Carbon tetrachloride poisoning in man, whether by inhalation or ingestion, is frequently associated with anatomical and clinical evidence of renal dam- age.Smetana (1) has shown that the distal tu- bule appears to bear the brunt of the renal patho- logical processes resulting in oliguria or anuria, and Woods (2) has demonstrated the identity of the renal pathology in this disease with that of the crush syndrome.This type of acute renal failure has therefore been included among the subclassifications of lower nephron nephrosis by Lucke (3).This author believes that the scant urine flow in this syndrome is adequately explained by the back- diffusion of the glomerular filtrate through the damaged tubular walls.This concept was first promulgated by Dunn, Haworth and Jones (4) working with experimental oxalate nephritis.Bywaters and Dible (5) concluded this to be the mechanism of anuria in the crush syndrome on the basis of morphology alone.A. N. Richards (6) was able to observe this phenomenon directly in the frog kidney poisoned with mercuric chlo- ride.He noted the absence of urine formation in spite of normal or augmented glomerular filtra- tion.Additional evidence cited for the occurrence of abnormal tubular permeability is the finding of negative TmD's 3 by Bobey et al. (7) and of de- creased creatinine/inulin clearance ratios by Rich- ards, Westfall, and Bott (8) in experimental uranium poisoning in dogs; the demonstration of negative TmPAH values by Redish, West, White- 1 Indebtedness is gratefully acknowledged to the U. S. Standard Products Co., of Woodworth, Wisconsin, for furnishing inulin in generous amounts for parenteral use in this work.2 Sarah Welt Fellow, permanent address:
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Sirota et al. (1949) studied this question.