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Sulphur containing amino acids in chronic renal failure with particular reference to homocystine and cysteine‐homocysteine mixed disulphide
Author(s) -
WILCKEN D. E. L.,
GUPTA VATSALA J.
Publication year - 1979
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1979.tb00888.x
Subject(s) - homocysteine , taurine , medicine , cystine , amino acid , methionine , renal function , endocrinology , cystathionine beta synthase , chemistry , creatinine , cysteine , kidney disease , chronic renal failure , biochemistry , enzyme
. We measured plasma sulphur amino acids in twenty‐two patients with chronic renal failure and compared the findings with those obtained in twenty‐two normal subjects. In fasting blood (08.00 hours) cysteine‐homocysteine mixed disulphide was significantly increased in the renal patients, mean values (± SD) being 8.2 ± 3.4 and 3.1 ± 1.0 μmol/l respectively ( P < 0.001). The increase was positively correlated with reduced renal function, as assessed by serum creatinine ( r = 0.62; P < 0.01). Homocystine was detected in nineteen patients, the mean concentration (± SD) being 1.7 ± 0.6 μmol/l; it was not found in any normal subject. Methionine levels were not different but there were significant increases in cystine ( P < 0.001) and taurine ( P < 0.05) in the patients. Similar values for these amino acids were found in a second blood sample drawn at 16.00 hours. Changes in the other neutral and acidic amino acids measured were in agreement with those reported in chronic azotaemia. We concluded that plasma levels of all the principal sulphur amino acids except methionine are elevated in chronic renal failure emphasizing the importance of the kidney in sulphur excretion. Prolonged accumulation of homocysteine and cysteine‐homocysteine mixed disulphide may be relevant to the development of accelerated vascular disease in patients with chronic renal failure by producing endothelial damage.