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首页> 美国政府科技报告 >The Origin and Effect of Guanidino Succinic Acidemia in Uremia
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The Origin and Effect of Guanidino Succinic Acidemia in Uremia

机译：喹喔啉琥珀酸血症在尿毒症中的起源与作用

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A method is described for the separation and identification of the principle guanidino derivatives in serum and urine. These include arginine, guanidinoacetate, guanidino-succinate, and methyl guanidine all of which are implicated in the uremic syndrome. A mechanism, involving the enzymatic regulation of nitrogen metabolism, is proposed for the production of unrecognized guanides in uremia and GSA is offered as a prototype. In this instance, retention of GAA, a normal metabolite and precursor of creatinine, due to renal insufficiency results in an increase in serum levels which suppresses the conversion of arginine to ornithine. To restore ornithine it is proposed that arginine is converted to GSA and this, in turn, accumulates resulting in depression of platelet activity and possible reduction in anabolic energy of the neuron. The process appears in rats to be reversed by providing an excess of methyl donor which serves to convert GAA to creatine and reinstitute the normal catabolic pathways for arginine. It is proposed to test this hypothesis in humans and thereby provide a prototype for the pharmacologic detoxification of nitrogen in uremia. (Author)

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