Tissue uptake of 125I-beta 2-microglobulin (beta 2-M) in anephric animals in the presence or absence of aluminium intoxication.

In long-term haemodialysis patients a new type of amyloidosis composed of beta 2-microglobulin (beta 2-M) has recently been described. The amyloid deposition has a particular predilection for articular structures. In the pathogenesis of this complication markedly elevated plasma beta 2-M concentrations, such as those observed in anuric patients, have a role. However, other as yet ill-defined factors must also be implicated, possible candidates being aluminium intoxication and the widely used regenerated cellulose (cuprophan) membrane. In the present experimental study, we examined tissue distribution of exogenous beta 2-M after i.v. injection of 125I-beta 2-M to bilaterally nephrectomised rats. One hundred and twenty minutes after injection, most radioactivity remained in the vascular compartment. The accumulation in tissues was weak, and no predilection for a particular tissue became apparent. Interestingly, chronically aluminium-overloaded, acutely anephric rats accumulated a significantly greater amount of 125I-beta 2-M in their spleens than anephric rats without prior aluminium intoxication. We then attempted to induce beta 2-M amyloid deposition in rats and mice, some of whom had undergone chronic aluminium intoxication and subcutaneous implantation of regenerated cellulose fragments for various periods of time. They were subsequently made anephric to obtain high plasma beta 2-M concentrations. None of the animals developed beta 2-M amyloidosis in spleen, liver, skin and mechanically altered joint synovium. In conclusion, chronic aluminium intoxication enhances splenic accumulation of exogenous 125I-beta 2-M in anephric rats. The factors required to form beta 2-M-amyloidosis in vivo have still to be defined.