[Analysis of selected inflammatory markers in patients with stable renal graft (RTx) 36 months after transplantation].

Chronic inflammation is an inherent feature of chronic renal failure. Successful renal transplantation (RTx) is the only known renal replacement therapy sufficient to reverse most of the metabolic disturbances of chronic uremia, although still some of these abnormalities may be present or even new problems may occur (mostly as the side effects of immunosuppressive drugs). The aim of this study was to evaluate the level of inflammation in 20 patients (9 F, 11 M, aged mean 44.0 +/- 11.8 years) with well-preserved renal function 36 months after kidney transplantation, using serum levels of selected cytokines (IL-6, IL-18, TNFalpha and soluble receptor for TNF - sTNFRII), acute phase proteins (CRP, fetuin A) and hepatocyte growth factor (HGF). Procalcitonin was also assessed as the sensitive indicator of active infection. Obtained results were compared with the control group of healthy subjects in a respective age. Serum levels of IL-6, TNF-R and IL-18 were significantly higher, and HGF and fetuin A--significantly lower in patients vs. controls (p < 0.05 for all differences). Significant negative correlations were noted between glomerular filtration rate (GFR) and serum TNF, sTNFRII and IL-18 in RTx patients, whereas strong positive relationship between GFR and fetuin A was observed. Serum creatinine correlated with IL-6, IL-18, TNFalpha, sTNFRII and hsCRP levels and serum urea-with TNFalpha, sTNFRII, IL-6 and IL-18. Significant negative associations were also noticed between serum fetuin A and most of the tested inflammatory markers: sTNFRII (r = -0.77; p = 0.0005), IL-6 (r = -0.63; p = 0.009), hsCRP (r = -0.62; p = 0.009) and IL-18 (r = -0.60; p = 0.01). Obtained results permit us to conclude that the increased activity of inflammation can still be noticed in RTx patients 36 months after successful engraftment. This process is inversely associated with the level of kidney function. The role of fetuin A as the 'negative' acute phase protein was also demonstrated in this group of patients.