Markers of inflammation before and during peritoneal dialysis.

In this study, we compared changes in inflammatory markers-C-reactive protein (CRP), pentraxin 3 (PTX3), serum component of amyloid A (SAA), and procalcitonin (PCT)-in 182 subjects: 69 from the general population (GP), 47 with CKD, 19 with an implanted intra-abdominal catheter for peritoneal dialysis ("prePD"), and 47 on peritoneal dialysis (PD). These were the results [median (95% confidence interval)] for the GP CKD, prePD, and PD groups respectively: CRP: 1.40 mg/L (1.15-2.10 mg/L), 5.30 mg/L (3.04-8.06 mg/L), 3.33 mg/L (2.15-12.58 mg/L), 7.25 mg/L (4.43-15.16 mg/L). SAA: 3.10 mg/L (2.90-3.53 mg/L), 7.77 mg/L (4.17-15.83 mg/L), 7.30 mg/L (4.81-10.96 mg/L), 9.14 mg/L (5.31-23.54 mg/L). PCT: 0.028 ng/mL (0.022-0.032 ng/mL), 0.121 ng/mL (0.094-0.166 ng/mL), 0.160 ng/mL (0.090-0.277 ng/mL), 0.363 ng/mL (0.222-0.481 ng/mL). PTX3: 0.54 ng/mL (0.33-0.62 ng/mL), 0.71 ng/ mL (0.32-1.50 ng/mL), 0.56 ng/mL (0.44-1.00 ng/ mL), 1.04 ng/mL (0.65-1.56 ng/mL). After catheter insertion, CRP showed a nonsignificant declining trend that disappeared throughout PD. The behavior of SAA was similar to that of CRP and was not modified by the changes induced by the start of PD. An increase in PTX3 was observed only with PD, which may be related to a local proinflammatory state caused by PD solution. We can conclude that catheter insertion for PD does not account for most of the local inflammatory changes observed in PD patients.

Inflammation markers, chronic kidney disease, and renal replacement therapy.

Chronic kidney disease (CKD) is associated with a proinflammatory state and an excess of cardiovascular risk. In this work, we describe changes in inflammatory markers-C-reactive protein (CRP), pentraxin 3 (PTX3), serum component of amyloid A (SAA), and procalcitonin (PCT)--in CKD patients compared with a control group of subjects with a normal estimated glomerular filtration rate (eGFR). Blood samples were obtained from 69 healthy individuals (GP) and 70 end-stage CKD patients--25 not yet on dialysis, 22 on peritoneal dialysis (PD), and 23 on hemodialysis (HD). These were the results [median (95% confidence interval)] for the GP CKD, PD, and HD groups respectively: CRP: 1.40 mg/L (1.19-2.11 mg/L), 6.50 mg/L (3.57-8.32mg/L), 7.60 mg/L (2.19-22.10mg/L), 9.60 mg/L (6.62-16.38 mg/L). SAA: 3.10 mg/L (2.90-3.53 mg/L), 7.11 mg/L (3.81-15.40mg/L), 9.69 mg/L (5.07-29.47mg/L), 15.90 mg/L (6.80-37.48 mg/L). PCT: 0.03 ng/mL (0.02-0.03 ng/mL), 0.12 ng/mL (0.09-0.16 ng/mL), 0.32 ng/mL (0.20-0.46 ng/ mL), 0.79 ng/mL (0.45-0.99 ng/mL). PTX3: 0.54 ng/mL (0.33-0.62 ng/mL), 0.71 ng/ mL (0.32-1.50 ng/mL), 1.52 ng/mL (0.65-2.13 ng/mL), 1.67 ng/mL (1.05-2.27 ng/mL). Compared with levels in the GP group, levels of SAA and CRP (systemic response) were significantly higher in CKD patients on and not on dialysis. Levels of PTX3 were higher only in dialyzed patients, significantly so in those on HD (greatly different from the CRP levels). These differing levels might be related to a local reaction caused by an invasive intervention (PD or HD). As eGFR declines and with the start of renal replacement therapy, PCT increases. Levels of PCT could potentially cause confusion when these patients are being evaluated for the presence of infection, and may also demonstrate some microvascular implications of dialysis therapy.