title: Glucose-free dialysis solutions: inductors of inflammation or preservers of peritoneal membrane?
abstract: OBJECTIVE
  Glucose and other bioincompatible factors of conventional peritoneal dialysis solutions may damage the peritoneal membrane. The aim of our study was to investigate whether replacement of glucose with icodextrin (ID) or amino acids (AA) affects inflammatory parameters or cancer antigen 125 (CA125).
  
  
  METHODS
  Either ID or AA was used, in random order, in one daily exchange during an 8-week period. After the first study period, the patients entered a washout period and then switched to the other study solution for an 8-week period. C-reactive protein (CRP) was measured in serum, and CA125, tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), and hyaluronan (HA) were measured in the overnight dwell dialysates at the beginning and end of the study periods.
  
  
  METHODS
  A university hospital.
  
  
  METHODS
  22 patients with duration on peritoneal dialysis of 1.5 - 6.3 months.
  
  
  METHODS
  Levels of serum CRP and dialysate CA125, IL-6, HA, and sICAM-1 during use of ID and AA were compared to levels during use of glucose-only-based solutions.
  
  
  RESULTS
  CRP increased significantly during use of ID. CA125 increased significantly during 8 weeks' use of AA, from 22.8 (5.4 - 89.0) to 42.9 (7.1 - 92.9) kU/L (p = 0.007). IL-6 increased during 8 weeks' use of AA, from 22.0 (9.0 - 108.0) to 36.5 (14.0 - 93.0) ng/L (p = 0.002) and ID, from 25.5 (8.0 - 82.0) to 40.0 (12.0 - 118.0) ng/L (p = 0.008). TNF-alpha also increased significantly during use of ID, but showed no significant changes during use of AA.
  
  
  CONCLUSIONS
  The use of glucose-free solutions, especially AA, may lead to preservation of mesothelial cell mass and host defense. However, activation of systemic and peritoneal inflammation may appear during the use of ID and to a lesser extent during use of AA.
authors.affiliation: Division of Nephrology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.
authors.forename: Terhi A
authors.initials: TA
authors.lastname: Martikainen
authors.forename: Anna-Maija
authors.initials: AM
authors.lastname: Teppo
authors.forename: Carola
authors.initials: C
authors.lastname: Grönhagen-Riska
authors.forename: Agneta V
authors.initials: AV
authors.lastname: Ekstrand
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000596:Amino Acids; D002097:C-Reactive Protein / Q000378:metabolism; D018394:CA-125 Antigen / Q000378:metabolism; D018592:Cross-Over Studies; D015314:Dialysis Solutions; D005260:Female; D005936:Glucans; D005947:Glucose; D006801:Humans; D006820:Hyaluronic Acid / Q000378:metabolism; D000077607:Icodextrin; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007674:Kidney Diseases / Q000378:metabolism* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000596:Amino Acids; D018394:CA-125 Antigen; D015314:Dialysis Solutions; D005936:Glucans; D015850:Interleukin-6; C482915:Nutrineal; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D000077607:Icodextrin; D006820:Hyaluronic Acid; D002097:C-Reactive Protein; D005947:Glucose