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Biomedical subjects

T Törnroth

Publications and source records attributed to T Törnroth.

At least 55 records · Page 3Linked to original sources

Atrophic gastritis in Sjögren's syndrome. Morphologic, biochemical, and immunologic findings.

Gastric studies were carried out in 16 patients with well-documented Sjögren's syndrome (SS), 43 matched rheumatic disease patients without SS, and 7 patients with chronic atrophic gastritis not associated with SS. Chronic atrophic gastritis was a much more common finding in the SS patients than in the rheumatic disease control patients. Significant hypopepsinogenemia was present in 11 of 16 SS patients. In 6 patients this was combined with hypergastrinemia, a combination highly specific for chronic atrophic gastritis. The lowest pepsinogen levels were seen in patients with primary SS associated with high levels of SS-B antibody. On a histologic and biochemical basis, it was not possible to distinguish the gastric findings in primary SS from those in secondary SS, nor to distinguish chronic atrophic gastritis associated with SS from that not associated with SS. We conclude that chronic atrophic gastritis is a prominent feature in SS and that the severity of the gastritis appears to correlate with some serologic parameters of SS.

Adult↗

Alterations in glomerular lectin binding sites of human kidney as detected by fluorescence microscopy.

Different lectins were used to study frozen sections of kidney samples showing alterations in routine immunofluorescence studies. Arachis hypogaea agglutinin (peanut lectin, PNA), lacking binding sites in normal glomeruli, bound to the glomeruli in two of the five samples studied, giving a granular fluorescence pattern. Concomitantly with the appearance of PNA-binding, binding sites for wheat germ agglutinin (WGA) appeared to be lost at glomeruli. Furthermore, changes in the expression of glomerular binding sites for Wistaria floribunda (WFA), Helix pomatia (HPA) and Dolichos biflorus (DBA) agglutinins could be seen in the kidneys studied, whereas the binding sites for Ulex europaeus agglutin (UEA I) in vascular endothelia seemed to be unaltered. The results show that kidney specimens presenting changes in routine immunofluorescence studies may also present altered binding for certain lectins. On this basis we propose that certain lectins may aid in characterizing these changes and are thus of potential use in studying diseased kidneys.

Fluorescent Antibody Technique↗

Glomerular sialic acid in Heymann nephritis and diacetylbenzidine induced nephropathy in rats.

Glomerular sialic acid was chemically measured in rats with experimental proteinuria induced by N,N'-diacetylbenzidine (DAB) or with autoimmune Heymann nephritis. In DAB nephrosis and in Heymann nephritis the relative amount of glomerular protein was increased. In DAB nephrosis the quantity of sialic acid expressed per amount of protein was decreased, but expressed per amount of DNA, which reflects the number of cells, there was no significant change. In Heymann nephritis the amount of sialic acid was not significantly altered when expressed per amount of protein or per amount of DNA. In individual animals, the amount of glomerular sialic acid expressed per amount of protein or per amount of DNA did not correlate with the severity of proteinuria. An increase in the total number of glomerular cells was found only in Heymann nephritis. The results suggest that proteinuria in the reported models is not the result of changes in glomerular sialic acid.

Animals↗

Primary amyloidosis with increased plasma carcinoembryonic antigen concentration. A case report.

A patient with suspected malignant disease had increased concentration of plasma carcinoembryonic antigen (CEA). Amyloidosis was demonstrated at autopsy. The amyloid fibril composition was characterized by immunohistochemical and immunochemical techniques and proved to be of the lambda light chain (AL) type. CEA was demonstrated in the liver parenchyma by using antihuman CEA antiserum. Increased plasma CEA concentration in a patient with primary amyloidosis has, to our knowledge, not been reported before.

Aged↗

Is amyloid A (AA) amyloidosis always secondary?

The case is reported of a patient with systemic AA amyloidosis associated with non-specific mesenteric lymphadenitis and chronic sideropenia. Renal, small bowel, and rectal biopsies showed amyloid deposits containing AA protein, as defined by potassium permanganate sensitivity and by reactivity with AA antiserum. Reversal of the nephrotic syndrome occurred during steroid-azathioprine therapy.

Adult↗

Recurrence of IgA nephropathy with nephrotic syndrome in renal allograft.

A 59-year-old female presented with peripheral oedema in association with an upper respiratory tract infection in August 1980. On examination she was found to have nephrotic range proteinuria, haematuria, slightly decreased renal function and elevated blood pressure. Renal biopsy showed mesangial proliferative glomerulonephritis with mesangial IgA and C3 deposits. She was treated with corticosteroids and later with cyclophosphamide, but without any response. 1 year after the onset of disease, she developed terminal renal failure. In December 1981, she received a cadaveric renal allograft; thereafter renal function became normal but she remained proteinuric, and developed fulminant nephrosis within 2 years. A transplant biopsy revealed alterations in the graft, indicating recurrence of the original disease.

Adrenal Cortex Hormones↗

Fine-needle aspiration biopsy at various stages of induction of Heymann nephritis.

Fine-needle aspiration biopsy (FNAB) has been successfully used for the monitoring of the in situ inflammatory response of rejection. We have evaluated FNAB as a technique for the quantification and cytological classification of infiltrating leukocytes during the induction of and manifest Heymann nephritis (HN). FNAB results were compared and supplemented with results of conventional histopathological and immunofluorescence (IFL) studies and with immunohistochemical studies to classify infiltrating T-lymphocyte subsets with immunoperoxidase (IP) technique. Rats (8/group) were killed three weeks after immunisation, and two and ten weeks after a booster. FNAB proved more sensitive than histopathological examination for the evaluation of interstitial infiltration in HN. Plasmablasts dominated the inflammatory picture three weeks after immunisation, when no glomerular or interstitial changes were observed histopathologically. The intensity and number of plasmablast reactions reached their peak two weeks after the booster, although disease was still not apparent. When membranous glomerulonephritis (MGN) was established, FNAB indicated plasmablasts in 4/7 rats, the reaction was strong in two. These rats had the most severe histopathological changes, too. FNAB indicated modest lymphocyte infiltration three weeks after immunisation. Immunohistochemical subtyping of T-lymphocytes showed initial T-helper infiltration, which gradually decreased after the booster, and had disappeared when MGN was manifest. At this stage T-suppressor infiltration was observed in the same two rats which had strong plasmablast reactions and severe HN with interstitial changes, as well. These observations suggest a role for cell-bound immunity in the induction of HN. Plasmablast reaction may initially be supported by the infiltrating T-helper lymphocytes, and it may imply local antibody production. Severe manifest disease was associated with both plasmablast and suppressor cell infiltration.

Animals↗

Renal allograft glomerulonephritis.

The analysis of 1282 renal transplantations revealed 14 cases of allograft glomerulonephritis (GN). Membranous GN was found in seven patients, in four of whom the GN appeared de novo. IgA GN was evident in three cases and focal segmental glomerulosclerosis and mesangiocapillary GN type 1 in two cases each. The signs of GN were detected 0.5-72 months after transplantation. The most common clinical sign indicating an allograft biopsy was nephrotic syndrome. Deterioration of the graft function was often seen and it was usually associated with chronic rejection.

Adolescent↗

Hypertension and progression of experimental nephritis. Interaction between immunological and haemodynamic factors.

Hypertension has been shown to accelerate the course of experimental nephritis. On the other hand, Heymann nephritic rats undergoing long-term DOCA-NaCl treatment develop hypertension with a malignant course. The present study examined the effect of a short-term DOCA-NaCl load on the development of hypertension and progression of nephritis. Heymann nephritic rats were treated with DOCA-NaCl between weeks 2 and 6 after the first immunization with brush border antigen. Within six weeks, hypertension developed in Heymann nephritis-DOCA-NaCl rats but not in Heymann nephritic rats without DOCA-NaCl treatment whereas DOCA-NaCl-treated rats developed a moderate elevation of blood pressure. During that time, anti-brush border antibodies and immune deposits typical of membranous nephropathy ensued, preceding appearance of proteinuria or histopathologically detectable renal changes in the immunized rats. After discontinuation of DOCA-NaCl treatments at week 6, blood pressure nearly normalized in DOCA-NaCl-treated rats. Within one year, however, blood pressure rose most markedly in nephritic rats treated initially with DOCA-NaCl. The rise in blood pressure at that time correlated with glomerular sclerosis, tubulo-interstitial changes and proteinuria. It is concluded that, during acute nephritis, immunological and hypertensinogenic mechanisms interact, leading to hypertension and aggravated course of nephritis. These experimental observations on nephritis-associated hypertension may have important bearings on human hypertension as well.

Animals↗

Lectins as markers for cells infiltrating human renal glomeruli.

This study describes a simple method for detecting mononuclear cells in human renal glomeruli using labeled lectins as probes. The lectins used in this study showed prominent binding to different cell types among the nonresident glomerular cells but not to normal glomerular elements. Monoclonal antibodies against monocytes/macrophages (OKM 1), T-cells (OKT 11), suppressior/cytotoxic T-cells (OKT 8), and anti-lysozyme antibodies were used in double-fluorescence studies with the lectins in an attempt to identify the lectin-positive cells. The results indicate that Bandeiraea simplicifolia I isolectin and Lotus tetragonolobus agglutinin in particular are useful for screening of kidney biopsies for cells of their monocyte/macrophage series and T-cells invading human renal glomeruli.

Antibodies, Monoclonal↗

Simultaneous anti-glomerular basement membrane and membranous glomerulonephritis: case report and literature review.

A 20-year-old male experienced a sore throat, fever, and lumbar pain. Examination revealed haematuria, proteinuria, and transiently impaired renal function. Renal biopsy revealed minor mesangial widening and small cellular crescents in 20% of the glomeruli under the light microscope, whereas immunofluorescence showed bright, linear staining of IgG along the glomerular basement membrane (GBM). Ultrastructural analysis showed minute subepithelial deposits analogous to early membranous glomerulonephritis (MGN). Anti-GBM antibodies were detected in the patient's serum. These findings were suggestive of simultaneous anti-GBM and immune complex glomerulonephritis in a patient with a mild, reversible renal illness.

Adult↗

Transformation of membranous glomerulonephritis into crescentic glomerulonephritis with glomerular basement membrane antibodies. Serial determinations of anti-GBM before the transformation.

This case report describes a patient who initially had a pleuritis and arthalgias. During the follow-up he developed first a membranous glomerulonephritis with nephrotic syndrome and subsequently a crescentic, rapidly progressive glomerulonephritis with glomerular basement membrane antibodies (anti-GBM). An analysis of the serum samples obtained during the follow-up revealed no infections at the onset of renal failure. However, anti-GBM could be demonstrated in the serum samples obtained 2 months before the deterioration of the renal function. The anti-GBM did not react with alveolar BM and the patient had no signs of pulmonary hemorrhage. The etiology and the sequence of the pathological events of rapidly progressive glomerulonephritis is discussed in the light of these observations.

Autoantibodies↗

Glomerulonephritis in renal allografts: results of 18 years of transplantations.

The analysis of 1282 renal transplantations revealed 13 cases of allograft glomerulonephritis (GN). Membranous GN was detected in seven patients, and mesangiocapillary GN type 1, IgA GN and focal segmental glomerulosclerosis in two patients each. The transplantation material included 13 patients with post-transplant nephrotic syndrome (NS), in 9 of whom it was evidently caused by GN. NS was the most common clinical sign of allograft GN. In addition, one patient developed low-grade proteinuria and one hematuria. In one case no signs of GN were detected at the time of graft biopsy. Loss of allograft function was associated with additional severe rejection changes. Five patients are living with a functioning graft, four have been started on hemodialysis and four have died form non-renal causes. It is concluded that NS is rare after renal transplantation and that it is most often caused by allograft GN. The prognosis of the graft is determined by co-existing rejection.

Adolescent↗

Mycoplasmal pneumonia associated with mesangiocapillary glomerulonephritis type II (dense deposit disease).

A 20-year-old man developed pneumonia and glomerulonephritis concomitantly with significantly rising Mycoplasma pneumoniae complement-fixing antibody titres. Renal biopsy showed mesangiocapillary glomerulonephritis type II (dense deposit disease). Attempts to demonstrate mycoplasmal antigen in the glomeruli failed. This is the third of five previously reported cases of glomerulonephritis associated with Mycoplasma pneumoniae and exhibiting dense deposit disease.

Adult↗

Nephritis among young Finnish men.

During an eight-year period (1975-1982) 174 military conscripts (out of a total of 314,000) were submitted to Helsinki University Central Hospital, Fourth Department of Medicine, on suspicion of renal disease. Eighty-four had isolated hematuria, 61 hematuria and concomitant proteinuria and 29 persistent proteinuria. In 100 of them the urinary abnormality was an incidental finding, 62 suffered from symptoms of infection and the rest had other complaints. A renal biopsy was performed, yielding a representative sample in 171 cases, after other causes of the urinary abnormality had been excluded. Morphological analysis showed that 131 patients had glomerulonephritis, IgA nephropathy being the most common type (70 patients). Tubulo-interstitial nephritis was seen in two cases, and nephrocalcinosis in one. Among 37 cases with apparently normal glomeruli under light microscopy, immunofluorescence analysis revealed glomerular deposits other than IgA in 19 cases and no deposits in 15 (three were inadequate for this analysis). On the basis of the figures in this study the average number of annually detected cases of nephritis was 48 per 100,000 Finnish conscripts. During the same period an annual average of 46 per 100,000 young men were exempted from military service because of nephritis, giving an overall figure of 94 cases of nephritis detected annually per 100,000 young Finnish men.

Adult↗