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  • Title: [Trypsin inhibitor in the urine of patients with glomerulonephritis].
    Author: Paskhina TS, Platonova LV, Poliantseva LR.
    Journal: Vopr Med Khim; 1988; 34(1):89-94. PubMed ID: 3369132.
    Abstract:
    Concentrations of urinary trypsin inhibitor (UTI) and acid stable antitryptic activity (AS-ATA) were estimated in morning urine of 50 patients with chronic glomerulonephritis and of 13 healthy persons in order to detect interrelationship between severity of kidney impairment and the content of the inhibitor in urine. In healthy persons concentrations of UTI and AS-ATA were equal to 1.05 +/- 0.15 micrograms/ml and 0.12 +/- 0.04 IU/ml, respectively. Similar values of the substances were detected in patients with latent form of glomerulonephritis and normal kidney function. Statistically distinct (P less than 0.01) increase of both these inhibitors was found in urine of patients with latent form of glomerulonephritis and impaired kidney function (4.77 +/- 1.24 micrograms/ml and 0.39 +/- 0.15 IU/ml, respectively) as well as with nephrotic form (26.17 +/- 7.55 micrograms/ml and 1.37 +/- 0.35 IU/ml, respectively) of glomerulonephritis of both primary type and caused by accompanying systemic diseases. Further increase in concentration of UTI up to 31.74 +/- 7.38 micrograms/ml and activation of AS-ATA in urine was observed in the patients with nephrotic form of glomerulonephritis at the step of chronic kidney insufficiency. The increase in UTI concentration observed did not correlate with the level of leukocyturia. Proteinases of monocytes, mast cells, fibroblasts, involved in inflammation and formation of connective tissue in kidney, but not of enzymes from polymorphonuclear leukocytes, appear to be responsible for formation of UTI out of its precursor inter-alpha-trypsin inhibitor in glomerulonephritis.
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