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Biomedical subjects

W Reichel

Publications and source records attributed to W Reichel.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Treatment of glomerulonephritis with heparin (author's transl)].

32 patients with different histologically proven forms of glomerulonephritis were treated with heparin for an average of 31 days. A dosage of heparin was chosen, which allowed an increase in thrombin time to 20-40 seconds. Histological findings alone do not allow any prediction concerning the therapeutic success of heparin treatment in glomerulonephritis. According to our results and comparable information given in the literature, the following therapeutic scheme can be recommended: Best results are seen in patients with a slow decrease of GFR (i.e. less than 30 ml/min) during the year preceding the beginning of the treatment. In rapid progredient glomerulonephritis, however, as in patients without any changes of GFR during this time, predictions as to the course of illness cannot be made. A high level of fibrin split products in serum may be expected to be the most valuable sign of therapeutic effect, as could be documented in 7 out of 8 successfully treated patients. Hypertension and proteinuria were not influenced by the treatment. Because of severe side effects the heparin treatment of glomerulonephritis should not be initiated in patients with severe hypertension.

Blood Coagulation Tests↗
PubMed1976

The different forms of glomerulonephritis morphological and clinical aspects, analyzed in 2500 patients.

Comparative morphological and clinical studies of 2,500 patients suffering from glomerulonephritis, enabled us to divide the different forms of diffuse glomerulonephritis into 3 distinct groups and to separate these groups from the focal glomerulonephritides. The different forms of diffuse glomerulonephritis in group I are: 1. endocapillary (acute) glomeruloenphritis (of the post-streptococcal type), 2. mesangioproliferative glomerulonephritis, 3. mesangioproliferative glomerulonephritis with focal crescents, 4. mesangioproliferative glomerulonephritis with focal scarring, 5. minimal proliferating intercapillary glomerulonephritis without nephrotic syndrome. It is emphasised that these forms can transform into one another, that they seldom occur with nephrotic syndrome, and with varying frequency with hypertension. Group II consists of: 1. minimal proliferating intercapillary glomerulonephritis with nephrotic syndrome, 2. focal sclerosing glomerulonephritis, 3. perimembranous glomerulonephritis, 4. membranoproliferative glomerulonephritis, 5. lobular glomerulonephritis. It is stressed that these glomerulonephritis forms usually do not develop out of group I type glomerulonephritis forms, and that in this group a nephrotic syndrome is the most prominent clinical syndrome. In the third group are 1. mesangioproliferative glomerulonephritis with diffuse crescents, 2. necrotising glomerulonephritis. It is shown that this form of glomerulonephritis does not usually develop from either group I of II forms. The fourth group of focal glomerulonephritis is uncommon. This disease is characterized by a necrotising and proliferative inflammatory lesion found segmentally and focally in the glomeruli. Most of the other glomeruli appearing normal. It is emphasised that in the literature the diagnosis focal glomerulonephritis is made far too often. This is because glomeruli in which the inflammatory process in a few lobules is of varying prominence, are included in the focal glomerulonephritis group. The classification of the different forms of glomerulonephritis into 3 groups here described, is thought of as a basic classification. It is compared with Ellis' classification (1942), with which it has much in common.

Basement Membrane↗
PubMed1976

Membranoproliferative glomerulonephritis with partial lipodystrophy: discordant occurrence in identical twins.

The course of disease of a patient with membranoproliferative glomerulonephritis and partial lipodystrophy is described. The case is further characterized by a deficiency of C3 and C3- activator, by normal values of C4, by evidence of the nephritogenic factor, by raised fibrin degradation products and by an unselective proteinuria. The course of the glomerulonephritis runs parallel to a pronounced susceptibility to infection (at first varicella, tonsillitis and measles, later pneumonia, meningitis, encephalitis and hepatitis). On account of a nephrotic syndrome and an initative impairment of the renal function, a cytostatic treatment was begun, which although raising the C3 level did not influence the further course of the disease. As the patient has a healthy identical twin sister without lipodystrophy, who shows no reduction in C3 and no nephritogenic factor, this case proves that these diseases are acquired and not genetically determined.

Adolescent↗
PubMed1976

[Differentiation of the proteinuria by microelectrophoresis in continuous polyacrylamide-gradient gels (author's transl)].

It is possible to differentiate the proteinuria of glomerulonephritis by means of microelectrophoresis in polyacrylamide-gradient gels. The advantages of this method (quick, cheap, concentration of the urine not required) led to its introduction into clinical use. Upon separating the urinary proteins according to their molecular weight and form, four patterns of proteinuria may be differentiated: low molecular, intermediate and high molecular. Those forms of glomerulonephritis which show constant morphological and clinical findings (e.g. minimal proliferative glomerulonephritis, mesangioproliferative glomerulonephritis with crescents) can be related to one of the four patterns of proteinuria, whereas the pattern of proteinuria in other forms of glomerulonephritis (e.g. (peri-)membranous glomerulonephritis, mesangioproliferative glomerulonephritis) are dependent on the phase of the disease.

Diagnosis, Differential↗
PubMed1976

[Rule of antibody structure. the primary structure of a monoclonal IgG1 immunoglobulin (myeloma protein Nie), I: Purification and characterization of the protein, the L- and H-chains, the cyanogenbromide cleavage products, and the disulfide bridges (author's transl)].

Myeloma protein Nie has been isolated from the serum of a myeloma patient by free flow continuous high voltage electrophoresis or by Pevicon-block electrophoresis. It was further purified by ion-exchange chromatography and gel filtration, and characterized by amino acid analysis and end group determination. Serologically, the protein belongs to the IgG1 subclass. It has been typed as Gm1+, 2-,4- and 17+. The L-chain is of the k-type. The L- and H-chains have been separated by gel-filtration after partial reduction and alkylation and characterized by amino acid analysis and end group determination. The F(ab)- and Fc-fragments, prepared by limited tryptic digestion, have been separated and characterized. Cyanogen bromide splitting products have been prepared both from the intact IgG and from the Fc-and the partially reduced and alkylated F(ab)-fragment. These splitting products have been purified and characterized by amino acid analysis and end group determination. By means of these cyanogen bromide splitting products and by partial reduction and alkylation, the disulfide bridges in the protein could be localized: one L-H-bridge, two inter-H-bridges and four loop forming intra-H-bridges.

Alkylation↗
PubMed1975

Proteinuria and distribution of fibrinogen split products in various forms of glomerulonephritis.

The microelectrophoresis on gradient gels allows differentiation between the different types of proteinuria in 1 h in a one-step procedure. Due to their different molecular weights and forms, fibrinogen split products are separated by this method. The determination of fibrinogen split products not only offers a possibility for dicrimination between the various forms of glomerulonephritis but also offers a possibility for following the course of the disease.

Electrophoresis, Polyacrylamide Gel↗
PubMed1975

Clinical significance of fibrinuria with fibrinogen split-product E following kidney allotransplantation.

Typical findings of disseminated intravascular coagulation were found in patients following kidney allotransplantation where quantitative determinations revealed fibrin degradation products in the urine. Split-product E, which was quantitatively determined in urine samples, contributes to this fibrinuria. Elevated levels of fibrinogen split products in serum as well as in urine are detectable several days prior to clinical signs of rejections and serve as an early indicator of impending rejection in patients with renal allografts.

Fibrin Fibrinogen Degradation Products↗