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  • Articles  (2)
  • Pharmacodynamic  (1)
  • kallikrein  (1)
  • 1
    ISSN: 1432-1041
    Keywords: Key words Cefepime ; Hemodialysis ; Pharmacokinetics ; Pharmacodynamic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: Among uremic patients on hemodialysis, infectious complications leading to a high incidence of morbidity and mortality are a well-documented problem. In this multi-dose study, the safety, tolerance, and pharmacokinetics of cefepime during high-flux hemodialysis were investigated and an improved dosing schedule is presented. Methods: Six long-term hemodialysis patients received 2 g cefepime i.v. at the end of hemodialysis three times per week. Results: Trough levels of cefepime were 23.3 ± 7.3 mg/l and peak serum concentrations 165.6 ± 48.7 mg/l. After 3.5 h of high-flux hemodialysis, 72.2 ± 6.4% of cefepime was eliminated. The intradialytic half-life was 1.6 ± 0.29 h and the interdialytic half-life 22.0 ± 2.14 h. Conclusion: A dosage of 2 g cefepime after each hemodialysis session achieved drug levels well above the minimal inhibitory concentration (MIC)90 for most of the target pathogens. Thus, the described dosing schedule is an efficient and cost saving antmicrobial therapy for severe infections in long-term hemodialysis patients with no residual renal function.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 22 (1982), S. 541-544 
    ISSN: 1432-1041
    Keywords: kallikrein ; nephrotic syndrome ; protease inhibition ; alpha1-antitrypsin ; alpha2-macroglobulin ; inter-alpha-trypsin inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary An inverse relationship between proteolytic activity in the presence of kallikrein 0.4 IU and urinary alpha1-antitrypsin concentration has been demonstrated. This protease inhibitor can directly inactivate kallikrein activity. The inhibition was abolished by removal of urinary alpha1-antitrypsin by trypsinsepharose treatment. Inhibition could be reversed by addition of purified alpha1-antitrypsin. These effects could not be demonstrated with inter-alpha-trypsin inhibitor or alpha2-macroglobulin. The inhibitory effect of alpha1-antitrypsin on kallikrein activity should be taken into account in studies in which kallikrein activity is estimated.
    Type of Medium: Electronic Resource
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