Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

GBM
8106
GLP
9358
Reference Values:
Reporting Limit: 80 ng/mL
Plasma insulin concentrations have been shown to increase only
when plasma glipizide concentrations exceeded 200 ng/mL.
Toxic range has not been established.
Test Performed by: Medtox Laboratories, Inc.
402 W. County Road D
St. Paul, MN 55112
Glomerular Basement Membrane Antibodies, IgG, Serum
Clinical Information: Antibodies to glomerular basement membrane antigens (GBM antibodies)
cause glomerulonephritis, Goodpasture syndrome (glomerulonephritis, often with rapid onset renal
failure, and pulmonary hemorrhage), and, less commonly, pulmonary hemosiderosis.(1) Nephrogenic
GBM antigens are associated with the noncollagenous carboxyl extension of type IV procollagen. The
immunologic stimuli that elicit production of GBM antibodies are not known. There is some evidence
of a genetic association with HLA-DR2. GBM antibody-mediated glomerulonephritis and Goodpasture
syndrome occur with a bimodal age distribution primarily in males ages 20 to 40 and in patients older
than age 50. Glomerulonephritis without pulmonary involvement is more common in the older age
group, and shows a female predominance.
Useful For: Evaluating patients with rapid onset renal failure or pulmonary hemorrhage, as an aid in
the diagnosis of Goodpasture syndrome
Interpretation: Positive results are consistent with Goodpasture syndrome. Glomerular basement
membrane antibodies detected by immunoassay have been reported to be highly specific for
Goodpasture syndrome. The sensitivity of this test approaches 87% in untreated patients with systemic
disease.(1)
Reference Values:
or =1.0 U (positive)
Reference values apply to all ages.
Clinical References: Pusey CD: Anti-glomerular basement membrane disease. Kidney Int
2003;64:1535-1550
Glucagon, Plasma
Clinical Information: Glucagon is a single-chain polypeptide of 29 amino acids that is derived
from a larger precursor peptide (big plasma glucagon), which is cleaved upon secretion. The main sites
of glucagon production are the hypothalamus and pancreatic alpha-islet cells. The function of
hypothalamic glucagon is incompletely understood and currently no clinical disorders of hypothalamic
glucagon function have been defined. Pancreatic islet glucagon is secreted in response to hypoglycemia,
with resultant increases in blood glucose concentration. Glucagon's hyperglycemic effect is produced by
stimulating hepatic glycogenolysis and gluconeogenesis; it has no effect on muscle glycogen. Once
blood-glucose levels have normalized, glucagon secretion ceases. Excessive glucagon secretion can lead
to hyperglycemia or aggravate preexisting hyperglycemia. Excessive and inappropriate glucagon
secretion can sometimes be observed in diabetes, in particular during ketoacidosis, and can complicate
management of the disorder. In rare cases, it also can occur in tumors of the pancreatic islets
(glucagonoma); carcinoid tumors and other neuroendocrine neoplasms and hepatocellular carcinomas.
Patients with glucagon-secreting tumors may present with classic glucagonoma syndrome, consisting of
necrolytic migratory erythema, diabetes, and diarrhea, but also can have more subtle symptoms and
signs. Decreased or absent glucagon response to hypoglycemia can be seen in type I diabetes
Current as of January 3, 2013 2:22 pm CST 800-533-1710 or 507-266-5700 or MayoMedicalLaboratories.com Page 823