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JAMA. 1970;214(11):2048-2049.

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Recent therapeutic successes of hemodialysis have provided renewed impetus to the search for uremic toxins. The search, of course, is not new. Nearly a century and a half ago, 20 years before Piorry and L'heritier¹ coined the term "uremia," Prevost and Dumas (Ann Chim Phys 23:90, 1821) had already discovered that removal of a dog's kidneys caused increased concentration of urea in its blood. Observations of similar increases in blood urea in patients with Bright's disease has since led to many experiments which at first tended to implicate this substance as the cause of the uremic syndrome, but later failed to substantiate this relationship. Similar failure followed attempts at incriminating other retained nitrogenous waste products or abnormally produced metabolites. Creatinine, uric acid, indican, phenol, oxalic acid, pseudouridine, methylguanidine, amino acid, microglobulins, aliphatic or aromatic amines—singly or in various combinations—could not account for the uremic syndrome. Thus frustrated, many . . . [Full Text PDF of this Article]

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