Bone Crystal Maturation in Renal Osteodystrophy in Humans

Abstract

A B S T R A C T Calcium, phosphorus, sodium, carbonate, magnesium, and hydroxyproline were measured in iliac crest biopsies of 22 normal volunteers and 24 selected patients with renal osteodystrophy. Histologic classification revealed that 10 were mildly abnormal, 8 osteomalacic, and 6 osteofibrotic. Bone density measurements were performed on an additional 12 normal, 11 mildly abnormal, 6 osteomalacic, and 10 osteofibrotic subjects. The results revealed an increase in magnesium and a decrease in carbonate apparent in the minimal and osteomalacic lesions and a much greater change in osteofibrosis. The bone density was decreased in patients with osteofibrosis. These observations would appear to be explained by postulation of an impairment of the normal maturational process of bone whereby there is an increase in amorphous calcium phosphate and a decrease in apatite crystal. The data suggest that the maturational defect is present as soon as any abnormality can be identified histologically, is present to the same degree in osteomalacia, and is most severe in osteofibrosis. In comparison of two sets of six patients matched for age and duration of dialysis, neither acidosis nor vitamin D therapy appeared to influence the severity of the maturational defect.

Normal maturational changes in bone matrix, mineral, and crystal size in the rat

“…Changes in ion distribution in bone mineral previously had been attributed largely to alterations in plasma values [7,21,22]. Serum Ca and/or Mg are known to change bone Mg by altering the Mg/Ca ratio for the newly forming bone [10].…”

“…The tibia for biochemical analysis was dried to an airstable weight (ASW). water content determined by heating to 100~ in vacuum overnight, whole bone density determined by a volume displacement method [7], and the bone powdered for Na determination by neutron activation [8], CO3 by direct manometric analysis [9], Ca and Mg by atomic absorption spectrometry, and P and OH-P by autoanalyzer modifications [7]. The percent mineral (and matrix) present in the mineralized tissue was calculated by summing the weight of the ions plus the water lost from the mineral on drying.…”

Estudio radiológico de la osteodistrofia renal

“…El déficit de 1, 25 ( OH) 2 D 3 no es el único causante del defecto en la mineralización. En los pacientes con IRC existe una alteración en la cristalización de las sales de calcio que puede ser debida al aumento de la concentración en el tejido óseo de magnesio y pirofosfato y a la disminución de la concentración de carbonatos 4 • Asimismo, la acidosis metabólica de la IRC juega un papel un tanto controvertido en la patogenia de la osteomalacia : se conoce la función amortiguadora de las sales cálcicas del hueso en la acidosis renal, pero la corrección de la acidosis no corrige las lesiones óseas, lo cual sugiere que su contribución no es tan importante como se pensaba 10 • La patogenia de otras lesiones óseas, como la osteoporosis y la osteoesclerosis, que también se observan en la osteodistrofia renal, si bien con menor frecuencia, es más oscura . Se piensa que en la pri-.…”

Renal Osteodystrophy: New Insights in Pathophysiology and Treatment Modalities with Special Emphasis on the Insulin-Like Growth Factor System

“…The contribution of metabolic acidosis to the pathogenesis of renal osteodystrophy is still controversially discussed [105, 106, 107]. However, the bulk of clinical data underline the impact of acidosis on bone [63, 108, 109, 110, 111].…”