Alternate reasons for atherogenesis in uremia.
The key to symptomatology in uremia is nitrogen retention leading to amidination and transmidination of a variety of substrates. The product of this activity is a series of guanidino acids which are methyl receptors converting S-adenosylmethionine to adenosine and homocysteine. Adenosine is a potent inhibitor of the enzyme ATPase and, in this way, contributes to the anemia, the bleeding diathesis and the CNS symptoms of uremia. Homocysteine is an inhibitor of pyridoxal phosphate-induced reactions and contributes to the angiitis and thromboembolism so unexpectedly encountered in chronic uremia.
D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D001161:Arteriosclerosis / Q000209:etiology*; D003545:Cysteine / Q000378:metabolism; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D009584:Nitrogen / Q000378:metabolism; D006435:Renal Dialysis; D014511:Uremia / Q000150:complications* / Q000378:metabolism
D006710:Homocysteine; D000251:Adenosine Triphosphatases; D003545:Cysteine; D009584:Nitrogen