Background: Chronic kidney disease (CKD) leads to a progressive decline in
kidney function that eventually progresses to end-stage renal disease. It is
critical to identify people at risk for renal disease and to intervene early to
avoid kidney damage. Tryptophan hydroxylase (TPH-1) is an accurate
biomarker for CKD early stage. The loss of tryptophan hydroxylase
contributes to kidney injury. N-acetylcysteine, glycine, and tryptophan can
arrest renal fibrosis development and progression through the anti-fibrotic
effect of tryptophan hydroxylase and the protective effect of Nacetylcysteine.
Objectives: This study aims to assess the metabolic effect of N-acetyl-lcysteine on kidney function as an EGFR inhibitor and its effect on AAs
depletion. In addition, to evaluate the effect of glycine and tryptophan on
kidney injury and renal fibrosis progression.
Results: Eight weeks of administration of pemetrexed led to a significant
increase in serum, urea, creatinine, and uric acid. Administration of Nacetylcysteine (NAC with pemetrexed) resulted in a significant decrease in
biochemical kidney function. Also, glycine and tryptophan directly affect
renal function; increased expression of tryptophan hydroxylase with decrease
expression of EGFR and transforming growth β (TGF-β), compared to Nacetylcysteine group.
Conclusion: N-acetylcysteine, glycine, and tryptophan can halt the depletion
of AAs in the presence of urea and EGFR. Glycine and tryptophan both have
a direct effect on renal function due to their uric acid-lowering properties |
