Myeloid bodies in drug-induced acute tubular necrosis.
A growing list of drugs, metals, and chemicals has been implicated as the cause of functional and structural damage specifically to the proximal tubular epithelium. Renal biopsies were obtained from three patients who had developed nephrotoxic agent-related acute renal failure. Two of the patients had received gentamicin and viomycin; the third patient had heavy exposure to chromium. All three biopsies showed acute tubular necrosis (ATN) on light microscopy. Electron microscopy revealed that the proximal tubular cells and, to a lesser degree, the distal tubular cells, contained abundant, variably sized myeloid bodies. In our previous experimental study of viomycin-induced ATN in rats, similar ultrastructural findings of a gradual increase in the number of myeloid bodies in the proximal tubular cells were also observed. The constant presence of myeloid bodies in the tubular epithelial cells following drug-induced tubular necrosis suggests that they may represent lysosomal isolation of drug-bound cytoplasmic structures, as a cellular mechanism to degrade toxic substances and, therefore, may serve as an ultrastructural marker of cellular drug uptake and drug disposition.
D058186:Acute Kidney Injury / Q000473:pathology*; D000328:Adult; D002857:Chromium / Q000009:adverse effects; D004848:Epithelium / Q000648:ultrastructure; D005260:Female; D005839:Gentamicins / Q000009:adverse effects; D006801:Humans; D002479:Inclusion Bodies / Q000648:ultrastructure*; D007683:Kidney Tubular Necrosis, Acute / Q000139:chemically induced / Q000473:pathology*; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000648:ultrastructure*; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D014756:Viomycin / Q000009:adverse effects
D005839:Gentamicins; D002857:Chromium; D014756:Viomycin