A neurophysiological bedside technique for monitoring uraemic brain dysfunction.
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Biomedical subjects
Publications and source records attributed to H Losse.
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An 18-year-old female with primary oxalosis, seen first when she was in advanced renal failure, developed a severe necrotizing angiopathy which began after a rapid decrease in renal function requiring chronic dialysis. Because of the severe angiopathy the preliminary diagnosis of an acute autoimmune vasculitis had been made. The correct diagnosis was revealed by renal biopsy and a renal transplantation performed. Soon after severe oxalosis led to failure of the renal transplant and death. The patient had also had familial spherocytosis, inherited from her father, while the oxalosis had been inherited from her mother. It is suggested that early transplantation at the onset of renal failure, as long as the blood oxalate level is still tolerably low, may give better results than have so far been reported.
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Plasma aluminium, zinc and copper were determined in 68 patients with chronic renal insufficiency and in 20 healthy individuals. In the renal insufficiency group 16 patients had received aluminium containing substances particularly phosphate binding drugs (aluminium hydroxide) for a long time. We observed that only the patients taking aluminium hydroxide showed elevated aluminium levels in plasma (controls: 0.86 +/- 0.27 mumoles/l; renal insufficiency: 3.05 +/- 1.63 mumoles/l). In two of these patients with symptoms of "dialysis dementia", plasma aluminium concentrations were markedly increased. The zinc concentrations in plasma of patients with renal insufficiency were slightly decreased (controls: 14.48 +/- 2.65 mumoles/l; renal insufficiency: 11.77 +/- 2.35 mumoles/l); the plasma copper concentrations were slightly increased (controls: 17.3 +/- 2.83 mumoles/l; renal insufficiency: 22.98 +/- 4.7 mumoles/l). There was a distinct decrease of plasma zinc concentrations in patients with raised aluminium levels. The clinical aspects of these changes are discussed.
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The etiology of retroperitoneal fibrosis still is largely unknown. Autoimmunologic mechanisms, traumata, systemic diseases, and drugs have been discussed as possible etiologic factors. The presented case was found to have a Klinefelter's syndrome besides retroperitoneal fibrosis. We do not believe that there is a relation between the two diseases. The retroperitoneal fibrosis of this case responded well to glucocorticosteroid therapy and the severly reduced renal function became normal.
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.
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