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Novel glomerular lesions were seen in male rabbits after intravenous administration of aluminum lactate. Eight rabbits in the treated group were given 0.1 mmol/kg of aluminum lactate 5 days a week for 4 weeks. The control group of 8 rabbits was given 0.3 mmol/kg of sodium lactate by the same injection protocol. In the treated group, the mesangial cells in the glomerular tufts in 6 of 8 rabbits were distended with grayish blue granular material, which was identified by laser microprobe mass spectrometry and acid solochrome azurine stain as an aluminum compound. Other consistent findings in the glomeruli included microaneurysm in 6 of 8 rabbits and segmental sclerosis in 6 of 8 rabbits. Less frequently observed glomerular changes included crescent formation, necrosis with calcification, fibrosis of the Bowman's capsule, cystic dilation of the Bowman's space, and exudation of erythrocytes into the Bowman's space. The mechanism by which aluminum lactate induces the glomerular changes is not certain. However, the pathogenesis may involve the deposition of aluminum in the mesangial cells, resulting in mesangiolysis which in turn causes microaneurysm. The sclerotic change is interpreted as a sequela of microaneurysm. The findings suggest that aluminum induces glomerular lesions in rabbits. This may serve as a good animal model to study mesangiolysis and microaneurysm formation.

In a previous paper (Yamaguchi et al. 1991) we informed that the administration of 1 ml. of 6% Na2EDTA every day intraperitoneally for two months led to the death of the guinea pigs, and autopsy revealed that the causes of death were right ventricular rupture ("rupturing") or severe right heart failure which was observed as extraordinary dilatation of the right ventricle ("non-rupturing"). The two different morphological causes of death were site dependent on the constriction of the pulmonary arteries, and the pulmonary arteries showed a fairly unique morphology. To analyze the morphological manifestations of the pulmonary arteries which were observed in the cases of extraordinarily dilated and thin ventricular luminal wall a decreased dose of Na2EDTA was administered every day for six months in order to maintain a reasonably long life of the animals through prevention of right ventricular rupture. In addition to the morphological manifestations reported in the previous paper, the longer term constriction of pulmonary arteries provoked aneurysmal changes, partially or totally, and the plexiform-like lesions which have been thought to be the most characteristic morphological one in pulmonary hypertension. The formative mechanisms are discussed.