[The participation of the kallikrein-kinin system in edema formation in glomerulonephritis].

Involvement of the kallikrein-kinin system in the pathogenesis of renal edemas may be mediated by increase of vascular permeability, proteinuria, diuresis and natriuresis. Proceeding from these points, in 27 patients with morphologically proved chronic glomerulonephritis and the nephrotic syndrome, the serum kallikrein activity and its 24-hour urinary excretion level were measured. According to their edematous syndrome severity, all the patients were divided into 2 groups: 1) 19 patients with moderate edemas; 2) 8 patients with severe ones. During the follow-up period, there were no essential changes in patients' body weights, and no significant differences between the groups in clearances and excreted fractions of sodium, potassium, chlorine, osmotically active substances, and in serum albumin and cholesterol levels, 24-hour protein losses and blood pressure. As compared to the healthy (n-20) in all the patients a substantial and statistically significant increase in kallikrein activity was revealed in serum and urine. Kallikreinemia and kallikreinuria were significantly higher in Group 2 than those in Group 1. In the total group of examinees a significant direct relationship was established between the urinary kallikrein activity and summary sodium and potassium excretion as well as between the serum kallikrein activity and chlorine clearance. A direct correlation between the serum kallikrein activity and proteinuria was also found. Thus, a role of the kallikrein-kinin system in development of glomerulonephritic edemas concurrent with the nephrotic syndrome is hetero-directional.(ABSTRACT TRUNCATED AT 250 WORDS)