Clinical significance of granulocyte-inhibiting proteins.

End-stage renal disease (ESRD) patients have a dialyser ultrafiltrate obtained from chronic haemodia-significant risk for bacterial infections. According to lysis patients and from peritoneal e ffl uent obtained Himmelfarb and Hakim [1] 15–20% of deaths in from CAPD patients. All these proteins inhibit in vitro haemodialysis patients are related to infectious com-glucose uptake and chemotaxis of PMNL [8]. Several plications. For more than 40 years 50% of patients studies have indicated that plasma light chain proteins with acute renal failure have died because of infections are elevated in uraemia [9,10]. [2]. These data indicate that microbial antigens are N-terminal amino acid sequence analysis of GIP II serious risk factors for patients with chronic and acute shows an amino acid sequence identical to b 2 -micro- renal failure. globulin. GIP II inhibits, at nanomolar concentrations The enhanced susceptibility to infection of patients in vitro , PMNL glucose uptake and oxidative metabol-with acute and chronic renal failure is multifactorial. ism However, commercially available b 2 -micro- Major factors in these patients are metabolic and globulin does not a ff ect PMNL metabolism and functional abnormalities of polymorphonuclear leuco-function. These data indicate that a modified form of cytes (PMNL), caused by: (i) iron overload (positive b 2 -microglobulin is responsible for PMNL inhibition. staining within the PMNL); (ii) accumulation of cal-In vitro experiments with mononuclear cells in culture cium within PMNL; (iii) bioincompatibility of dialysers and peritoneal dialysis solutions; and (iv) low- and high-molecular-mass