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  • Interferon alpha-2b  (1)
  • Postinfectious glomerulonephritis  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Interferon alpha-2b ; Nephrotoxicity ; Urinary enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The nephrotoxic potential of alpha-interferon (IFN alpha-2b) was analysed in 21 patients with chronic myeloid leukemia. As particularly sensitive parameters in the detection of subclinical renal injury we measured the excretion of the following urinary enzymes: lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), leucine arylaminidase (LAP), β-galactosidase (GAL) and N-acetyl-beta-glucosaminidase (NAG). Additionally, protein excretion and urinary sediment were analysed. In 18 of 21 patients a significant increase in the excretion of LDH, LAP, GGT and NAG was found, in 6 patients there was an additional rise in the output of GAL. Eleven patients developed proteinuria up to 2 g/l, one patient excreted up to 9 g/l. Enzymuria and protein excretion decreased in all patients after reduction of the IFN alpha-2b dosage and disappeared in two patients following cessation of therapy. The high incidence of nephrotoxic events in patients with CML during IFN alpha-2b therapy might be mostly due to immunological or substance-specific effects.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Rapid progressive (crescentic) glomerulonephritis ; Postinfectious glomerulonephritis ; Membrane plasma separation ; Immunosuppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since 1971 we observed 31 patients with histologically proven rapidly progressive (crescentic) glomerulonephritis. At the onset of therapy 16 patients presented with end stage renal failure, the others with impaired renal function. 21 patients received combined immunosuppressive therapy, consisting of prednisone, cyclophosphamide and azathioprine. 8 patients were treated with membrane plasmapheresis, additionally. 10 patients received no specific therapy. After 5 years 13 patients were on hemodialysis, 4 had impaired renal function and 10 patients were dead. Two patients died due to the progression of underlying diseases, the others were lost following infectious diseases. There was no additional positive effect in the group treated with membrane plasma separation compared with patients treated only immunosuppressive. Only in 4 patients without specific therapy normalization of renal function occurred. In these patients RPGN appeared after an infectious disease. We conclude that an infectious disease associated RPGN is an own entity of glomerulonephritis that has a very good prognosis and needs only antibiotic therapy.
    Type of Medium: Electronic Resource
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