title: Strong correlation of B2-microglobulin (B2-m) with procalcitonin (PCT) in the serum of chronic hemodialysis patients: a role for infections in the dialysis-related amyloidosis?
abstract: BACKGROUND
  Infections trigger the activation of defensive cells capable to produce and release B(2)-microglobulin (B(2)-m). Procalcitonin (PCT), secreted by a wide range of human cells, included the aforementioned defensive cells, is generally considered a sensitive and specific marker of infection. In this prospective study, we examined the possibility that infections, as detected by increased levels of PCT, increase the serum levels of B(2)-m in chronic hemodialysis (CHD) patients, possibly affecting the rate of progression of dialysis-related amyloidosis (DRA).
  
  
  METHODS
  For a period of four months, 76 CHD patients, 45 men/31 women, mean age 63 +/- 15.7 years, with no residual renal function and in HD for 46 +/- 50 months were studied bimonthly. Blood was drawn, at baseline T(0), two months T(2), and four months T(4), for measuring hematocrit (Ht), white blood cells (WBC), erythrocyte sedimentation rate (ESR), blood urea and serum creatinine, protein (albumin, globulin), C-reactive protein (CRP), and PCT kappa alpha iota B(2)-m. Any events (especially infections) in the preceding 10-day period were recorded.
  
  
  RESULTS
  At baseline, 100% of all B(2)-m measurements were abnormal (>2.4 mg/L), 13.4% of PCT values were increased (>1.5 ng/mL), and 49.4% of CRP values exceeded the lower limit of 5 mg/L with no statistically significant differences between the results of the three periods of the study. Statistically significant, in all periods, was the linear positive correlation of B(2)-m with PCT (T[0]: p < 0.001, T[2]: p < 0.004, T[4]: p < 0.001). Also, statistically significant (p < 0.005) was the positive correlation of B(2)-m to HD vintage.
  
  
  CONCLUSIONS
  In this study, the strong positive correlation of B(2)-m to PCT probably signifies that the (mainly subclinical) infections increase B(2)-m production in CHD patients intensifying the problem of HD-related amyloidosis.
authors: Center for Nephrology G. Papadakis, General Hospital of Nikea, Piraeus, Greece.
authors: Petros
authors: P
authors: Kalocheretis
authors: Ioanna
authors: I
authors: Revela
authors: Eleni
authors: E
authors: Spanou
authors: Apostolos
authors: A
authors: Drouzas
authors: Ioanna
authors: I
authors: Makriniotou
authors: Christos
authors: C
authors: Iatrou
mesh_terms: D000368:Aged; D000686:Amyloidosis / Q000382:microbiology*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D002116:Calcitonin / Q000097:blood*; D015740:Calcitonin Gene-Related Peptide; D005260:Female; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D007239:Infections / Q000382:microbiology; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011498:Protein Precursors / Q000097:blood*; D006435:Renal Dialysis / Q000009:adverse effects*; D001613:beta 2-Microglobulin / Q000097:blood*
chemical_list: D015415:Biomarkers; C000606589:CALCA protein, human; D006023:Glycoproteins; D011498:Protein Precursors; D001613:beta 2-Microglobulin; D002116:Calcitonin; D002097:C-Reactive Protein; D015740:Calcitonin Gene-Related Peptide