26.07.2013 Views

Untitled - D Ank Unlimited

Untitled - D Ank Unlimited

Untitled - D Ank Unlimited

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

nephelometry 528 network theory<br />

VLA-4<br />

Melanoma cell<br />

VCAM-1<br />

CD44<br />

Melanoma cell attached to endothelial cell surface through VLA-4–<br />

VCAM-1 interaction.<br />

diminishing CD4 lymphocyte levels reflects the progression<br />

of HIV-1 infection to clinical AIDS.<br />

Lens<br />

Nephelometry.<br />

Antigen<br />

+<br />

Antibody<br />

Lens<br />

Detector<br />

nephelometry<br />

A technique to assay proteins and other biological materials<br />

through the formation of a precipitate of antigen and<br />

homologous antibody. The assay depends on the turbidity or<br />

cloudiness of a suspension and is based on determination of<br />

the degree to which light is scattered when a helium–neon<br />

laser beam is directed through the suspension. The antigen<br />

concentration is ascertained using a standard curve devised<br />

from the light scatter produced by solutions of known antigen<br />

concentration. This method is used by many clinical<br />

immunology laboratories for the quantification of complement<br />

components and immunoglobulins in patients’ sera or<br />

other body fluids.<br />

nephritic factor<br />

C3 nephritic factor (C3NeF) is found in the sera of patients<br />

with type II membranoproliferative glomerulonephritis<br />

70°<br />

(i.e., dense-deposit disease). This factor can activate the<br />

alternate complement pathway; it is an immunoglobulin that<br />

interacts with alternate complement pathway C3 convertase<br />

and stabilizes it. Thus, it activates the pathway and leads to<br />

the generation of biologically active complement fragments.<br />

C3NeF is an autoantibody against alternate pathway C3 convertase.<br />

Membranoproliferative glomerulonephritis patients<br />

have a genetic predisposition to develop the disease. The<br />

excessive C3 consumption leads to hypocomplementemia.<br />

nephritic factor autoantibodies<br />

The most frequently encountered of the four types of<br />

autoantibodies reactive with the complement system in<br />

membranoproliferative glomerulonephritis (MPGN) are<br />

antibodies to a neoepitope on the Bb moiety of C3bBb<br />

(properdin-independent C3NeF). These autoantibodies are<br />

designated C3NeF (or as Nfa, NFII, or C3bBb stabilizing<br />

factor). They belong to the immunoglobulin G (IgG) or IgM<br />

class and are found in type II (dense-deposit) MPGN. They<br />

have also been found in partial lipodystrophy (PLD), poststreptococcal<br />

glomerulonephritis, systemic lupus erythematosus,<br />

idiopathic rapidly progressive glomerulonephritis, and<br />

rarely in MPGN types I and III. The sera of patients with<br />

MPGN contain anti-idiotypic antibodies. C3NeF (Nfa) interaction<br />

with inhomologous antigen induces prolonged in vitro<br />

C3bBb C3-cleaving activity half-life and decreased serum<br />

C3 concentrations. The presence of these antibodies is used<br />

to distinguish types of MPGN and monitor treatment.<br />

nephritic syndrome<br />

A clinical complex of acute onset characterized by hematuria<br />

with red cell and hemoglobin casts in the urine, oliguria,<br />

azotemia, and hypertension. There may be limited proteinuria.<br />

Inflammatory reactions within glomeruli cause injury<br />

to capillary walls which permits the release of erythrocytes<br />

into the urine. Acute diffuse proliferative glomerulonephritis<br />

is an example of a primary glomerular disease associated<br />

with acute nephritic syndrome.<br />

nephrotic syndrome<br />

A clinical complex that consists of massive proteinuria with<br />

the loss of greater than 3.5 g of protein per day, generalized<br />

edema, hypoalbuminemia (i.e.,

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!