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T Törnroth

Publications and source records attributed to T Törnroth.

At least 73 records · Page 4Linked to original sources
PubMed1984

Nephritogenic and non-nephritogenic epithelial antigens in autoimmune and passive Heymann nephritis.

The proximal tubular brush border (BB) membrane fraction isolated from rat kidneys contains antigens which induce anti-BB autoantibodies and autoimmune Heymann nephritis in immunized rats. Rabbits immunized with the BB membrane fraction form anti-BB antibodies which, after injection into rats, induce passive Heymann nephritis in rats. Various rat epithelia share antigens with renal tubular BB. However, it is still a controversial issue whether these nonrenal tissues can induce either autoimmune Heymann nephritis in rats or nephritogenic anti-BB antibodies by immunization of rabbits. To test this we have immunized rats and rabbits with different amounts of kidney BB membrane fraction and with tissue fractions known to contain antigens cross-reacting with kidney BB. Using immunohistologic, histologic, and electron microscopic techniques, we studied the development of kidney lesions typical of Heymann nephritis after active or passive immunization of rats. Rat and rabbit anti-BB antibodies were characterized by immunoprecipitation techniques. Both serum anti-BB antibodies and antibodies eluted from the kidneys of the nephritic rats bound to several nonrenal rat epithelia, suggesting that these tissues contain nephritogenic antigens. However, although immunization with 5 micrograms of BB membrane protein could induce glomerular lesions typical of autoimmune Heymann nephritis in a rat, none of the rats immunized with 50 to 600 times greater amounts of nonrenal tissue proteins developed these lesions. Similarly, antibodies from rabbits immunized with rat kidney BB membranes, but not from rabbits immunized with nonrenal epithelia, induced passive Heymann nephritis in rats. The results suggest that the nephritogenic activity is confined to kidney tissue.

Animals↗
PubMed1983

Predominantly vascular amyloid deposition in the kidney in patients with minimal or no proteinuria.

A series of nine patients with secondary (AA type) renal amyloidosis with little or no proteinuria is reported. Renal failure was the presenting sign of renal disease in seven patients. Renal biopsy revealed a predominantly vascular deposition of amyloid in all patients. Three patients had no glomerular amyloid deposits. This pattern of amyloid deposition was found in 12.5% of our renal biopsies from patient with amyloidosis. No significant clinical differences, other than the lack of proteinuria, were noted between these patients and patients with the usual pattern of amyloid deposition.

Adult↗
PubMed1982

Renal biopsy findings in orthostatic proteinuria.

Percutaneous renal biopsy was performed on 15 patients with orthostatic proteinuria and 6 control subjects without proteinuria in order to investigate possible renal alterations. The light-microscopic findings were either normal or showed slight mesangial proliferation in the orthostatic group but were normal in the control subjects, while the immunofluorescence-microscopic study revealed mesangial, capillary or arteriolar deposits of complement C3 and/or immunoglobulins in 10 out of 12 cases with orthostatic proteinuria; complement C3 was seen in only one control subject. The electron-microscopic findings were similar in the two groups, showing slight subepithelial, intramembranous and mesangial alterations. Focal loss of the epithelial foot processes was seen in only one case with orthostatic proteinuria. It is concluded that there are no histological, electron microscopical or immunohistochemical alterations specific for orthostatic proteinuria. A finding of complement in the glomeruli in about half and of immunoglobulin in some of the patients with orthostatic proteinuria is in favour of an association to present or previous glomerulonephritis.

Adult↗
PubMed1981

Aggravation of hypertension in spontaneously hypertensive rats by Heymann nephritis.

1. To explore the effect of nephritis on development of genetic hypertension we immunized 10-week-old spontaneously hypertensive rats with purified rat kidney brush-border antigen. This induces Heymann nephritis (autologous immune complex nephritis), which does not elevate blood pressure in normal rats. 2. Nephritis developed in 11 of the 12 immunized animals, and systolic blood pressure rose to a significantly higher level than in the non-immunized spontaneously hypertensive rats within 4 weeks. Blood pressure remained higher in the immunized rats at 17 weeks, heart weights were greater, but creatinine clearance remained unchanged. 3. At 6 weeks, urinary sodium excretion was greater in the immunized spontaneously hypertensive rats, whereas at 17 weeks, sodium excretion was decreased in these animals along with reduced serum protein concentration, packed cell volume and plasma renin activity, as compared with that of the controls. 4. Development of hypertension in nephritic rats, therefore, appeared unrelated to sodium excretion; signs of volume expansion emerged later. 5. Acceleration of the development of spontaneous hypertension by Heymann nephritis, also leading to sustained higher blood pressure levels than in spontaneously hypertensive rats, offers a new approach to experimental study of immune mechanisms behind acceleration of pre-existing hypertension. This may have important bearings on essential hypertension as well.

Animals↗
PubMed1981

Heymann nephritis-DOCA-NaCl hypertension in the rat. Role of nephritis, DOCA, NaCl, and vascular lesions in the development of hypertension.

In order to explore the impact of nephritis on the development of hypertension, rats with Heymann nephritis were given 0.9% NaCl to drink, in combination with or without DOCA injections, for up to 6 months. Combined nephritis-DOCA-NaCl resulted in severe hypertension and shortened life span, whereas nephritis-NaCl combination failed to induce hypertension or shorten life span. All immunized rats developed membranous glomerulonephritis but creatinine clearance did not decrease. DOCA-NaCl-treated nephritic rats had a heavier proteinuria and more marked renal lesions than NaCl-treated nephritis rats. Proliferative-sclerotic glomerular lesions were seen in the nephritis-DOCA-NaCl group only, correlating to the severity of hypertension. Other renal and extrarenal vascular lesions, increasing with time, also appeared related to the severity of hypertension. This suggests a secondary relationship of vascular damage to hypertension in this model. Appearance of proteinuria preceded the establishment of hypertension, suggesting that nephritis sensitized to the development of hypertension during DOCA-NaCl treatment. Sodium excess alone, however, did not induce hypertension in Heymann nephritic rats. The present Heymann nephritis-DOCA-NaCl hypertension model appears a useful model for the study of hypertension complicating glomerulonephritis.

Animals↗
PubMed1980

An improved colloidal iron stain for glomerular sialoproteins.

The thick sialoglycoprotein coat of the glomerular epithelial cells is a part of the glomerular filtration barrier. It can be demonstrated in paraffin histoslogy by means of the colloidal iron procedure. We have studied the special requirements of tissue processing to obtain reproducible results by this staining method. The requirements include proper fixation, avoiding heat during sectioning and ample rehydration. We have further tested a colloidal iron-PAS procedure for simultaneous demonstration of the glomerular epithelial coat and the basement membrane.

Animals↗
PubMed1980

Hyperreninemia, lysozymuria, and erythrocytosis in Fanconi syndrome with medullary cystic kidney.

Adult onset Fanconi syndrome with medullary cystic kidney was diagnosed in a 30-year-old male with muscular weakness, hypokalemia, normal BP, hyperreninemia, and secondary aldosteronism. He also had non-specific aminoaciduria, lysozymuria, and beta 2-microglobulinuria. Urinary concentrating and acidifying capacity was impaired, and both sodium and potassium were lost into the urine. I.v. pyelography revealed medullary cystic kidney. Renal biopsy showed juxtaglomerular hyperplasia, heavy subintimal deposits and C3 and IgG in preglomerular arteriolar walls, and degenerative changes in the tubules, including loss of brush border and "macula densa-like" lesions. Polycythemia with elevated serum erythropoietin levels, and raised blood ACTH values with features of cortisolism were also present. Indomethacin therapy decreased plasma renin activity (PRA), plasma aldosterone, and urinary loss of potassium and sodium, while serum potassium approached normal levels. Metoprolol, a beta-adrenergic blocking agent, caused similar effects. Insensitivity to the pressor effect of angiotensin II was reversed by indomethacin treatment. Somatostatin infusion lowered PRA and aldosterone without affecting BP. Several biochemical aberrations of this patient resemble Bartter's syndrome, including the effect of indomethacin.

Adult↗
PubMed1980

Autologous immune complex nephritis and DOCA-NaCl load: a new model of hypertension.

In order to explore immunological features of hypertension, we studied autologous immune complex nephritis (Heymann nephritis) combined with DOCA-NaCl treatment. This combination resulted in hypertension and increased heart weight whereas DOCA-NaCl treatment alone induced only a slight elevation of blood pressure and a moderate increase in heart weight. Nephritic rats without DOCA-NaCl load remained normotensive, their heart weights being comparable to those of controls. This new model of hypertension was neither characterized by azotemia nor by reduced renal excretory capacity. Hypertension was not renin-angiotensin-dependent. DOCA-NaCl treatment accelerated the development of proteinuria. In the hypertensive rats, systolic blood pressure to daily urinary protein excretion. Renal histopathology revealed changes resembling those of malignant nephrosclerosis. Immunohistology and electron microscopy showed a typical membranous glomerulonephritis in all immunized animals. It was concluded that immune complex disease of the Heymann nephritis type may interfere with normal hemodynamic adaptation to hypervolemic sodium load, resulting in hypertension.

Animals↗
PubMed1980

Fibronectin as a marker for the glomerular mesangium in immunohistology of kidney biopsies.

Antibodies against fibronectin have been used as a marker for the glomerular mesangium in routine immunofluorescence microscopy of renal biopsies. Rhodamine-conjugated antibodies against fibronectin were used in this study of 22 human kidney biopsies and four histologically normal kidneys in combination with routinely employed fluorescein-conjugated antibodies against immunoglobulins, complement components, and fibrin. The distribution of fibronectin was similar to mesangial material demonstrable by silver impregnation. By the double staining procedure localization of deposits in relation to the mesangium was considerably facilitated. Variations in the mesangial fibronectin were observed; staining was increased in seven of 11 cases of mesangial glomerulonephritis, and decreased or absent in four of four cases of membranous glomerulonephritis and three of three cases of amyloidosis. Abnormal localization of fibronectin was observed in glomerular crescents and in the intertubular area together with fibrin in kidney transplants. The results suggest that antibodies against fibronectin are useful markers for the glomerular mesangium and that alterations in mesangial fibronectin may reflect the functi-nal state of the glomerulus. Abnormal localization in extramesangial areas may result from local synthesis or increased adsorption of circulating fibronectin to fibrin or collagen.

Adult↗
PubMed1980

Heymann nephritis induced by kidney brush border glycoproteins.

Heymann nephritis developed in rats immunized with brush border membrane fractions isolated from rat kidney tubules. Glomerular autoantibodies eluted from cryostat sections of nephritic kidneys reacted in immunoelectron microscopy with the outer surface of isolated brush border membrane vesicles. This indicates that the autoantigens are plasma membrane components. To characterize further the chemical nature of the nephritogenic autoantigens, we treated the brush border membranes with trypsin and sodium deoxycholate, and the solubilized membranes were then fractionated by lectin affinity chromatography. The polypeptide composition of the fractions was analyzed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. The capacity of the membrane fractions to induce Heymann nephritis was assessed by observing the development of typical renal lesions, antibrush border autoantibodies, and proteinuria in rats immunized with these fractions. The results suggest that the nephritogenic autoantigen is an integral component of the brush border membrane of kidney proximal tubules and has an affinity for Lens culinaris agglutinin. This indicates that it is a glycoprotein and has mannosyl and/or glycosyl groups exposed in its oligosaccharide side chains.

Animals↗
PubMed1979

Fatal renal vasculitis and minimal change glomerulonephritis complicating treatment with penicillamine. Report on two cases.

Two cases with different and not previously described fatal renal complications during treatment with penicillamine are reported. A man with seronegative rheumatoid arthritis with features of systemic lupus erythematosus was treated with penicillamine for six months and developed a mild membranous glomerulonephritis and a severe renal vasculitis leading to uremia and death. A woman with primary biliary cirrhosis was treated with penicillamine for nine months and developed a nephrotic syndrome, the renal biopsy showing minimal change glomerulonephritis. The nephrotic syndrome responded to prednisone but the patient died, probably from septicemia. Penicillamine may thus cause glomerular damage without deposition of immune complexes. A restricted use of the drug is recommended.

Female↗
PubMed1979

Renal transplantation in amyloidosis.

During a three-year period renal transplantation was performed in 12 patients with amyloidosis. This disease was primary (or the cause unknown) in two cases and secondary in ten. In the latter cases the primary disease was rheumatoid arthritis in six, ankylosing spondylitis in one, osteomyelitis in two and tuberculosis in one. Five of the 12 patients were alive one year after transplantation. Two years after transplantation four out of seven were alive. Graft survival was the same. At the end of the three-year period five patients were alive. In two of these cases renal biopsy showed amyloid deposits in the transplant two and three years, respectively, after the transplantation.

Adult↗
PubMed1979

Resolution of renal amyloidosis secondary to rheumatoid arthritis.

A patient with seronegative rheumatoid arthritis developed a nephrotic syndrome. Histological examination of renal biopsy disclosed moderate amyloidosis. Ultrastructurally the glomerular amyloid deposits were seen to be located both within the mesangium and subepithelially in the peripheral capillaries. The patient was treated with prednisone and cyclophosphamide for two years. The nephrotic syndrome remitted and a follow-up biopsy showed almost total disappearance of Congo red positive amyloid substance. Electron microscopy showed abundant finely granular material but only small amounts of fibrillar amyloid in the mesangial regions and intramembranous lucent areas containing few amyloid fibrils but no subepithelial deposits in the peripheral capillaries. We conclude that the mesangial amyloid substance was degraded to granular material and that the subepithelial amyloid deposits were resolved by mechanisms similar to those involved in the resolution of subepithelial immune complex deposits, i.e. through slow washing out and incorporation into the basement membrane.

Amyloidosis↗
PubMed1979

Granulomatous glomerulonephritis in a patient with rheumatoid arthritis treated with gold salts.

The clinical course of rheumatoid arthritis in the patient described was characterized by two episodes of microhaematuria, both occurring shortly after the administration of gold salt. The second of these episodes developed into progressive renal failure. Renal biopsy disclosed a rarely described granulomatous glomerulonephritis. Various known pathogenic mechanisms of renal injury are evaluated concerning their applicability in this patient. However, although it is believed that the gold salt therapy was the main agent in the pathogenesis of this fatal renal complication, the mechanism whereby such a pathogenesis proceeded remains unclear.

Aged↗