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Biomedical subjects

A J Fish

Publications and source records attributed to A J Fish.

At least 55 records · Page 3Linked to original sources
PubMed1980

Pregnancy and systemic lupus erythematosus.

Eleven patients with 18 pregnancies occurring during the course of systemic lupus erythematosus (SLE) were reviewed. Ten had long-standing lupus glomerulonephritis and a single patient developed glomerulonephritis during pregnancy. Patients were divided into those without (Group A) and those with (Group B) clinical evidence of renal disease or active SLE at conception. In Group A there were 10 pregnancies in five patients; all pregnancies were uncomplicated, except for mild superimposed pre-eclampsia in two, and all resulted in term delivery. Eight pregnancies in six patients occurred in Group B; four pregnancies were complicated by severe (2) or mild (1) superimposed pre-eclampsia and the onset of glomerulonephritis (1), resulting in three premature deliveries and a spontaneous abortion. The remaining four pregnancies were uncomplicated but resulted in one term delivery, one elective abortion, and two spontaneous abortions. None of the patients developed either renal failure or a rapidly progressive course following pregnancy.

Adult↗
PubMed1979

Immunofluorescence studies of dense deposit disease. The presence of railroad tracks and mesangial rings.

Immunopathologic analysis was carried out on renal tissue from patients with membranoproliferative glomerulonephritis, nine with type I and nine with type II (dense deposit disease). A specific finding in all patients with type II, but not type I, was the presence of C3 along the margin but not within the central portion of dense deposit material in the glomerular basement membrane giving a double linear appearance (railroad tracks); C3 was also present within the mesangium, outlining numerous circular structures (mesangial rings). By phase contrast, electron microscopy, and dual label fluorescence studies, the railroad tracks and mesangial rings were shown to outline dense deposit material. Mesangial rings contained properdin (four of nine patients); railroad tracks contained properdin (five of nine patients) and C4 (four of nine patients); no other complement components or immunoglobulins were present. Studies using rhodamine-conjugated rabbit antibody to human glomerular basement membrane demonstrated no reactivity with the dense deposit material itself. In type I and to a lesser extent in type II, granular deposits of C3, C4, properdin, IgM, and IgG were present along the glomerular basement membrane, suggesting that immune complexes play a role in both diseases. Dense deposit transformation of the glomerular basement membrane may be a consequence of a highly specific injury.

Autoantibodies↗
PubMed1979

Spatial orientation and distribution of antigens within human glomerular basement membrane.

Antibodies to GBM have a linear staining pattern along the GBM by immunofluorescence. In this study, we have examined the distribution of human GBM antigens using Goodpasture antibody and heterologous rabbit anti-human GBM antibody. Goodpasture sera and Goodpasture antibody eluted from diseased kidneys reacted as a single linear component within the GBM. Rabbit anti-human GBM was shown to react along distinctly separate zones of the inner and outer aspects of the GBM; the central portion of the GBM seemed to be nonreactive with this antibody. In comparison, Goodpasture antibodies reacted along the inner zone of the GBM but at a locus external to that reacting with heterologous rabbit anti-GBM antibody. These observations of linear binding of antibody to different sites along the GBM suggest a spatial organization of antigen not previously observed.

Anti-Glomerular Basement Membrane Disease↗
PubMed1978

Histopathology and electron and immunofluorescence microscopy of gingivitis granulomatosa associated with glossitis and cheilitis in a case of Anderson-Fabry disease.

A 17-year-old white boy with signs, symptoms, and family history of angiokeratoma corporis diffusum universale, Anderson-Fabry disease (AFD), developed recurrent and then persistent swelling of both lips, erythematous hyperplastic gingivae, and a pebbled tongue. Positive blood findings were raised serum IgE, decreased T-cell level, and increased B-cell level. Histopathology of the gingiva showed noncaseating granulomas with multinucleate giant cells containing Schaumann bodies and large plasma-cell infiltrates in which immunofluorescence demonstrated immune globulins of several classes. Electron microscopy and histochemistry demonstrated ceramide in the vasculature. No glycolipid was found in the macrophages or giant cells of the granulomas which, in contrast, resembled sarcoid reactions. Plasma cells with Russell bodies and immune reaction-induced degranulation of mast cells were also identified. The pathogenesis of the oral findings possibly relates to altered immune reactivity associated with damage to the microvasculature analogous to that in Melkersson-Rosenthal syndrome.

Adolescent↗
PubMed1978

The immunohistopathology of glomerular antigens. II. The glomerular basement membrane, actomyosin, and fibroblast surface antigens in normal, diseased, and transplanted human kidneys.

Immunofluorescent studies have demonstrated that actomyosin (AMY) is present in the mesangium in a restrictive pattern, whereas fibroblast surface antigen (FSA) has a more extensive mesangial distribution. Antibody to glomerular basement membrane (GBM) is localized to the GBM. One hundred ninety-six tissue samples, including 17 from normal subjects, 94 from patients with primary renal diseases, and 85 from transplanted kidneys, were examined for changes in distribution of AMY, FSA, and GBM antigens. The distribution of AMY and FSA in the mesangium is markedly increased in width in patients with diabetic nephropathy, and the GBM is thickened. AMY and FSA are mildly increased in patients with glomerulonephritis and GBM is normal. Patients with membranoproliferative glomerulonephritis (MPGN) show a loss of all glomerular antigens. Increased mesangial AMY was found in 12 of 37 transplanted kidneys in diabetic patients vs 4 of 33 nondiabetics 0 to 4 years after transplantation (P < 0.025). This difference is more notable at 2 to 4 years, with 5 of 9 diabetics showing increased AMY vs 0 of 6 nondiabetic patients (P < 0.0005). In MPGN, 5 of 8 tissues showed decreased mesangial AMY vs 3 of 36 diabetic patients (P < 0.0005) and 1 of 32 patients with other glomerulopathies (P < 0.0005). GBM thickening is not associated with specific pretransplant diseases. In transplanted kidneys, the pattern of FSA is dissociated from that of AMY: over half of all patients have increased FSA, even when AMY is normal. Whether this unique finding in transplanted kidneys reflects an increase in the synthesis of FSA by mesangial cells or the failure to clear this (circulating) antigen from the mesangial matrix is unknown.

Actomyosin↗
PubMed1978

Human glomerular cells in culture. Three subcultured cell types bearing glomerular antigens.

In this paper, we describe three cell types from the explanted human glomerulus: the circular glomerular cell (CGC), the rhomboid glomerular cell (RGC), and the small ovoid glomerular cell (SOGC). These cells were compared with subcultured human umbilical vein endothelial and smooth muscle cells, uterine smooth muscle cells, and skin fibroblasts. Immunochemical comparisons utilized antiserums to antigens in the human glomerulus: antiglomerular basement membrane, antifibroblast surface antigen (FSA) (reactive extensively with the mesangium), antiactomyosin (AMY) localizing more restrictively in the mesangium, and antihemophilic factor (AHF) localizing to the endothelium. No cultured glomerular cells bore the AHF marker of endothelial cells. The epithelioid CGC excrete most GBM antigen as an orderly palisade of granules from the cell surface. FSA is rapidly lost from the cell surface. RGC have a typical multilayered smooth muscle morphology and have a most prominent complex AMY pattern of periodic aggregates and fibrils. FSA adheres to the cell surface. SOGC form an initial nonoverlapped monolayer resembling endothelial cells but elongate and form multilayers after confluency. The AMY fibril pattern of SOGC is distinctively multidirectional. The translation of in vitro characteristics into in vivo identification must be interpreted cautiously: CGC may derive from glomerular epithelial cells; RGC may derive from mesangial cells; and SOGC may represent a more rapidly proliferating, less differentiated form of the epithelial cell or another, unidentified, glomerular cell type.

Antigens↗
PubMed1978

C3b receptors on human glomeruli in vitro. Loss in culture.

C3b receptors, easily demonstrated on isolated human infant glomeruli, are lost as cells grow in culture. This suggests that epithelial cells are dedifferentiated or that the C3b receptor is not intrinsic to the epithelial cell.

Cells, Cultured↗
PubMed1977

Systemic lupus erythematosus within the first two decades of life.

Forty-nine patients with systemic lupus erythematosus (SLE) during childhood and adolescence presenting over a period of 17 years were followed during treatment with prednisone and azathioprine. The average period of follow-up was 5.7 years. Detailed analyses of clinical parameters of renal function and sequential changes in glomerular abnormalities by percutaneous renal biopsy are reported. Therapy was directed towards normalizing the results of urinalysis and renal function, eliminating proteinuria and maintaining normal serology (normal serum complement and negative antiDNA titers). The 10 year survival of the entire group was 86 per cent. A survival of 73 per cent and 87 per cent over this interval in patients with diffuse and focal proliferative lupus nephritis, respectively, was achieved. The major cause of mortality in this series was infection. It appears that intensive observation and monitoring of serologic parameters in SLE, along with aggressive steroid and immunosuppressive therapy, lead to a prognosis in SLE more favorable than previously reported.

Adolescent↗
PubMed1976

Human glomerular smooth muscle (mesangial) cells in culture.

Glomerular smooth muscle cells were grown and subcultured from human glomeruli in vitro. These cells, stained with antiserum to smooth muscle actomyosin and examined by immunofluorescence, had brightly stained intracellular fibrils similar to those seen in smooth muscle cells. Actomyosin fibrils were altered by conditions affecting actomyosin in vitro. Glomerular smooth muscle cells lacked the antihemophilic factor and blood group antigens present in endothelial cells, and are, therefore, most likely derived from the smooth muscle cells of the glomerular mesangium. By radio-labeled amino acid analysis, they synthesize a collagen differing from that of fibroblasts, and which probably differs from basement membrane collagen. Other cell types could be grown and subcultured using a different glomerular isolation technique, culture medium and method of subculture.

Actomyosin↗
PubMed1975

The role of complement, immunoglobulin and bacterial antigen in coagulase-negative staphylococcal shunt nephritis.

We describe three patients with arrested hydrocephalus in whom glomerulonephritis developed secondary to Staphylococcus epidermidis bacteremia from an infected ventriculoatrial shunt. Investigation of the immune-mediated renal disease associated with this chronic infection showed that (1) complement depletion during the acute phase of bacteremia and nephritis was predominantly via the classic pathway; (2) rheumatoid factor was associated with bacteremia, fever, proteinuria and low complement levels; (3) early complement components (C1q, C4, C3), immunoglobulin (predominantly immunoglobulin M [IgM], Staph. epidermidis antigen(s) and electron denxe subendothelial deposits were localized within the renal glomerulus; (4) C1q, and IgM derived from patient serums, were the most prominent in vitro immunoreactants to Staph. epidermidis cell walls; and (5) the causative organisms, Staph. epidermidis, shared common antigens with Staph. aureus, and antibody from patient serums cross reacted with extracts from both of these organisms.

Antigens, Bacterial↗
PubMed1975

Human glomerular cells in tissue culture.

Cells from human glomeruli explanted in tissue culture were grown and subcultivated up to 12 to 13 times. Light and electron microscopic studies revealed these cells to be morphologically distinct from fibroblasts. By electron microscopy, an extracellular material resembling basal lamina was seen and prominent intracellular microfilaments were evident. Immunofluorescent microscopy demonstrated reactivity of heterologous antiglomerular basement membrane antibody with aggregates of extracellular material. Absorption experiments using antiglomerular basement membrane antibody showed that the extracellular materiial shared some antigenic components with glomerular basement membrane. Antibody to cultured glomerular cells stained the mesangium and glomerular basement membrane of normal human kidney. This antibody was nephrotoxic in monkeys, induced proteinuria with proliferative glomerulonephritis, and localized to the mesangium and glomerular basement membrane of monkey glomeruli. These findings and the presence of prominent intracellular microfilaments (contractile elements) suggest that the glomerular cells may be of mesangial origin.

Adult↗
PubMed1974

The glomerular mesangium. II. Studies of macromolecular uptake in nephrotoxic nephritis in rats.

These studies were designed to explore the effects of nephrotoxic serum (NTS) in rats on the uptake and processing by the glomerular mesangium of intravenously administered protein macromolecules (radiolabeled aggregated human IgG, [125I]AHIgG). Measurements of [125I]AHIgG levels in preparations of isolated glomeruli correlated well with qualitative estimates of glomerular IgG deposition seen by immunofluorescent microscopy. Rats given 2 ml NTS received 25 mg/100 g body wt [125I]AHIgG 48 h later and were sacrificed at varying time intervals thereafter. NTS-treated animals demonstrated a marked increase in glomerular uptake of [125I]AHIgG as compared with concurrent controls but a normal ability to clear [125I]AHIgG from the mesangium over 72 hr. Animals given 1.0, 0.5, and 0.25 ml NTS had neither proteinuria nor significant light microscopic changes, yet had increased uptake of [125I]AHIgG of 4.4, 3.0, and 2.1 times control values, respectively at 8 h after the infusion of aggregates. Rats given 1 ml NTS and 12.5, 6.25, and 3.125 mg [125I]AHIgG/100 g body wt had increased glomerular uptake at 8 h, but there was, within both NTS and control groups, a disproportionate decrease in uptake at lower [125I]AHIgG doses. Rats given cobra venom factor (CoF) followed by a NTS shown to be complement dependent (proteinuria reduced by prior complement depletion with CoF) had less mesangial [125I]AHIgG uptake than NTS controls but greater uptake compared with normal controls. CoF itself had no effect on mesangial or reticuloendothelial system [125I]AHIgG uptake. These studies demonstrate a striking change in glomerular mesangial activity after fixation of nephrotoxic antibodies to the glomerular basement membrane, even in the absence of proteinuria and suggest that subtle alterations of the filtration surface can influence mesangial function. The effect of NTS on the mesangium is due, in large part, to the glomerular injury and proteinuria which nephrotoxic antibodies produce.

Animals↗
PubMed1974

The immunohistopathology of glomerular antigens. The glomerular basement membrane, collagen, and actomyosin antigens in normal and diseased kidneys.

The immunofluorescent localization of antisera to human glomerular basement membrane (GBM), collagen, and smooth muscle actomyosin was examined in 15 specimens of normal renal tissue and 98 specimens from patients with renal disease. The anti-GBM and anticollagen antisera normally localize to GBM, while antiactomyosin localizes to the mesangium. Diabetic nephropathy revealed a striking expansion of mesangial material reacting with antiactomyosin. In contrast, the expanded mesangium in membranoproliferative glomerulonephritis did not react with antiactomyosin, and the GBM localization of anti-GBM and anticollagen sera was similarly lost. The thickened GBM in diabetes mellitus and membranous nephropathy reacted with anti-GBM and anticollagen, but with accentuation of staining on the inner aspect of the GBM. In proliferative glomerulonephritis there was a moderate increase in the distribution of actomyosin. Glomerular sclerosis and hyalinization in all diseases studied was accompanied by a loss of immunofluorescent staining for all glomerular antigens, including collagen.

Actomyosin↗
PubMed1974

Hematogenous Streptococcus faecalis pyelonephritis in the rat. A histologic, immunopathologic and bacteriologic study.

The demonstration of bacterial antigens in active pyelonephritis in man has been inconsistent. In this paper we have studied 110 rats with experimental pyelonephritis induced by a single intravenous injection of Streptococcus faecalis. The animals were studied at intervals up to 1 year; bacteremia, urine and renal parenchymal bacterial counts were monitored. In these animals it was observed that bacteriuria and positive bacterial cultures of renal tissue persisted up to 1 year in some rats. Bacteria and their antigenic products in small foci were detected by immunofluorescence in the pyelonephritic lesions. The highly focal distribution of the bacterial antigens in bacteriologically positive tissues of this model suggest the need for careful fixation technics, availability of large tissue specimens and careful control of immunologic factors. These specific requirements to detect bacterial antigens may preclude the practical study of human pyelonephritic kidneys.

Animals↗
PubMed1973

The glomerular mesangium. 3. Acute immune mesangial injury: a new model of glomerulonephritis.

A mechanism of immune glomerular injury is described based on the fixation of antibody (Ab) to an antigen (Ag) that has localized in the glomerular mesangium. Rabbits were given, intravenously (i.v.), aggregated human IgG (AHIgG) or albumin (AHSA) and 10 h later, when the Ag by immunofluorescent microscopy was present in the mesangium, a kidney was removed and transplanted into a normal rabbit. The recipient then received, i.v., rabbit anti-HIgG or anti-HSA. Within minutes of Ab infusion, glomeruli of the donor kidney had polymorphonuclear (PMN) infiltration that over the next few hours became marked and was associated with glomerular cell swelling. At 24 h a decrease in PMN's and early mesangial proliferation was seen. By 3 days there was marked mesangial hypercellularity and increased mesangial matrix. Within minutes after Ab administration rabbit IgG, C3, and fibrin were seen in the glomerular mesangium. There was a fall in complement titer by 1 min after Ab infusion that was due to complement consumption by the donor kidney. Complement then returned to normal levels by 48 h. Significant glomerular injury did not occur (a) in the recipient's own kidney, (b) from Ag administration and transplantation without recipient Ab administration, or (c) from transplantation and Ab administration without prior Ag administration. These studies demonstrated that Ag localized in the glomerular mesangium can react with circulating Ab and complement resulting in severe glomerular injury.

Animals↗