Biomedical subjects

C G Hipp

Publications and source records attributed to C G Hipp.

3 recordsLinked to original sources

PubMed1986

The epithelial antigen phenotype of glomerular crescent cells.

There is controversy over the origin of cells in glomerular crescents. Although crescent cells were once considered to be of epithelial lineage, recent data have suggested that they are derived from the mononuclear phagocyte system. To further define the histogenesis of crescents, the authors evaluated 26 renal biopsy specimens having cellular crescents, using immunoenzyme and immunofluorescence microscopy, and a battery of 11 antibodies reactive with renal epithelial cells and 5 antibodies reactive with leukocytes. Although minor populations of macrophages were present in most crescents, in only 1 of 23 specimens evaluated with anti-macrophage antibodies were these the major cell type. Of 23 specimens evaluated with anti-epithelial antibodies, all but one had crescents with most of the cells expressing one or more epithelial antigens. Crescent cells shared antigens with glomerular and tubular epithelial cells, but the antigen phenotype of crescents often differed from that of normal tubular or glomerular epithelial cells.

Antibody Specificity↗

PubMed1985

C1q nephropathy: a distinct pathologic entity usually causing nephrotic syndrome.

The presence, distribution, and intensity of glomerular C1q localization were evaluated by direct immunofluorescence microscopy in 800 renal biopsy specimens which were also studied by light and electron microscopy. Identified were 15 patients with extensive (mean: 3.6 + out of 4 +), predominantly mesangial, C1q localization along with C3 and immunoglobulins, but no evidence for systemic lupus erythematosus. Pathologically, this lesion most closely resembled lupus nephritis. Clinical and pathologic data from these 15 C1q nephropathy patients were compared to data from 30 lupus nephritis and 223 other proliferative glomerulonephritis patients, and the C1q nephropathy patients were found to be dissimilar to both groups. The 15 C1q nephropathy patients had an average age of 17.8 years, 8 males, 7 females, 9 Black, 100% had proteinuria (mean 7.5 g/d), 40% hematuria, 0% hypocomplementemia, and 0% antinuclear antibodies. By electron microscopy, 100% had mesangial dense deposits, 20% capillary wall dense deposits, and 0% endothelial tubuloreticular inclusions. Nine patients treated with steroids had no definite resolution of proteinuria. We proposed that C1q nephropathy is a distinct clinicopathologic entity, usually causing steroid-resistant nephrotic syndrome in older children and young adults.

Adolescent↗

PubMed1985

Immunohistopathologic evaluation of C1q in 800 renal biopsy specimens.

The frequency, distribution, and intensity of C1q localization were evaluated in 800 renal biopsy specimens, and these observations were correlated with light, immunofluorescence, and electron microscopy findings. Intense C1q immunostaining was most frequent in proliferative and membranous lupus glomerulonephritis and in a recently described form of proliferative glomerulonephritis designated "C1q nephropathy." Moderate intensity C1q immunostaining was observed in most cases of type I but not type II, membranoproliferative glomerulonephritis. Unlike lupus membranous glomerulopathy, non-lupus membranous glomerulopathy usually did not have extensive C1q localization. C1q was scanty or absent in IgA nephropathy and antiglomerular basement membrane antibody mediated glomerulonephritis. C1q, along with IgM and C3, was often present at sites of glomerular sclerosis, especially in focal segmental glomerulosclerosis. Extraglomerular C1q was most frequent and most intense in cases of lupus nephritis having extraglomerular immune deposits. The presence or absence and intensity of C1q immunostaining were shown to be useful in the differential diagnosis of some glomerulopathies.

Autoantibodies↗