1999 Fiscal Year Final Research Report Summary
Homocysteine metabolism and oxygen stress in chronic renal failure
Project/Area Number |
10671013
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | Hyogo College of Medicine |
Principal Investigator |
TAKAMITSU Yoshihiro Hyogo College of Medicine, Professor, 医学部, 教授 (90107053)
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Co-Investigator(Kenkyū-buntansha) |
NAKANISHI Takeshi Hyogo College of Medicine, Assistant Professor, 医学部, 助教授 (70217769)
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Project Period (FY) |
1998 – 1999
|
Keywords | progression of renal failure / oxygen stress / homocysteine / cysteine / nitric oxide / urine protein / macrophage / マクロファージ |
Research Abstract |
We have already demonstrated that homocysteine (Hcy) and NO metabolites (NO3) are increased, as the renal function is decreased. Hcy and cysteine (Cys), those are amino acids with SH-base, as well as NO might accelerate the generation of O2-・, OH・ and peroxynitrite. As the rise in oxygen radical is associated with the deterioration of renal function, we determined the relation between sulfur amino acids, as well as NO metabolites and the rate of deterioration of renal function in patients with chronic renal failure. Serum creatinine level was over 2.5 mg/dl in all patients, who have been followed up for at lease 9 months. The rate of deterioration of renal function was expressed as the timed change of reciprocal of creatinine (SL-ICR). SL-ICR was not correlated with pHcy, but was invertedly correlated with pCys and pCys/pHcy. And it was significantly correlated with the daily excretion of urine protein and pNO3. From these results, the deterioration of renal function might be related with sulfur amino acids metabolism, especially cysteine synthesis. On the other hand, renal function decreased rapidly as NO synthesis increased. It might be suggested that NO synthesis from macrophage in renal tissue might injure the renal function.
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