CD62P and P10 as predictive markers for assessing the efficacy of hemodialysis in treating end-stage renal disease.

BACKGROUND: CD62P is a platelet α-granule membrane protein, and P10 is a platelet membrane glycoprotein thrombospondin. To better understand the effects of hemodialysis (HD), we have conducted this study to investigate CD62P and P10 in assessing the efficacy of HD in treating patients with end-stage renal disease (ESRD). METHODS: The case group consisted of 111 patients suffering ESRD treated with regular HD and the control group enrolled 117 healthy subjects. Before and after HD treatment, a series of parameters were observed, based on which, CD62P and P10 levels were detected in the patients in two groups before and after HD therapy. The correlation analysis analyzed the correlations of CD62P and P10 markers with serum creatinine (Scr), blood urea nitrogen (BUN), and subjective score; and logistic regression analysis was performed to reveal factors affecting the efficacy of HD. RESULTS: BUN, Scr, serum phosphorus, intact parathyroid hormone (iPTH), fibrinogen, and ß2-microglobulin (ß2-MG) decreased while hemoglobin, albumin, and activated partial thromboplastin time increased in the patients suffering ESRD; patients presented with improvements in subjective symptoms and an increase in dry weight. CD62P and P10 levels were lower in post-treatment patients. CD62P and P10 positively correlated with Scr, BUN and subjective score; post-treatment CD62P and P10 levels, BUN, hemoglobin, albumin, triglyceride, iPTH, ß2-MG, and fibrinogen were correlated with the efficacy of HD. CONCLUSION: CD62P and P10 might be correlated to the efficacy of HD in treating ESRD, in turn providing predictive markers for assessing the ability of HD in treating ESRD.

Microinflammation is involved in the dysfunction of arteriovenous fistula in patients with maintenance hemodialysis.

BACKGROUND: Vascular access (VA) dysfunction is a major clinical complication in the hemodialysis population and has a direct effect on dialysis outcome. This study was conducted to explore the role of microinflammation in the VA dysfunction in maintenance hemodialysis patients. METHODS: Forty-seven patients (male 35 and female 12) receiving maintenance hemodialysis were included for this study. They were divided into three groups: group 1 (n = 15), patients with initial hemodialysis and new arteriovenous fistula (AVF); group 2 (n = 18), patients treated with hemodialysis for long term with well-functional VA; group 3 (n = 14), maintenance hemodialysis patients with VA dysfunction. Biochemical parameters and serum tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were determined. High-sensitivity C-reactive protein (hs-CRP) was determined by latex-enhanced immuno-nephelometric method. Tissues of radial artery were taken from group 1 and group 3 for the histological study. Expression of CD68 and MCP-1 in the radial artery was determined by immunohistochemistry. RESULTS: Serum hs-CRP in group 3 was significantly higher than those in group 1 and group 2 ((7.40 +/- 2.42) mg/L vs (4.21 +/- 1.62) mg/L and (5.04 +/- 3.65) mg/L, P < 0.01 and P < 0.05, respectively). Serum TNF-alpha in group 3 was significantly higher than those in group 1 and group 2 ((64.03 +/- 9.29) pg/ml vs (54.69 +/- 12.39) pg/ml and (54.05 +/- 7.68) pg/ml, P < 0.05 and P < 0.01, respectively). Serum IL-6 in group 3 was also significantly higher than those in group 1 and group 2 ((70.09 +/- 14.53) pg/ml vs (56.43 +/- 10.11) pg/ml and (60.77 +/- 9.70) pg/ml, P < 0.01 and P < 0.05, respectively). Patients in group 3 had a thicker internal layer of vessels than in group 1 ((0.356 +/- 0.056) mm vs (0.111 +/- 0.021) mm, P < 0.01). Expression of CD68 and MCP-1 in the fistula vessel walls in group 3 were much higher than those in group 1 (P < 0.01). Moreover, serum hs-CRP level was positively correlated with the neointimal hyperplasia, the expression of CD68 and MCP-1 in fistula vessel (P < 0.01, respectively). CONCLUSION: Microinflammation might be involved in the dysfunction of AVF in patients with maintenance hemodialysis.