title: Serum beta2-microglobulin and immunoglobulin levels in young hemodialysis patients.
abstract: Amyloidosis is a complication of long-term hemodialysis treatment. The major histological feature of hemodialysis-associated amyloidosis (HAA) is the deposition of amyloid fibrils in the affected lesions, due, in part, to elevated serum beta2-microglobulin (beta2M) levels. In vitro studies reveal that serum immunoglobulin light and heavy chains co-deposit with beta2M in tissues affected by HAA. Only one study of HAA has been performed in young dialysis patients. We therefore assessed risk factors for HAA in a group (n=30) of young (18.7+/-0.9 years) patients receiving chronic, uninterrupted hemodialysis using cellulose acetate membranes. All patients initiated dialysis before reaching 18 years of age. The pre-dialysis serum beta2M level was 49.7+/-3.9 mg/l (normal 0-2.4 mg/l). Since serum albumin was normal (4.3+/-0.1 mg/dl) and serum protein/albumin was elevated (1.7+/-0.0, normal 1.2-1.5), indicating increased circulating protein, we assayed immunoglobulins in the same patients. The serum immunoglobulin levels (expressed as a percentage of the total level of serum proteins) were elevated (21.3+/-0.9%, normal 11.1%-21.0%). The Kt/v was 1.37+/-0.03, suggesting that the high levels of serum beta2M and immunoglobulins were not due to inadequate dialysis in these patients. Patients with residual renal function (Kr) did display significantly lower serum levels of beta2M (33.2+/-2.3, P=0.03). Furthermore, improved clearance of beta2M correlated with higher values of Kr (r=0.914). In contrast, serum levels of immunoglobulin (22.6+/-3.7, P=0.5) were unaffected by Kr. In addition, there was no correlation between older age at onset of dialysis and serum levels of either beta2M (r=0.107) or immunoglobulins (r=0.321). Finally, the length of time on dialysis had no effect on serum levels of either beta2M (r=0.105) or immunoglobulins (r=0.092). Taken together, these results indicate that young hemodialysis patients may be at risk for HAA.
authors.affiliation: Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York, USA.
authors.forename: M P
authors.initials: MP
authors.lastname: Dixit
authors.forename: M R
authors.initials: MR
authors.lastname: Cabansag
authors.forename: J
authors.initials: J
authors.lastname: Piscitelli
authors.forename: I
authors.initials: I
authors.lastname: Greifer
authors.forename: D M
authors.initials: DM
authors.lastname: Silverstein
mesh_terms: D000293:Adolescent; D000328:Adult; D000686:Amyloidosis / Q000097:blood* / Q000209:etiology; D001798:Blood Proteins / Q000032:analysis; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007136:Immunoglobulins / Q000097:blood*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy; D008297:Male; D006435:Renal Dialysis / Q000009:adverse effects*; D012307:Risk Factors; D001613:beta 2-Microglobulin / Q000378:metabolism*
chemical_list: D001798:Blood Proteins; D007136:Immunoglobulins; D001613:beta 2-Microglobulin