ATLAS DE OSTEODISTROFIA RENAL
There are two forms, according to the degree or rate of mineralization. The classic form is Osteomalacia; as previously mentioned, this is associated with mineralization defect and a marked excess of osteoid. A few decades ago, this was the most disturbing form since it was often accompanied by serious bone fractures. Incidence varied from region to region, indicating that factors other than the uremic state itself, and related with dialysis techniques, were involved in its genesis. This is the case of aluminum present in in inadequately purified water used for dialysis. When aluminum is deposited at the mineralization front, it induces serious forms of osteomalacia (fracturing osteodystrophy), as reflected by the presence of wide lamellar osteoid and delayed tetracycline labeling. Tetracycline double labels may appear as unseparated bands or be totally absent. Proper water treatment with Reverse Osmosis has led to the virtual disappearance of aluminum-induced osteomalacia. Nowadays, Osteomalacia is rarely found associated with long-term hypophosphoremia and/or metabolic acidosis.
The next form of low turnover is that called “Adynamic Bone Disease”. Originally described in relation to cases of aluminium intoxication, this is today the most frequent histological form, presenting in 40% and even 60% of patients in some series, especially in the aged and diabetic patients. This disorder is characterized by low cellular activity adjacent to the trabecular surface, but without evidence of mineralization defects, although tetracycline labeling is not usually observed. In other words, excess osteoid is not apparent. Bone mass tends to be diminished, such that it sometimes presents as a form of osteopenia or osteoporosis. This bone is relatively resistent to calcium incorporation, which is considered a risk for extraosseous calcification. Abusive use of vitamin D analogs has been seen to possibly favor the appearance of this entity.