{'fraction_non_alphanumeric': 0.03580562659846547, 'fraction_numerical': 0.0017050298380221654, 'mean_word_length': 5.747126436781609, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Accumulation of the endogenous L‐arginine analogue NG‐monomethyl‐L‐arginine in human end‐stage renal failure patients on regular haemodialysis

We measured plasma levels of L‐arginine, its analogue NG‐monomethyl‐L‐arginine (L‐NMMA), and related amino acids in normal subjects and uraemic patients (n = 31), before and after haemodialysis. Plasma levels of L‐arginine were reduced to less than half of normal values in uraemic subjects compared with controls, and were not affected by haemodialysis. L‐NMMA was not detectable in non‐uraemic subjects, but markedly elevated in uraemic patients. In parallel, we used human red blood cells as a model to study the effect of L‐NMMA upon the transport of L‐arginine. L‐NMMA trans‐stimulated L‐arginine transport significantly, confirming that L‐arginine and L‐NMMA share common transport pathways. Our results suggest altered L‐arginine metabolism and the presence of an increased concentration of a NO synthase inhibitor in uraemia. We propose that alterations in plasma L‐arginine levels and increased production of L‐arginine analogues will alter NO synthesis and may help to explain some pathological changes seen in uraemia.