Biomedical subjects

B J Van Damme

Publications and source records attributed to B J Van Damme.

10 recordsLinked to original sources

PubMed1996

Isolated zygomycosis in a bought living unrelated kidney transplant.

We report the first case of zygomycosis by Absidia corymbifera, only localized in an unrelated living donor kidney was bought and transplanted in India. Zygomycosis was diagnosed 2.5 months post-transplantation, in the clinical setting of rapid transplant failure, following an episode of cytomegalovirus (CMV) colitis, CMV nephritis, and acute rejection. Treatment consisted of transplantectomy. One year later, the patient is doing well, without clinical or serological evidence of persistent mycotic or virological infections. We speculate that this isolated mycotic infection originated with the donor or was due to the poor hygienic conditions in the operating theater or surgical ward. Another possibility is that this isolated renal involvement resulted from a subclinical pulmonary infection with hematogenous dissemination to the kidney in a manner comparable to renal tuberculosis. The patient received no amphotericin and was cured with transplantectomy alone.

Humans↗

PubMed1996

Detection of prostate specific antigen in pancreas and salivary glands: a potential impact on prostate cancer overestimation.

PURPOSE: We explored the immunohistochemical expression of prostate specific antigen (PSA) in pancreas and salivary glands. MATERIALS AND METHODS: We investigated 62 specimens from male and female subjects, representing normal cases and several pathological conditions of pancreas and salivary glands. Two commercially available monoclonal antisera for PSA and 1 for prostatic acid phosphatase were used. RESULTS: A consistently positive reaction for PSA and prostatic acid phosphatase, independent of patient sex, was noted in ductal cells of normal pancreas and normal salivary glands, as well as pleomorphic adenoma, adenocarcinoma and all oncocytic epithelial cells of Warthin's tumor. Reaction was absent in normal stromal and acinar cells, and squamous carcinoma. CONCLUSIONS: PSA is detectable in normal and cancer tissues far from the prostate. Therefore, we may not entirely rely on specificity of PSA alone to diagnose metastatic prostate cancer.

Female↗

PubMed1995

Active Heymann nephritis in complement component C6 deficient rats.

The mechanisms of renal injury that result in proteinuria in active Heymann nephritis (AHN) remain unclear, though data suggest that in analogy of the passive form of the disease the membrane attack complex C5b-9 may be involved. AHN was induced in an inbred strain of PVG/c-rats that are totally deficient in the C6 component of complement and are unable to form the lytic C5b-9 complex, as well as in non-complement deficient PVG/c+ rats that are immunologic identical to the deficient strain. In both groups of animals comparably high titers of anti-Fx1A autoantibodies were found after three weeks and persisted at 40 weeks. Proteinuria was also similar in both groups, and was first evident at six weeks. High levels of urinary protein, ranging from 200 mg/24 hr to 500 mg/24 hr, were found after 10 weeks and persisted up to one year. Renal biopsy findings at various times post-immunization were identical in both groups, including immunofluorescence staining for Ig and C3 deposits, and also EM findings of subepithelial electron-dense deposits were not different. The injection of heterologous rabbit complement, that partially and temporarily restored the CH50 activity in PVG/c- rats did not alter or hasten the disease. Long-term follow-up showed that all rats in both groups continued to have severe proteinuria and that most animals died between 8 to 12 months after disease induction, without renal impairment. EM findings in serial biopsies demonstrated that the growth of the subepithelial deposits as measured by surface area occurred between weeks 4 and 12. A positive correlation (r = 0.94) between the size of the deposits and the level of proteinuria was found. These studies demonstrate that the membrane attack complex of complement does not play a major role in AHN. The relationship of the size of the immune deposits to the level of proteinuria suggests that the growth of the immune deposits on itself initiate secondary mechanisms that damage the permselective characteristics of the glomerular membrane.

Animals↗

PubMed1994

A new single nephron model of focal and segmental glomerulosclerosis in the Munich-Wistar rat.

The hypothesis that damage to the visceral epithelial cell plays a central role in the pathogenesis of focal and segmental glomerulosclerosis was tested by injecting saponin solutions of increasing concentration (0.1, 0.3, 0.6 and 1.0 mg/ml) in Bowman's space of superficial glomeruli in the Munich-Wistar rat. The microinjections were performed both with and without intermittent clamping of the renal vessels during two minutes. After 8 to 14 days the injected glomeruli were examined by light microscopy. The injected glomeruli were classified as, normal (NL), showing visceral epithelial cell damage (VECD), showing focal and segmental glomerulosclerosis (FSGS) or showing global sclerosis (GS). Swelling and intracellular vacuolation of the visceral epithelial cells (VEC) were considered as VECD. FSGS-lesions were seen most frequently in the glomeruli injected with 10 nl of a saponin solution with a concentration higher than 0.3 mg/ml. In view of the light microscopic lesions four glomeruli in a 0 mg/ml, the 0.1 mg/ml and the 0.6 mg/ml saponin groups were examined after 40 minutes with transmission electron microscopy (TEM) to evaluate the selectivity of the lesions. In the 0 and 0.1 mg/ml group only occasional limited fusion of the foot processes of the podocytes was seen. In the 0.6 mg/ml group segmental lysis of the VEC without ultrastructural damage to the capillary basement membrane or the endothelial and mesangial cells was seen. It is concluded that it is possible to induce direct segmental lysis of the visceral epithelial cells in a single glomerulus, and that this damage to the visceral epithelial cells is related to the development of focal and segmental glomerulosclerosis.

Animals↗

PubMed1994

Hereditary C6 deficiency in a strain of PVG/c rats.

A chance observation has led to the discovery of a strain of PVG rats (PVG/c-) which are deficient in complement (C) component C6. Analysis of total haemolytic activity (CH50) of PVG/c- serum revealed an absent CH50 activity compared with serum of other rat strains and of a PVG/c rat (PVG/c+) that showed normal C activity. Thus, the PVG/c- rat was unable to activate the C5b-9 membrane attack complex. To gain insight into the complement abnormalities, analysis of individual C components was performed. Testing the PVG/c- serum in a C6 haemolytic assay and using deficient human sera showed a deficiency of C6 in the PVG/c- rat. Highly purified human C6 and human sera deficient in other components were able to reconstitute the CH50 activity of the PVG/c- rat. The possibility that an inactivator of C was present in PVG/c- serum was excluded. The deficiency was found to be inheritable and under the control of an autosomal recessive gene. Furthermore, tissue antigens and immunity of the PVG/c- rat were found to be identical to those determined in the PVG/c+ rat. With regard to their health status, the PVG/c- animals seem to have no disadvantages compared with PVG/c+ rats when held under the same conditions within the protected environment of animal facilities. Taken together, both rat strains provide an unique animal model for studying the biological role of C, particularly the C5b-9 membrane attack complex in experimental medicine.

Animals↗

PubMed1990

[Clinico-pathological correlations in IgA-nephropathy].

67 renal biopsies of children with IgA nephropathy, collected from 1970 to 1983 were analyzed semiquantitatively. Glomerular, tubular, vascular and interstitial lesions were scored and compared with clinical data in 56 patients. The number of cases registered and the severity and type of the glomerulopathy varied widely between centres. Histological parameters influencing significantly the outcome of the disease could not be detected.

Biopsy↗

PubMed1988

Erythromycin-induced hepatitis: simulator of malignancy.

A 67-year-old patient was admitted with a 2-week history of epigastric discomfort that began after an episode of upper respiratory tract infection treated with erythromycin. Results of liver function tests were abnormal. Abdominal ultrasound (US) and computed tomography showed multiple, poorly demarcated irregular lesions in both hepatic lobes, suggestive of diffuse metastatic invasion. Histologic examination of the biopsy specimen revealed drug-induced hepatitis. Ten weeks after withdrawal of the erythromycin, US showed complete resolution of the hyperechogenic liver lesions.

Aged↗

PubMed1988

Renal thorium deposition associated with transitional cell carcinoma: radiologic demonstration in two patients.

Abdominal radiography, excretory urography, retrograde pyelography, and computed tomography were performed in two patients who had undergone retrograde pyelography with thorium dioxide (Thorotrast) approximately 40 years ago. Both patients developed a transitional cell carcinoma due to suburothelial thorium deposition. Typical thorium densities were demonstrated at CT in the peripelvicalyceal area as well as in retroperitoneal lymph nodes. Elderly patients in whom radiographic examination reveals retained Thorotrast in the kidney should be followed up because of the high risk of renal carcinoma.

Aged↗

PubMed1978

Experimental glomerulonephritis in the rat induced by antibodies directed against tubular antigens. IV. Investigations into the pathogenesis of the model.

Heterologous immune complex glomerulonephritis can be induced in various strains of rats by one injection of heterologous antibody directed against antigens present in the brush border of the proximal. Although it is generally believed that an immune complex glomerulonephritis is caused by the deposition of soluble immune complexes from the circulation in the glomerular basement membrane, there are reasons for doubting whether this mechanism is also operating in the type of experimental glomerulonephritis presented here. In a study using injections of extra antibody and extra antigen to influence the formation and deposition of immune complexes, it is demonstrated that this type of glomerulonephritis is induced in a state of antibody excess. The theory that only immune complexes formed in antigen excess can deposit in the glomerular basement membrane, warrants the assumption that in our model a different pathogenetic mechanism is operating. The hypothesis is put forward that in the heterologous immune complex glomerulonephritis free antibody crosses the glomerular basement membrane to combine with the antigen. This antigen either crosses the glomerular basement membrane separately or is already present as an integral part of this structure.

Animals↗

PubMed1978

Experimental glomerulonephritis in the rat induced by antibodies directed against tubular antigens. V. Fixed glomerular antigens in the pathogenesis of heterologous immune complex glomerulonephritis.

In heterologous immune complex glomerulonephritis glomerular deposition of immune complexes occurs immediately after an injection with heterologous antibody directed against antigen, derived from the brush border of the tubules. The injected antibody is thought to combine with circulating Fx1A antigen to form immune complexes which subsequently are deposited in the glomeruli. However, perfusion of rat kidneys in absence of this antigen likewise resulted in prompt localization of immune complexes along the glomerular basement membrane. Further, Fx1A antigen was shown to be present in the capillary wall, especially in the filtration slits and on the cell membrane of epithelial cells. From these findings it was concluded that in this model of glomerulonephritis the deposited immune complexes are formed locally instead of being deposited from the circulation. This concept of "fixed antigen" may also be relevant to the pathogenesis of other forms of experimental glomerulonephritis and probably also for human glomerulonephritis.

Antigen-Antibody Complex↗