Renal tubular damage without glomerular damage after cytotoxic drugs and aminoglycosides.
Cytotoxic agents and aminoglycosides when given for a maximum of eleven days damaged the renal tubules as indicated by an increased urinary beta 2-microglobulin (beta 2-m), N-acetyl-beta-D-glucosaminidase (NAG) and total protein. Methotrexate (MTX) caused the greatest changes among the cytotoxic agents studied. Prophylactic doses of aminoglycosides in surgical patients also caused tubuloproteinuria. The tubular damage was greatest when aminoglycosides were given to treat septicaemia complicating haematological malignancies in patients who had previously had cytotoxic drugs. However, even in these patients there was no evidence of glomerular failure or increased glomerular permeability seven days after beginning chemotherapy.
D000118:Acetylglucosaminidase / Q000652:urine; D000328:Adult; D000419:Albuminuria / Q000652:urine; D000617:Aminoglycosides / Q000009:adverse effects*; D000970:Antineoplastic Agents / Q000009:adverse effects*; D003404:Creatinine / Q000097:blood; D005260:Female; D006801:Humans; D007684:Kidney Tubules / Q000187:drug effects*; D007700:Kinetics; D008297:Male; D008727:Methotrexate / Q000009:adverse effects; D008875:Middle Aged; D011507:Proteinuria / Q000652:urine; D001613:beta 2-Microglobulin / Q000378:metabolism
D000617:Aminoglycosides; D000970:Antineoplastic Agents; D001613:beta 2-Microglobulin; D003404:Creatinine; D000118:Acetylglucosaminidase; D008727:Methotrexate