Biomedical subjects

M N Koss

Publications and source records attributed to M N Koss.

4 recordsLinked to original sources

PubMed1976

The nature and incidence of cryoproteins in hepatitis B antigen (HbsAg) positive patients.

Hepatitis B (HbsAg) surface antigen has been detected in the serum of patients with a variety of diseases and immune complexes of this antigen and antibody have been implicated in tissue damage to various organs. Previously we have demonstrated that serum cryoproteins occur in a variety of immune complex disorders and represent pathogenic complexes of antigen and specific antibody. Sera from patients with acute HbsAg positive hepatitis, chronic hepatitis B antigenemia, acute and chronic HbsAg negative hepatitis, as well as a variety HbsAg negative miscellaneous liver diseases and normals were studied for the presence and nature of cryoproteins. Cryoproteins were detected in a large number of patients with acute and chronic HbsAg positive hepatitis and chronic HbsAg carriers. The quantity of these cold insoluble precipitates was highest in acute hepatitis. Cryoproteins were detected with much less frequency in HbsAg negative patients and were not found in normals. The precipitates in HbsAg patients contained either HbsAg, anti-HBsAg or both, along with immunoglobulins and occasionally complement and rheumatoid factor. The cryoproteins in these patients had biological properties attributable to immune complexes and several of the patients had clinical manifestations of acute or chronic serum sickness. Cryoproteins from HbsAg negative patients did not contain HbsAg or antibody to HbsAg and did not have biologic properties of immune complexes. In HbsAg positive patients HbsAg and antibody to HbsAg were concentrated in the cryoprecipitate. The preliminary studies suggest that investigation on cryoproteins in hepatitis may be of clinical and immunopathogenic value.

Antigen-Antibody Complex↗

PubMed1976

Experimental Bence Jones cast nephropathy.

C3H mice received intraperitoneal injections of a single dose of 50 to 200 mg. of purified lambda Bence Jones protein. Control animals received injections of comparable amounts of ovalbumin. The mice which received 200 mg. of lambda Bence Jones protein developed extensive cast formation in the distal renal tubules. By electron microscopy, the casts were found to contain elongated crystalloid structures. In some areas, these crystalloids appeared to penetrate into or be engulfed by tubular epithelial cells. By immunofluorescence, only lambda Bence Jones protein was detectable in the casts during the first 5 days. Thereafter, Tamm-Horsfall protein was also found in increasing amounts. The casts induced an inflammatory response characterized by the sequential appearance of polymorphonuclear leukocytes and mononuclear cells. The secondary tubular cell changes included atrophy, degeneration, and regeneration. Giant cells were present around many casts, but it could not be determined whether these derived from tubular epithelial or mononuclear inflammatory cells. Elevated blood urea nitrogen was found terminally in most animals. Smaller doses of the same protein as well as preliminary studies with two other lambda Bence Jones proteins failed to produce comparable changes. This experimental model of Bence Jones nephropathy closely resembles the morphologic features of so-called "myeloma kidney" in man.

Animals↗

PubMed1975

Nephropathy associated with sickle cell anemia: an autologous immune complex nephritis. I. Studies on nature of glomerular-bound antibody and antigen identification in a patient with sickle cell disease and immune deposit glomerulonephritis.

The nature of the glomerular-bound antibody and the putative antigen was investigated in one of the patients with sickle cell disease and immune deposit membranoproliferative glomerulonephritis by immunohistologic and glomerular antibody elution. Renal proximal tubular epithelial antigen was localized in association with immunoglobulins G (IgG), M (IgM), Clq fraction of the first component of complement (Clq) and the third component of complement (C3) in a granular pattern along the glomerular basement membrane of the patient's kidney. IgG and IgM were eluted from glomeruli. These immunoglobulins fixed to the proximal tubules of normal human kidney by direct immunofluorescence. This localization was abolished by absorption of the eluted immunoglobulins with renal tubular epithelial (RTE) antigen. The IgG eluted from the glomeruli blocked the fixation of rabbit anti-RTE antigen to normal proximal tubular brush border. These studies suggest that the nephritis in this patient was due to deposition of complexes or RTE antigen and specific antibody. An autologous immune complex nephritis may develop in some patients with sickle cell anemia secondary to RTE antigen released possibly after renal ischemia or some other phenomenon causing renal tubular damage.

Adolescent↗

PubMed1975

The human choroid plexus and autoimmune nephritis.

The choroid plexus resembles the glomerular basement membrane (GBM) and may be a site of injury or source of antigen in Goodpasture syndrome. Immunohistologic studies were performed on the choroid plexus of a patient with auto-immune nephritis and pulmonary hemorrhage. The studies showed linear deposition of host IgG, IGM, and beta1c. Antibody eluted from the diseased kidney fixed in a linear pattern to normal choroid plexus and could be absorbed by either choroid plexus or GBM. Antibody to choroid plexus fixed to GBM and the linear staining was no longer observed after absorption with GBM or choroid plexus. Antibody to GBM fixed to normal choroid plexus and was obsorbed by both choroid plexus and glomerular basement membrane. The studies suggest an immunologic relationship between choroid plexus and GBM and a role for the choroid plexus in autoimmune nephritis.

Animals↗