H protein, which compromises its fluid-phase regulatory function.
Atypical Hemolytic-Uremic Syndrome
Factor H autoantibodies are identified in ~10% patients with aHUS (Dragon-Durey, et al 2005, Moore, et al 2010). Most but not all patients with aHUS who develop Factor H autoantibodies are homozygous for a known polymorphism, del(CFHR3-CFHR1). Homozygosity for this deletion is seen in 15% of patients with aHUS as compared to 5% of controls of northern European ancestry (Zipfel et al 2007, Skerka et al 2009). The Factor H autoantibodies in aHUS patients bind to and block the C-terminal region of the Factor H protein, which interferes with its surface regulatory function (Józsi et al 2007).
Sensitivity >99%
Comments:
Please print, complete and submit the Kidney Testing Requisition Form from the Molecular Otolaryngology & Renal Research Laboratories, to Specimen Control/Mailouts with the specimen and the Epic Requisition.
Methodology:
Enzyme Linked Immuno-Sorbent Assay (ELISA) is used to assay the
presence of Factor H autoantibodies.
CPT Code:
83516