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Biomedical subjects

K J Assmann

Publications and source records attributed to K J Assmann.

98 records · Page 6Linked to original sources
PubMed1980

Jejunal lymphoma in a patient with primary adult-onset hypogammaglobulinemia and nodular lymphoid hyperplasia of the small intestine.

A patient is presented with primary adult-onset hypogammaglobulinemia and nodular lymphoid hyperplasia of the small intestine complicated by a jejunal lymphoma. The tumor was resected and was classified as a malignant diffuse histiocytic lymphoma with involvement of mesenteric lymph nodes. Gastroenterological, immunological, histological, and immunopathological studies on this case are reported. The possibility that nodular lymphoid hyperplasia of the small intestine in hypogammaglobulinemia is a premalignant condition is discussed.

Adult↗
PubMedDate not supplied

Renal biopsy and family studies in 65 children with isolated hematuria.

We have investigated 65 children with isolated hematuria persisting for at least a year. Renal biopsy specimens were studied by light microscopy, electron microscopy and immunofluorescence with antisera specific against basement membrane components. The majority of the biopsies (62/65) showed variable histologic abnormalities. Four categories could be distinguished on combined histological and clinical criteria: Alport syndrome (n = 8), benign hematuria (n = 33, familial in 23), IgA nephropathy (n = 16) and increase in mesangial cells and matrix (n = 5). On the basis of our results, we suggest that a renal biopsy can establish diagnosis and prognosis in those children with isolated hematuria where the family history is negative. If the family has adult male individuals with isolated hematuria, a biopsy can usually be avoided, since this family history effectively excludes Alport syndrome. The use of antisera against basement membrane components did not allow a differentiation between Alport syndrome and benign hematuria. Goodpasture serum immunofluorescence was variable in the former and normally present in the latter.

Basement Membrane↗
PubMedDate not supplied

Decreased PMN accumulation and glomerular damage by clodronate liposome treatment in PMN-dependent anti-GBM nephritis in mice.

BACKGROUND: Intravenous administration of clodronate (dichloromethylene bisphosphate)-containing liposomes (clodro-L) has been reported to induce selective depletion of tissue macrophages (M phi) with little or no effect on polymorphonuclear granulocytes (PMN). Therefore, we used clodro-L treatment to study the role of M phi in a PMN-dependent model of anti-glomerular basement membrane (GBM) nephritis. METHODS: C57BL/6J mice received clodro-L i.v. at days -2 and -1 before i.v. injection of anti-GBM antibodies. The albuminuria of the first 24 h was measured by radial immunodiffusion in 18 hour urine samples and glomerular changes were studied histologically and immunohistologically. RESULTS: Treatment with clodro-L, in doses that adequately destroyed the Kupffer cells, failed to reduce glomerular M phi numbers, but markedly inhibited glomerular PMN accumulation. Compared to control mice, clodro-L-pretreated C57BL/6J mice showed considerable reduction of both albuminuria and glomerular damage at day 1 after injection of rabbit anti-GBM antibody. CONCLUSIONS: In this PMN-dependent model, the inhibitory effect of clodro-L treatment on the development of nephritis very likely due to the inhibition of glomerular PMN accumulation. Our results indicate the clodro-L treatment as a method of selective M phi depletion has its limitations, especially in models in which PMN are involved as effector cells.

Albuminuria↗