The results of our clinical observations of 122 patients with chronic glomerulonephritis with normal function of kidneys and chronic renal failure, experimental investigations of white Wistar rats with induced hyperkynureninemia and hyperkynureninuria, and experimental studies of the influence of kynurenine and related components on kidney tubular cells and fibroblasts in tissue culture, allow us to conclude that the impaired tryptophan - nicotinic acid pathway associated with elevated accumulation of kynurenine in blood serum is a pathogenetic basis in development of injury of tubular epithelial cells and hematuria, as well as of arterial hypertension in patients with chronic glomerulonephritis. Our studies have shown that hyperkynureninemia in chronic glomerulonephritis can develop in cases of pyridoxal-5-phosphate (P-5-P) deficiency (hyperkynureninemia at fasting state and/or after L-tryptophan load), as well as through the stimulation of the immune system followed by increase of activity of indolamine 2,3 dioxygenase and guonisine triphosphate cyclohydrolase/(hyperkynureninemia at fasting state, increase of serum neopterin concentration) or in chronic renal failure (increased serum kynurenine and neopterin concentrations at fasting state and after L-tryptophan load, increased serum creatinine concentration). Therefore, the L-tryptophan peroral loading test and determination of serum kynurenine and neopterin are helpful for the differentiation of the pathogenetic basis of the diagnosis in patients with chronic glomerulonephritis.
|Journal||Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.|
|Publication status||Published - 1998|
- chronic glomerulonephritis
- pyridoxal-5-phosphate deficiency
Field of Science*
- 3.1 Basic medicine
- 1.1. Scientific article indexed in Web of Science and/or Scopus database