POS-452 SERUM LEVELS OF PLASMINOGEN ACTIVATOR UROKINASE RECEPTOR AND CARDIOTROPHIN-LIKE CYTOKINE FACTOR 1 IN PATIENTS WITH NEPHROTIC SYNDROME

Abstract

The pathogenesis of primary focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) remains unknown to date. Some circulating permeability factors are discussed. This work assessed molecule candidates for permeability in serum samples of patients with nephrotic syndrome (NS). Forty-one patients with chronic glomerulonephritis (CGN) were included in our study. Seventeen patients had FSGS, 7 patients had MCD, 5 patients had membranoproliferative glomerulonephritis (MPGN), 6 patients had IgA nephropathy, and 6 patients had membranous nephropathy (MN). The laboratory data were compared with the clinical and histological features of nephritis. Serum levels of uPAR and CLCF-1 were measured by ELISA. Levels of uPAR in the serum of patients with CGN The levels of uPAR in serum did not correlate with daily proteinuria (Rs=-0.114, p=0.51), serum creatinine/eGFR (Rs=0.032, p=0.847 and Rs=-0.054, p=0.747, respectively), arterial hypertension (Rs=0.015, p=0.926), glomerulosclerosis percentage (Rs=0.364, p=0.07) or tubulointerstitial fibrosis (Rs=-0.189, p=0.517). There was no correlation with serum C-reactive protein levels (Rs = 0.226, p=0.173) Regarding the morphological forms of glomerulonephritis, the levels of uPAR were not significantly higher in FSGS patients than in MCD, IgA nephropathy, membranous nephropathy or membranoproliferative glomerulonephritis patients (Figure 1). However, the uPAR levels were significantly higher in FSGS patients before immunosuppressive treatment. In FSGS patients who already received immunosuppressive treatment, the uPAR levels were lower and comparable to those of the other groups (Figure 2). CLCF-1 in the serum of patients with CGN No correlations were found between the levels of CLCF-1 in serum and creatinine levels/glomerular filtration rate (Rs=0.285, p=0.079/Rs=-0.268, p=0.099), arterial hypertension (Rs=0.212, p=0.195), percentage of sclerosed glomeruli (Rs=0.28, p=0.127) or severity of tubulointerstitial fibrosis (Rs=0.238, p=0.413). There were no significant differences between the histological variants of nephritis (Figure 1). The levels of CLCF-1 did not depend on the therapy (Figure 2).However, we found correlations between CLCF-1 levels and proteinuria (Rs = 0. 397; p = 0.015) and lipid levels (Rs = 0. 475; p = 0.003). Additionally, correlations between CLCF-1 levels and triglyceride levels (Figure 3), very low-density lipoprotein (Rs = 0.467, p=0.045), and high-density lipoprotein levels (Rs = - 0.599, p=0.031) were found. View Large Image Figure ViewerDownload Hi-res image Download (PPT) Our data indicate a significant increase in the serum suPAR levels in untreated FSGS; immunosuppressive treatment can decrease the suPAR levels. CLCF-1 levels in serum did not depend on histological forms of nephritis or treatment, but it correlated with proteinuria and lipid levels in patients with nephrotic syndrome.