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ATTEMPTS to correlate the clinical course of uremic patients with changes in certain serum constituents have been unsuccessful.1 Similarly, efforts to link the development of uremia to specific "toxins" have been inconclusive.2 , 3 To date, no etiologic factor has been identified for the uremic state4 — irrespective of any possible relation between diverse mechanisms that terminate in uremia — that is, "renal failure with retention of nitrogenous catabolites."5 In a previous study reported from this laboratory, uremia was produced in dogs by bilateral ureteral ligation.6 In these animals it was demonstrated by filter-paper electrophoresis that prolongation of the uremic state effected . . .
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Finkle et al. (1956) studied this question.
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