ARTICULAR TOXICITY OF ALUMINUM - POSSIBLE INVOLVEMENT IN DIALYSIS-ASSOCIATED ARTHROPATHY

Several factors, in addition to beta 2M amyloid may play a role in the pathogenesis of dialysis-associated arthropathy, In order to investig ate the articular toxicity of aluminum derivatives in vivo, an insolub le derivative (hydroxide) or a soluble one (lactate) were single-injec ted into the rabbit knee or the synovial-like air pouch cavity in the rat. Histological and laboratory studies were carried out on rabbits w hereas the air pouch model served for studying the release of eicosano ids. Aluminum levels were measured in liver, kidney and synovium of ra bbits, 48 h after intra-articular injection. After injection into rabb it knee, aluminum lactate resulted in an hemorrhagic effusion and a co ngestive synovitis. Perivascular edema was associated with sparse infi ltration of inflammatory cells in the synovium. These lesions coexiste d with an apparent loss of proteoglycan in superficial zones of tibial and femoral cartilages. Aluminum hydroxide did not affect joint struc tures. In the air experiment, aluminum hydroxide increased leukocyte c ount in pouch-washout fluid from 3 to 24 hours after its injection whe n PGE2 and LTB4 levels were little modified. In contrast, aluminum lac tate increased PGE2 levels from 3 to 10 hours after its injection, in the absence of leukocyte migration into the cavity. LTB4 levels peaked less markedly after 6 hours. Aluminum compounds may damage joint stru ctures either directly or through stimulating the secretion of eicosan oids by synovial-like cells. These mechanisms could be of some relevan ce in hemodialyzed patients with aluminum overload, who develop dialys is-associated arthropathy.