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ORIGINALLY uremia signified the end stage of organic renal disease when urea was demonstrable in the serum. This was Bright’s concept1 based on the chemical analyses of Christison. Although it was later shown that the blood normally contained urea and that excessive urea concentration could not by itself reproduce the complex manifestations of uremia, the term “uremia” nevertheless became permanently rooted in medical texts and no one would think seriously of displacing it. Probably one of the chief reasons for this was the complete failure throughout the last hundred years to demonstrate any single metabolite or toxin the retention of which could be responsible for uremia. Each of the normally present urinary constituents has been shown to be capable of producing one or more of the major symptoms of the uremic state. But none has met the rigid scientific tests of (1) reproduction of the general state of uremia, (2) effectiveness in causing important symptoms at or near the concentration of the substance in the blood in natural uremia (Table 1).

For example, ammonium salts were implicated early in the etiology of uremia.2 Intravenous injection of ammonium salts produces hyperpnea, convulsions, coma and death. The urine in the end stages of renal disease contains little ammonia, if bacterial infection or contamination is excluded, suggesting that ammonia is retained in the blood. Yet it took another 70 years before Nash and Benedict3 showed that there is practically no ammonia in normal blood and no increase in uremic blood. In fact, the. . .



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