CCL18 in peritoneal dialysis patients and encapsulating peritoneal sclerosis

Abstract

This is the first report of high levels of CCL18 in the spent dialysate and serum from long-term PD patients. These levels correlated with dysfunction of peritoneal membrane transport status, therefore following CCL18 in a longitudinal study may be of interest.

Sustained low peritoneal effluent CCL18 levels are associated with preservation of peritoneal membrane function in peritoneal dialysis

“…Moreover, effluent levels of CCL18 at the second and third year of PD treatment were significantly higher in the patients who developed PMF. In the cross-sectional study, we also confirmed significantly higher effluent concentrations of CCL18 in the patients who ultimately developed PMF and/or EPS, in agreement with previous findings [10,15]. Because it is probably not feasible to evaluate CCL18 periodically in these patients, a ROC curve was used to analyze the predictive value of effluent CCL18 for development of PMF in samples from patients at the third year of PD treatment.…”

“…We found that high levels of CCL18 in peritoneal effluent were associated with UFF and with later development of EPS in a small number of patients [9]; similar data have been reported by other authors [15]. Our objective was to analyze the predictive capacity of CCL18 levels in serum and peritoneal effluent to herald peritoneal membrane damage, as shown by functional data [1], or the development of EPS.…”

“…Moreover, coculture of M2 with fibroblasts enhances the production of collagen and this is partly dependent on CCL18 [13,14]). CCL18 chemokine is produced by peritoneal M2 macrophages and is notably present at easily measurable levels in the effluent of patients treated with PD [10,15]. High plasma CCL18 levels have been involved in progressive fibrosing disorders such as pulmonary and liver fibrosis [14,16].…”

Recommendations for pathological diagnosis on biopsy samples from peritoneal dialysis patients

“…Recent clinical studies are compatible with those findings; recurrent peritonitis may cause increased permeability and decreased UF in time dependent manner after episode of peritonitis [60,61]. The activated peritoneal macrophages are involved via producing fibrosis chemokine (C-C motif) ligand 18 (CCL18) [62,63], and high level of CCL15 in PD effluent was detected together with elevated IL-6 and monocyte chemotactic protein-1 (MCP-1) [64]. Otherwise inflammation derived fibrosis formation are produced by tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/ Fn14 [65] and T helper 17 cell/IL-17 [66] (for review [67]).…”

Subepithelial collagen deposition, profibrogenic cytokine gene expression, and changes after prolonged fluticasone propionate treatment in adult eosinophilic esophagitis: A prospective study

“…The most significant results, however, were for CCL18. This chemokine has been related to bronchial asthma, 24,25 atopic dermatitis, 26 and other chronic fibrosing diseases, such as scleroderma 27 and encapsulating peritoneal sclerosis, 28,29 but until now, its role in esophageal diseases was unknown. We have observed that CCL18 was the most highly upregulated gene in patients with EoE when compared with both control groups (P 5 .008), with a significant downregulation after long-term topical steroid treatment (P 5 .01).…”