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  • 1
    Electronic Resource
    Electronic Resource
    Granulocyte lysosomal factors and plasma elastase in uremia: A potential factor of catabolism (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 218-224 
    Details
    ISSN: 1432-1440
    Keywords: Granulocyte lysosomal factors ; Elastase ; Acute and chronic uremia ; Catabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In uremic intoxication proteolytic activity in plasma and striated muscle is enhanced. To get further insights into the underlying mechanisms the lysosomal factors of polymorphonuclear (PMN) leukocytes and the plasma elastase-α 1-proteinase inhibitor complex were investigated in patients with acute and chronic renal failure. Lysosomal activity was evaluated in peripheral blood smears by the lysis of erythrocytes and plasma (halo formation) around each neutrophil induced by 0.25 M NaCl borate buffer. In about half of the patients with chronic renal insufficiency on dietary treatment lysosomal activity of PMN leukocytes was reduced. The plasma concentration of elastase-α 1-proteinase inhibitor complex was normal in most subjects, but increased in three patients with the highest serum creatinine levels (〉13 mg/dl). In the patients with acute renal failure (ARF) of various origin (postoperatively, septicemia, pancreatitis, or dye-induced) halo formation was either reduced or absent. The plasma elastase-α 1-proteinase inhibitor complex was increased in 5/6 of the patients by a factor of two to four. Also in the patients on regular hemodialysis treatment halo formation of PMN leukocytes was substantially reduced, whereas the plasma levels of elastase-α 1-proteinase inhibitor complex was slightly increased. The finding of reduced lysosomal activity of PMN neutrophils in uremia may be partly due to an enhanced release of neutral proteinases into the circulation as indicated by the elevated plasma levels of elastase-α 1-proteinase inhibitor complex in some patients. This release might be in part due to the effect of “uremic toxins”. In the patients on hemodialysis treatment the contact of the blood with the dialyzer (cuprophane) membrane might be an additional factor. Moreover, in the patients with acute renal failure the underlying disease (infection, shock, trauma) contributes to the release of proteinases. These disturbances may be harmful to the patient if the blood concentration or function of the most important proteinase inhibitors (α 1-proteinase inhibitor,α 2-macroglobulin) is reduced.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01721047
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Independence of enhanced protein catabolism from glucocorticoids in chronically uremic rats (1989)
    Springer
    Research in experimental medicine 189 (1989), S. 339-345 
    Details
    ISSN: 1433-8580
    Keywords: Chronic renal failure ; Catabolism ; Corticosterone ; RU 38 486 ; Nt-methylhistidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with chronic renal failure are prone to develop negative nitrogen balance resulting clinically in wasting and malnutrition. To study the role of glucocorticoids in the pathogenesis of uremic catabolism, we determined urinary excretion rates of urea and Nt-methylhistidine in chronically uremic rats with and without RU 38 486, a potent antiglucocorticoid. In comparison to pair-fed non-uremic animals, chronically uremic rats displayed significantly enhanced ureagenesis, as demonstrated by increased urinary urea excretion, and myofibrillar protein breakdown, as indicated by increased excretion rates of urinary Nt-methylhistidine. The administration of RU 38486 to chronically uremic rats, however, did not result in a normalization of urinary excretion of Nt-methylhistidine. Similarily, the antiglucocorticoid did not influence the extent of ureagenesis in our uremic animals, as it was demonstrated by comparable levels of urinary urea excretion. This suggests that glucocorticoids are not involved in the pathogenesis of enhanced catabolism in chronic renal insufficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01855039
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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