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Biomedical subjects

H W Intorp

Publications and source records attributed to H W Intorp.

At least 19 recordsLinked to original sources

[The phenomenon of double line of IgG in immunoelectrophoresis (author's transl)].

Immunoelectrophoretic studies of patients' sera occasionally reveal a parallel splitting of the IgG precipitation line if the test is performed with polyvalent antihuman antiserum directed not only against the Fc-part of the IgG molecule. This phenomenon has been studied in a patient with discoid lupus erythematosus and another patient with lymphadenopathy of unknown origin. Apparently, this finding was not due to a monoclonal gammopathy: In the cellulose membrane electrophoresis no extragradient could be observed and assays with antisera directed against free and bound light chains showed a regular pattern. The splitting of the IgG precipitate is much rather caused by polyclonal IgG with a high proportion of slowly diffusing heterogenous IgG-x, as has been found in studies using the immunoelectrophoresis as well as the analytical ultracentrifuge. It was not due to Fab fragments.

Female↗

[Light-chain plasmacytoma with reversible renal insufficiency after intravascular application of thorotrast (author's transl)].

Thirty-three years after intravascular injection of Thorotrast, a light-chain plasmacytoma with hypercalcemia and renal insufficiency was diagnosed in a 60-year-old man. The question of causal relation between Thorotrast deposit and plasmacytoma is discussed. The accumulated radiation load to the bone-marrow as caused by thorium dioxide deposition amounts to circa 3000 rem. According to casuistic and epidemiological communications, induction of plasmacytomas by external X-irradiation may be regarded as possible. A distinct increase in myeloproliferative diseases but only small numbers of plasmacytomas are reported in extensive epidemiological Thorotrast studies. From combination of results of the three most comprehensive epidemiological Thorotrast studies is obtained a numerical ratio of 1:5 for the spontaneous rate against the number of plasmacytomas observed. Identical correlations are yielded by investigations at Hiroshima and Nagasaki. Hence it is to be supposed that also plasmacytomas can be induced by thorotrastosis of the reticulohistiocytic system.

Acute Kidney Injury↗

Pathogenetic mechanisms in tubular renal disease.

Injections of heterologous tubular material into rabbits caused the formation of immune complexes deposited predominantly on the tubular basement membrane. Much fainter deposits were found on the glomerular basement membrane. Immunohistological studies revealed that the antigen involved originated from cells of the proximal tubules. In other animal experiments, purified tubular material was used for immunisation in order to analyse the antigenic structure of renal tubules. These rabbits were found to produce autoantibodies against an antigen present in the tubular as well as the glomerular basement membrane. Morphological studies of the kidneys from the immunised animals revealed alterations in the tubular epithelial cells and interstitial tissue which were characterised microscopically and electron microscopically by swelling and degeneration of the epithelial cells, and cellular infiltrates in the interstitium.

Animals↗

Renal disease in pregnancy.

Renal biopsy was obtained in 11 primiparous and 9 multiparous patients with severe pre-eclampsia. The large number of patients with renal disease allowed for single-case evaluation. Eclamptic convulsions and fetal deaths were observed in association with renal disease without foci of additional primary glomerular endotheliosis. The data indicate that pregnancy can exacerbate renal disease and allow for early diagnosis. Fluorescence angiography revealed changes in patients in whom the optic fundi were normal. Tissues of glomerulonephritis stained by immune fluorescence against immunoglobulins and on occasion against human fibrinogen. Primary endotheliosis and nephrosclerosis stained against fibrinogen only. There was no pattern of laboratory data to make the differential diagnosis between primary endotheliosis and various forms of renal disease. Fibrinogen breakdown products were inconsistently increased in contrast to fibrin monomer formation, which was increased regardless of the underlying morphology. It is our feeling that renal biopsy with subsequent pathologic classification is the only technique we have at present which provides relevant information on the effect of renal disease on pregnancy and vice versa.

Biopsy↗

[Enzyme activities of beta-hexosaminidase in urine from patients with renal diseases (author's transl)].

Enzymatic activities of beta-hexosaminidase and beta-galactosidase were determined in 24 h urine specimens from patients with renal diseases, from individuals with essential hypertension and patients with other diseases. Patients suffering from various renal diseases had significantly higher activities of the beta-hexosaminidase than individuals with essential hypertension or other diseases. However for beta-galactosidase only the mean value of the enzymatic activities was elevated. The possible mechanisms causing an increase of these enzymes in 24 h urine samples are discussed.

Galactosidases↗

Malignant nephrosclerosis during pregnancy and in the postpartum period (the uremic hemolytic syndrome).

Histologic, immunohistologic, and ultrastructural features are presented of two cases with malignant nephrosclerosis during pregnancy. Primary malignant nephrosclerosis emerges as a clinical entity which can be distinguished from toxemia of pregnancy in the midtrimester and post partum. The first description of malignant nephrosclerosis dates from 40 years ago, but only a few cases were reported associated with pregnancy. Although disseminated intravascular coagulation seems involved, the morphology is different from that of toxemia. Malignant nephrosclerosis reveals a close similarity to the hemolytic uremic syndrome. Early diagnosis by renal biopsy and proper treatment may prevent a lethal outcome due to progressive failure.

Adult↗