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  • Nephrotoxicity  (2)
  • Glukagon  (1)
  • Monoclonal antibody  (1)
  • 1
    ISSN: 0009-8981
    Keywords: Human kidney ; Isoenzyme ; Monoclonal antibody ; Renal cell carcinoma ; gamma-Glutamyltransferase (EC 2.3.2.2)
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 651-657 
    ISSN: 1432-1440
    Keywords: Uremia ; cAMP ; lipolysis ; Glucagon ; Uremic metabolic disturbances ; Urämie ; cyclisches AMP ; Glukagon ; Lipolyse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Vergleichend wurde der Effekt einer intravenös gegebenen Einzeldosis von Glukagon auf das Verhalten der cAMP-Konzentration im Plasma untersucht. Die Untersuchungen erfolgten an 7 gesunden Personen, 10 Patienten mit chronischer Niereninsuffizienz und 10 Patienten, die auf Grund des chronischen Nierenversagens einer Langzeithämodialysebehandlung bedurften. 10 min nach Glukagonanwendung zeigten die urämischen Patienten einen signifikanten (p 〈 0,0001) größeren Anstieg von cAMP im Vergleich zu der Kontrollgruppe. Die Glukosekonzentrationen zeigten nach Glukagon zwischen den beiden Gruppen keine Differenz. Die Lipolyse war in der urämischen Patientengruppe weniger stark ausgeprägt, als bei den Kontrollen (p 〈 0,003). Die Resultate ließen sich nicht auf Unterschiede in der Insulinantwort zurückführen. Die Befunde weisen auf ein unterschiedliches Verhalten der hepatischen Adenylatcyclase und der cAMP-Bildung zwischen gesunden und urämischen Personen hin. Diese Änderungen der cAMP-Aktivität können eine grundsätzliche Rolle bei der Pathophysiologie metabolischer Störungen bei Urämie spielen.
    Notes: Summary The effect of a single, intravenously administered dose of glucagon on plasma cyclic adenoside monophosphate (cAMP) was studied in seven normal subjects, ten patients with chronic renal failure (CRF), and ten patients with terminal renal insufficiency (TRI) receiving long-term haemodialysis treatment (HD). Ten minutes following glucagon administration, uremic patients displayed a significantly (P 〈 0.0001) greater increase in cAMP than control subjects. Glucose levels after glucagon administration did not differ significantly between the normal and uremic groups, and lipolysis was less pronounced in the uremic patients than in the controls (P 〈 0.003). These results could not be attributed to differences in serum insulin response. The findings demonstrate differences in the hepatic adenylate cyclase and cAMP response between normal and uremic subjects. These alterations in cAMP responsiveness may play a role in the pathophysiology of the metabolic disturbances associated with uremia.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 44 (1993), S. S33 
    ISSN: 1432-1041
    Keywords: Nephrotoxicity ; Cell repair ; drug induced nephrotoxicity ; growth factors ; specific proteinuria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Nephrotoxic drugs may account for approximately at least 20 % of clinically observed cases of acute renal failure in whom tubular lethal or sublethal damage is a predominant finding. Acute toxic tubular cell injury is characterized by loss of cellular polarization, intrinsic energy deficiency, calcium overload, release of toxic proteases and free oxygen radicals, derangement of the cytoskeleton, and vacuolar transformation of brush border microvilli. These events may finally lead to irreversible cell death. Shedding of membrane enzymes and cytoskeletal components in urine (kidney tissue proteinuria) may serve as a noninvasive early marker for assessing tubular cell injury. Successful recovery of renal function depends on early repair of lethally or sublethally damaged nephrons, in which intrinsic nephrogenic adaptive and proliferative responses cooperate in concert with auto/para/-juxtacrine growth promoting factors and cytokines. Exogenously administered growth factors may enhance renal cell recovery, as shown in animal models. Increased expression of immediate early genes in tubular cells after renal injury reflects the ongoing mitogenic activity necessary for reepithelialization and remodeling (new, polarized, differentiated cells). Further progress in understanding the molecular mechanisms of renal tubular injury will probably influence the diagnostic modalities and therapeutic approaches to acute drug induced renal failure.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1041
    Keywords: Nephrotoxicity ; cephamandol ; cephazolin ; cephacetrile ; cephalothin ; brush border enzymes ; urine alanine-aminopeptidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Cephamandol 6.0 g, cephazolin 6.0 g or cephacetrile or cephalothin 8.0 g were administered as short-term infusions on 3 consecutive days to informed volunteers, who had no history or evidence of impairment of renal funktion. There were 15 subjects in the cephamandol, cephacetrile and cephalothin groups and 14 subjects in the cephazolin group. Alanine-aminopeptidase, a characteristic tubule enzyme, was determined in a 24-hour urine 2 days before administration, during the 3 day administration and on the 4 subsequent days. In addition, alanine-aminopeptidase was also estimated immunologically in concentrated urine with the aid of an anti-brush border antibody. Cephamandol, cephazolin and cephalothin were completely without effect on the proximal tubule. Cephacetrile, on the other hand, showed clear reactions in 9 out of 15 subjects, in the form of elevated AAP activity in urine and in 6 of the cases membrane elimination was demonstrable immunologically. After withdrawal of the medication, the values of the responder group returned spontaneously to normal, i. e. no cumulative effect was detected. These investigations show that elimination of alanine-aminopeptidase in the urine is a very sensitive index of the action of cephalosporins on renal tubules.
    Type of Medium: Electronic Resource
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