The epiphyseal growth plate of femora (proximal and distal), tibiae, radii and ulnae of seven uremic children were studied to clarify the histopathogenesis of epiphyseolysis. Epiphyseolysis was found to be result of three different processes: (1) growth arrest, (2) excessive erosion of the growth cartilage and of the trabeculae of metaphyseal spongiosa and (3) disturbance of vascularisation of hypertrophic cartilage. By resorptive destruction, secondary hyperparathyroidism causes loss of the chondro-osseous continuity. The ordered trajectoral pattern of the trabeculae in the primary spongiosa is transformed into a dense lace of mechanically inferior trabeculae consisting of woven bone. Impairment of primary mineralization could not be demonstrated. Intensive subperiosteal osteoclastic resorption leads to a reduction of metaphyseal width and to fractures of the unsupported lateral parts of the growth cartilage. There were notable differences between the growth plates in different localisations: in growth plates subjected to axial compression (distal femur, tibia) signs of growth arrest prevailed (reduction of hypertrophic cartilage, occlusion of the growth plate by a transverse plate of bone); in growth plates subjected to shearing forces (upper femur, radius, ulna) epiphyses were seen to slip sideway.