Urinary concentrations of tenascin and TIMP-1 are elevated in association with renal disease and may reflect specific aspects of renal fibrosis.

Objective Evaluation of the inflammatory activity in patients on chronic peritoneal dialysis (PD) and patients on chronic hemodialysis (HD) in comparison to patients with chronic renal insufficiency without dialysis treatment and healthy volunteers. Design Open, non randomized prospective study. Setting Nephrology Department, including HD and PD therapy in a university hospital. Patients Twenty -four patients on chronic PD, 21 patients on chronic HD therapy using a cuprophan dialyzer, 16 patients with chronic renal insufficiency without dialysis treatment, and 33 healthy volunteers; 8 additional patients before and after initiation of chronic HD therapy. All patients and controls were without infection or immunosuppressive therapy. Main Outcome Measures As a marker of the inflammatory activity in the different patient groups, C-reactive protein (CAP) was measured serially using a sensitive, enzyme-Iinked, immunosorbent assay in order to detect values below the detection limit of standard assays. Results All patient groups had CAP levels higher than the normal controls (p < 0.01). Patients on HD had CAP levels significantly higher than PD patients (p < 0.01) whose levels were comparable to patients without dialysis therapy. Accordingly, longitudinal measurements before and after initiation of chronic HD showed a significant increase in CAP levels after the beginning of HD treatment (p < 0.04). Conclusions The results suggest that induction of the inflammatory activity is lower during PD compared to HD, since stimulation by the dialyzer membrane, dialysate buffer, or bacterial fragments in the dialysate is avoided. This observation might indicate a possible lower risk of long-term complications in patients with PD.

Conflicting results have been published concerning the systemic induction of the cytokine tumor necrosis factor alpha (TNFα) during hemodialysis (HD). We therefore evaluated in vitro TNFα production in whole blood as well as in vivo variability of TNFα levels in patients on long-term HD. Whole blood was incubated at room temperature (RT) with or without exogenously added endotoxin (ET), and plasma-TNFα was measured after 5, 30, 120, 240, and 960 min by specific enzyme immunoassay. Additionally, plasma-TNFα before and after 120 and 240 min HD was studied longitudinally once a week over a period of 4 weeks in 36 patients on Cuprophan® (CU, n=23) or polysulfone-F60 (PSu, n=13) HD. Mean plasma TNFα levels in vitro rose from (mean) 8 pg/ml after 5 min to 12 pg/ml (120′) and 32 pg/ml (960′) even without ET addition, and to 18 pg/ml (after 120′) and 88 pg/ml (after 960′) when 0.1 μg/ml ET were added. Pre-dialytic as well as intradialytic TNFα levels in patients showed high intra-individual variability. A substantial (> 100%) increase in plasma TNFα was observed during only 14 out of 84 treatments with CU and 20 out of 47 with PSu, however, the increase in TNFα was not statistically significant in either group. We conclude that the sampling procedure, if not carefully standardized, is a potential source of artifacts with regard to “systemic” TNFα levels. The high intra and inter-individual variability of plasma TNFα suggests that results of cross-sectional studies are questionable.

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