Procalcitonin in patients undergoing chronic hemodialysis.

Accessible online at: www.karger.com/journals/nef Dear Sir, Procalcitonin (PCT), the precursor of calcitonin, is a new diagnostic parameter for infections. There is evidence for PCT being a more specific parameter indicating systemic bacterial and fungal infections than the nonspecific acute-phase markers C-reactive protein (CRP) or apoferritin. Experimental data and clinical observations have shown that the main stimuli for PCT release are bacterial endotoxins and proinflammatory cytokines as seen in septicemia and bacteremia [1, 2]. Both uremia and bioincompatibility of hemodialysis (HD) result in a chronic systemic inflammatory syndrome. Even when ultrapure dialysate is used, there is evidence for endotoxins or endotoxin fragments (lipid A, muramyl peptides, molecular weight !1 kD) crossing both lowand high-flux membranes, leading to the activation of monocytes and subsequent release of several proinflammatory cytokines, such as interleukin 1 and tumor necrosis factor alpha [3, 4]. The aim of our investigation was to characterize PCT serum levels in patients without systemic infections undergoing chronic dialysis therapy. Thirty-six patients on chronic HD and 10 patients on continuous ambulatory peritoneal dialysis (CAPD) were selected for the study on the basis of absence of any clinical evidence for infections during the last 3 weeks prior to the study and being without active immunologic or acute thromboembolic disorders, malignancies, or major surgical procedures (28 men and 18 women with a mean age of 58 B 24 years). All patients had been on dialysis therapy for at least 3 months. Informed consent was obtained from all patients. Causes of chronic renal failure were chronic glomerulonephritis (n = 14), diabetic nephropathy (n = 10), interstitial nephritis (n = 7), hypertensive nephropathy (n = 6), nephroangiosclerosis (n = 1), and undetermined causes (n = 6). HD therapy was performed using high-flux membranes (polysulfone F60S, Fresenius, Bad Homburg, Germany; polyarylethersulfone H4, Hospal, Lyon, France) and bicarbonate-based dialysate. In 16 patients ultrapure dialysate was used. The endotoxin count was always below 50 U/ml. Blood samples were taken from the vascular access site prior to dialysis therapy (basal state) and from the efferent line at 15 min (time 15) and at the end of the HD session (time 240). In the CAPD patients blood was drawn from a peripheral vein at routine visits. The PCT levels were assayed using the LUMLtest®, an immunoluminometric assay. The reference range is below 0.5 ng/ml, but in healthy subjects the PCT levels are usually below 0.1 ng/ ml [5]. CRP, leukocytes, and ferritin were sampled at the same time points in EDTA and serum tubes (Sarstedt) and analyzed by autoanalyzer. PCT was above the detectable level of 0.1 ng/ml in all 36 chronic HD patients before and at the end of HD. The PCT levels were above 0.5 ng/ml in 16 patients (44%) at baseline versus 9 patients (25%) at the end of HD. On average the PCT levels decreased from 0.58 B 0.35 ng/ml at baseline to 0.44 B 0.32 ng/ml at the end of HD (fig. 1, p ! 0.05). In 1 of the 10 CAPD patients, the PCT serum level was 0.8 ng/ml, in the remaining 9 patients the PCT levels were between 0.1 and 0.3 (0.23 B 0.11) ng/ml. CRP was below Fig. 1. Mean PCT and CRP levels in 36 patients on chronic HD without systemic infections. 0.3 0.3 0.4 0.4 0.5 0.5 C R P (m g /d l)