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W Thoenes

Publications and source records attributed to W Thoenes.

At least 73 records · Page 4Linked to original sources

[New aspects of amyloidosis (author's transl)].

Amyloid is a substance that has the same composition of the basic qualities even in the different patterns of amyloidosis. Electron microscopic investigations have revealed that all forms of amyloidosis do not only exhibit homogeneous basic qualities but also common principle of accumulation. This may be commented as follows: Fibrils of amyloid are always found in close connection with basement membranes or basement membrane-like substances respectively produced by cells with the property of contracting (myocytic or "myopotent' cells). Collagen fibres of different types do not display a regular relation to the substance of amyloid. The origin and development of the various forms of amyloidosis depends on the three following factors: 1. On the extent of the production of amyloidogenic proteins which may belong to different types of proteins according to the basic disease; 2. On the way of protein silting (hematogenic silting-generalized amyloidosis; local enrichment--local amyloidosis); 3. On the site of predilection of all deposits of amyloid in the areas of basement membranes or basement membrane-like substances resp. produced by cells with the properties of contracting. A new classification should be made on the basis of these principles.

Amyloid↗

Cell fusion as a mechanism for the formation of giant cells (Langhans' type). Autoradiographic findings in autoimmune tubulo-interstitial nephritis of the rat.

The formation of multinuclear giant cells of the Langhans' type in tubulo-interstitial auto-immune nephritis in the rat has been investigated by means of autoradiography. While in the majority of giant cells all nuclei were radiolabeled, in a few both labeled and unlabeled nuclei were present. This latter finding represents strong evidence in favour of the hypothesis that giant cells do not form by endomitotic processes but rather through fusion of certain precursor cells. According to previous studies this precursor cell population consists mainly of epitheloid cells, i.e. modified monocytes.

Animals↗

The glomerular lesions in endotheliotropic hemolytic nephroangiopathy (hemolytic uremic syndrome, malignant nephrosclerosis, post partum renal insufficiency).

The term "Endotheliotropic Hemolytic Nephroangiopathy" (EHN) comprises various clinically or pathomorphologically defined disease states with severe renal lesions (e.g. hemolytic uremic syndrome, malignant nephrosclerosis, post partum renal insufficiency) which, to date, have been considered as different entities. We attempted to assign accompanying glomerular changes based upon light and electron microscopy to the above mentioned clinical pictures and their various stages. The accordingly classified glomerular lesions (G1--G3 and Ga) are of critical importance in pathohistological differential diagnosis. Since it is assumed that fibrin is a causing event in the pathogenesis of the vascular lesions, quantitative evaluation of glomerular fibrin deposits was done. The results, when viewed with respect to time, lead to the conclusion that the microthrombotic component represents a secondary phenomenon. Thus, the primary and hence pathogenetically most important finding is a severe damage to the endothelium of the terminal renal vasculature. This endothelial damage although being expressed with variable intensity has to be regarded as the common denominator inherent to all types of glomerular lesions in EHN.

Acute Kidney Injury↗

Subtypes of acute postinfectious glomerulonephritis. Synopsis of clinical and pathological features.

42 kidney biopsies from adults and children suffering from acute postinfectious glomerulonephritis were examined by light microscopy, immunofluorescence and electron microscopy. The biopsies were obtained within 9 weeks of the onset of the first clinical symptoms. The results show not only a range of variation in the histological picture (particularly in the accumulation of leukocytes in the capillary lumens, and in the degree of cell proliferation) but also different immunofluorescent patterns which we have called the "starry sky", "garland" and "mesangial" patterns. These patterns correspond to characteristic differences in the electron microscopic picture. The "starry sky" pattern (IgG, IgM and/or IgA, combined with C3) occurs mainly in the first weeks of the disease and is associated with an endocapillary-mesangial glomerulonephritis. This may turn into a "mesangial" pattern (mostly C3 alone) which is associated mainly with mesangial proliferation. Four types of immune deposits can be observed electron microscopically in all three patterns (subendothelial, subepithelial, mesangial and intramembranous), but their different quantitative distribution determines the characteristic picture. Subepithelial deposits (so called "humps") often considered characteristic of poststreptococcal glomerulonephritis play a dominant role in the "garland" pattern. The cases with a "garland" pattern often show strikingly high levels of proteinuria (greater than 5 g/24 hr). It is believed that in patients with postinfectious glomerulonephritis deposition of immune complexes of various composition is responsible for producing the described subtypes depending on their different distribution in the glomeruli. It seems possible that these subtypes have different clinical significance, something which could be confirmed by performing follow-up studies.

Acute Disease↗

Characterization of cells involved in the formation of granuloma. An ultrastructural study on macrophages, epitheloid cells, and giant cells in experimental tubulo-interstitial nephritis.

In experimental tubulo-interstitial (anti-basement membrane) nephritis of the rat, granulomatous inflammation develops around immunologically altered tubular basement membranes. The present light- and electron microscopic studies indicate that in the course of the granulomatous reaction, tissue monocytes evolve from blood monocytes and pursue two independent pathways of differentation. On the one hand they may differentiate into macrophages ("distant from tubules") or, alternatively, into epitheloid cells ("adjacent to tubules"). The latter, through cell fusion, develop into multinucleated giant cells of the Langhans' type. The cytoplasmic components of the epitheloid cells and the multinucleated giant cells should be interpreted as an activation of cellular biosynthesis. Its products, upon being secreted at the immunodefective basement membrane, will obviously serve immune defense mechanisms.

Animals↗

Interstitial nephritis in a patient with atypical Sjögren's syndrome.

A patient was observed with interstitial nephritis which resulted in renal tubular acidosis (distal type), tubular proteinuria and defective urinary concentrating ability in the absence of edema, elevated arterial blood pressure, glomerular proteinuria or abnormal urinary sediment. The presence of interstitial nephritis was established by renal biopsy which showed dense infiltrates in the interstitium, interstitial fibrosis and thickening and splitting of the pericapillary basal membranes. Immunofluorescence was non contributory. Extrarenal symptoms were discrete (arthralgia of both hands, Raynaud's syndrome upon cold exposure). Mixed connective tissue disease (MCTD) was suspected because of a positive ANF test (speckled pattern), which was completely abolished by ribonuclease pretreatment. However, in hemagglutination tests, no antibodies against ribonuclear protein (ENA) could be demonstrated. The diagnosis of Sjögren's syndrome was established by demonstration of antibodies against SSA and SSB antigens. The observation suggests that in patients with interstitial nephritis the diagnosis of Sjörgren's syndrome must be considered even if extrarenal symptoms of Sjögren's disease are minimal or lacking. The diagnosis can be established with recent serological techniques.

Adult↗

[Clinico-pathological data in infants with different types of nephrotic syndrome (author's transl)].

Case reports including light- and electron microscopy about 4 children with infantile nephrotic syndrome are given. Histologic lesions were microcystic renal disease ("Finnish type"), diffuse glomerular mesangial sclerosis, glomerular mesangial proliferation and minimal changes in the 4 patients, respectively. Knowledge of the individual histologic lesion is essential for adequate therapy and the prognosis in all infants with nephrotic syndrome, except in cases with data proving the Finnish type; in some cases, the identification of individual histologic type will lead to adequate genetic counselling of the family.

Biopsy↗

[Current problems of glomerulonephritis (author's transl)].

Setting out with the theory of glomerulonephritis from Volhard and Fahr (1914) and the fundamental patho-anatomical examinations on this subject by Theodor Fahr (1925, 1934) the actual problems of glomerulonephritis are described. Progress in nephropathology and immunopathology which was partly conditioned by progress in the methodical fields has come to the result that, nowadays, an appropriate characterization of glomerulonephritic diseases is only possible by the synopsis of the three categories: Immunopathogenesis, pathomorphology and clinic. Each of these categories has its own classification. The nosology of the various GN types results from the (constant or variable) combination of the components of these three systems. By this means, some known types of glomerulonephritis were confirmed, some were newly defined, and new entities with variable clinical relevance were layed bare. Because immunopathogenetic events very often induce characteristic structural alterations in the glomeruli, it is the pathomorphological nomenclature which -- as pars pro toto -- still is the best suited for common interchange.

Antigen-Antibody Complex↗

[Histopathology of the kidney in pseudo-Bartter's Syndrome induced by chronic abuse of diuretics (author's transl)].

A 38-year-old female patient developed a Pseudo-Bartter's-Syndrome with hypokalemic alkalosis, hyponatremia and hyperrenism as the result of the abuse of diuretics (furosemide, spironolactone, thiabutacide) for a period of more than 10 years. The needle biopsy specimen from the kidney showed a hyperplasia of the juxtaglomerular apparatus and of the mesangium cells as the morphologic basis of hyperrenism, a focal vacuolisation of the proximal tubular epithelium and a focal atrophy of the distal tubules. The pathogenesis of the tubular alterations and their possible relation to hypokalemia, hypoxemia or drug-toxicity is discussed, a satisfactory interpretation, however, cannot be given. The encroachment of proximal tubular epithelium on the parietal layer of Bowman's capsule is another striking pathoanatomical finding, and considered a compensatory mechanism under the continuous loss of water.

Adult↗

Architecture and cell structures in the distal nephron of the rat kidney.

Using semi-thin sections of marked tubules of the rat kidney, the distal part of the nephron is represented in toto for the first time and reconstructed in its course from the thick part of HENLE's loop to its junction with another collecting tubule. The shape of the model accords well with observations in vivo. On the basis of observations with light and electron microscopy, four types of cells are differentiated: Type 1 (Mittelstück) cell; type 2 (intermediate) cell; type 3 (light) cell and type 4 (intercalated) cell. According to the distribution of these different types of cells, the distal nephron is divided in the following way: Pars recta and pars convoluta of the distal nephron consist of type 1 (Mittelstück) cells; pars arcuata and pars recta of the cortical collecting duct exhibit type 3 (light) and type 4 (intercalated) cells; in the connecting portion of the distal tubule all four types are represented, type 2 (intermediate) and type 4 (intercalated) being the most frequent. The demarcation of the connecting portion according to our definition points to a dynamic relationship of the cell structures of the distal nephron, which gains clarity when conditions are experimentally varied. Hence the question for a morphological proof of where exactly the two nephrogenic blastemata join gives place to the more important question of what these cell structures and their variability mean as signs of functional adaptation-reactions.--The existence of the connecting portion, contested until now, is affirmed; a cytological characterization of it is given and a definition is recommended.

Animals↗

The obsolescent renal glomerulus--collapse, sclerosis, hyalinosis, fibrosis. A light- and electron microscopical study on human biopsies.

By light and electron microscopical examination it is shown that four structural components can contribute to obsolescent glomeruli: capillary basement membranes, enriched mesangium matrix, "vascular" hyalin and collagen fibers. Each of these components can bring about glomerular damage alone. One non-reactive form--a glomerular collapse with only basement membrane remnants--can be separated from three reactive forms: the accumulation of mesangium matrix (sclerosis or matrix-sclerosis), deposition of vascular hyalin (hyalinosis in the narrow sense), and fiber development within the former urinary space (fibrosis or fibro-sclerosis). The use of the term "fibrinoid" in place of the descriptive term "hyalin" is not supported by objective results. Knowledge of the various constituents which accumulate in the reactive types of glomerular obsolescence might be important in the diagnosis of the underlying disease, though mixed pictures were often observed. To avoid terminological overlap we suggest that the term "hyalinization" is replaced by "obsolescence" or "scarring" with specification of the structural components involved.

Adult↗

Formation of basement membrane in extracapillary proliferates in rapidly progressive glomerulonephritis.

In the extracapillary proliferations (crescents) of the glomeruli in glomerulonephritis, basement membranes appear and in addition "secretory bodies" are formed in the cisternae of the rough endoplasmatic reticulum. The findings permit the conclusion that proliferated visceral epithelial cells are involved in the crescent formation to a greater extent than previously assumed.

Basement Membrane↗