BackgroundUremic pruritus is a common, but unpleasant, complication of end-stage renal disease. The uremic burden may differ between hemodialysis (HD) and peritoneal dialysis (PD) patients. This difference may also change the clinical characteristics of uremic pruritus between the 2 modalities. In this study, we investigated the uremic pruritus between patients on HD and PD.MethodsA total of 425 HD and 223 PD patients from the Clinical Research Center registry in Korea were included. Patients were assessed for pruritus intensity, scratching activity, pruritus distribution, and frequency of pruritus-related sleep disturbance using the visual analog scale and questionnaire.ResultsThe prevalence of uremic pruritus was higher in PD patients than that in HD patients (62.6% vs. 48.3%, P = 0.001). In the multivariable logistic analysis, PD treatment was significantly associated with the prevalence of uremic pruritus (odds ratio, 1.76; 95% confidence interval, 1.20–2.57, P = 0.004) after adjustment for clinical variables. The visual analog scale score, representing a subjective intensity of itchiness, was significantly higher in PD patients (PD 2.11 ± 2.32 vs. HD 1.65 ± 2.28, P = 0.013) compared with HD patients. The intensity of uremic pruritus was independently related with serum albumin levels (β = –0.143, P = 0.006) in HD patients and total weekly Kt/V (β = –0.176, P = 0.028) in PD patients.ConclusionOur data demonstrate the difference in prevalence, intensity, and risk factors of uremic pruritus between HD and PD patients. These findings suggest that careful consideration for uremic pruritus might be needed in end-stage renal disease patients according to the dialysis modality.
Background:A decrease in the number of tissue eosinophils is known to reflect the malignancy potential of neoplastic lesions and even prognosis. Increased levels of the chemokines CCL11 and CCL24 in serum and tissue are also known to have diagnostic value as serum tumor markers or prognostic factors. The aim of this study was to evaluate the correlation between the degree of tissue eosinophilia and the expression of these chemokines in the glandular and stromal cells of colorectal neoplastic lesions ranging from benign to malignant tumors.Methods:We counted the number of infiltrating eosinophils in neoplastic lesion tissue and we evaluated the expression of CCL11 and CCL24 in glandular cells and stromal cells by immunohistochemical staining.Results:The results showed that the number of eosinophils decreased significantly and the expression of CCL11 and CCL24 in glandular cells decreased with tumor progression, whereas the stromal expression of CCL11 and CCL24 appeared to increase.Conclusions:The discrepancy in CCL11 and CCL24 expression between glandular cells and stromal cells might shed light on how colorectal cancer evades the immune system, which would enable further development of immunotherapies that target these chemokines. Further research on eosinophil biology and the expression pattern of chemokines in tumor cells is needed.
BackgroundEvidence of antibody-mediated injury in the absence of donor-specific HLA antibodies (HLA-DSA) has recently emerged, suggesting a role of antibodies in targeting non-HLA antigens expressed on renal allograft tissue. However, the clinical significance of pre-transplant non-HLA antibodies remains unclear. We compared the histological and clinical impact of pre-transplant HLA-DSA and non-HLA antibodies, especially angiotensin II type I receptor (anti-AT1R) and MHC class I-related chain A (anti-MICA), in kidney transplant patients.MethodsPre-transplant HLA-DSA, anti-AT1R, and anti-MICA were retrospectively examined in 359 kidney transplant patients to determine the effect of each antibody on allograft survival and clinical characteristics.ResultsPre-transplant HLA-DSA, anti-AT1R, and anti-MICA were detected in 37 (10.3%), 174 (48.5%), and 50 patients (13.9%), respectively. Post-transplant antibody-mediated rejection was associated with a pre-transplant HLA-DSA (+) status only. The development of microvascular inflammation (MVI) was associated with pre-transplant HLA-DSA (P=0.001) and anti-AT1R (P=0.036). Anti-AT1R (+) patients had significantly lower allograft survival compared with anti-AT1R (−) patients (P=0.042). Only pre-transplant anti-AT1R positivity was an independent risk factor for allograft failure (hazard ratio 4.824, confidence interval 1.017–24.888; P=0.038). MVI was the most common histological feature of allograft failure in patients with pre-transplant anti-AT1R.ConclusionsPre-transplant anti-AT1R is an important risk factor for allograft failure, which may be mediated by MVI induction in the allograft tissue.
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