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The influence of the tumor injury on the kidney functional state among the patients with localized renal cell cancer (RCC) was studied. We examined 46 patients with RCC without clinical signs of CRD and 13 healthy people. We studied the content of cystatin C, L-FABP, KIM-1, IL-18, kallikrein (K), prekallikrein (PK), total activity of trypsin-like proteinase (ATP), activity of carboxypeptidases N (ACE), α-1-proteinase inhibitor (α-1PI) and α-2-macroglobulin (α-2M), renin (R), angiotensin-I (AT-I), cortisol and aldosterone in blood and urine. We have revealed the decrease of the ratio coefficient of cystatin C in blood and urine by 1.8 times or its increase by 1.4 times in expression of IL-18 and L-FABP: in blood by 2.6 and 1.9 times; in urine 2.3 and 1.5 times. K was increased by 2.3 and 2.0 times, ACE – by 1.3–1.4 times; the activity of α-1PI and α-2M in blood was increased more than 2 times, the coefficient of interaction of K/α-2М was increased and α-1PI/α-2М was decreased. The concentration of TP in urine was higher and the inhibitors of proteolysis were lower as compared with the norm. R, АТ-I, aldosterone and cortisol were substantially increased as compared with the norm. On the background of decrease of the ratio of K/R the ratio coefficient of renin/АТ-I was increased by 2.5 times, К/АТ-I by 1.6 times, cortisol/АТ-I – by 1.5 times (p<0.05). The tumor injury of kidney is accompanied by the tubulointerstitial disfunction, displacement of the proteinaseinhibitor equilibrium toward activation of proteolysis, dysregulation of the adaptation mechanisms, disturbance of the local renal metabolism on the level of microcirculation and kidney parenchyma.
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Keywords: localized renal cancer, markers of renal injury, kallikrein-kinin system, renin-angiotensin-aldosterone system