The concentration of interleukin-17 in the blood and urine of patients with chronic glomerulonephritis with nephrotic syndrome

BACKGROUND. In the mechanisms of immune inflammation in chronic glomerulonephritis (CGN), activation of T-cells plays an important role. The role of Th1 and Th2 cells in the pathogenesis of some forms of CGN has been well studied, while the activation of Th17 cells in CGN has been only evaluated in isolated studies. THE AIM: to evaluate the value of determining the level of IL-17 in urine and blood serum in chronic glomerulonephritis.

PATIENTS AND METHODS. Adult patients with active CGN (N=40) were recruited aged from 18 to 75 years. Ten patients had focal segmental glomerulosclerosis, 6 had membranoproliferative glomerulonephritis, 15 had IgA nephropathy, and 9 had membranous nephropathy at histological examination. The control group included 10 healthy subjects. The IL-17A levels in the urine and blood serum were determined by enzyme-linked immunosorbent assay (ELISA). The IL17A levels in the urine were calculated as the ratio to urinary creatinine. The levels of IL-17 in urine and blood serum were compared with the indicators of proteinuria, albumin, creatinine, serum sodium, also the severity of hypertension, edema and daily sodium excretion.

RESULTS. The results of our study showed a significantly higher concentration of IL-17 in urine in patients with a marked decrease in renal function. Also, the levels of IL-17 in urine directly correlated with serum sodium and inversely correlated with eGFR. We also found an association between increase levels of IL-17 in urine with arterial hypertension and the severity of edema. There were no significant correlations of IL-17 in blood serum and other laboratory indicators of nephritis activity.

CONCLUSION. Patients with CGN have increase levels of IL-17 in the urine compared to healthy subjects. A more significant increase of IL-17 in urine is observed in patients with high clinical activity of HCG. IL-17A may participate in the mechanisms of sodium retention, the development of hypertension and edema in patients with nephrotic syndrome.

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