Coen G, Mazzaferro S, Ballanti P, Sardella D, Chicca S, Manni M, Bonucci E, Taggi F
Renal Pathophysiology and Hypertension Unit, Department of Experimental Medicine and Pathology, La Sapienenza University, Rome, Italy.
Nephrol Dial Transplant. 1996 May;11(5):813-9. doi: 10.1093/oxfordjournals.ndt.a027404.
Renal osteodystrophy has been studied less extensively in predialysis than in dialysis patients. Different types or histological patterns in their natural evolution from moderate to advanced severity of renal insufficiency are only partially known, with special regard to adynamic bone disease and its relationship with osteomalacia.
We conducted a cross-sectional retrospective study on 76 unselected patients with chronic renal failure undergoing conservative treatment, with a wide range of severity of renal insufficiency. All the patients were subjected to bone biopsy for histological and histomorphometric evaluation. The patients, 44 males and 32 females ranging in age from 18 to 72 years and with serum creatinine 1.2-11.4 mg/dl, had not been exposed to aluminium-containing drugs and had never been treated with vitamin D or calcitriol.
Ten patients had normal bone, nine were diagnosed with adynamic bone disease, 26 with mild mixed osteodystrophy, seven with predominant osteomalacia, 22 with advance mixed osteodystrophy, and two with predominant hyperparathyroidism. Patients with adynamic bone disease had less severe chronic renal failure than the other pathological subgroups, intact PTH above the upper limit of normal, normocalcaemia, and reduced serum osteocalcin in line with a significantly lower ObS/BS. Osteomalacia was found in a more advanced stage of chronic renal failure with relative hypocalcaemia and more severe metabolic acidosis. A creatinine clearance of 20 ml/min served as a clear demarcation between this histological group and adynamic bone disease.
It is postulated that adynamic bone disease is a form of renal osteodystrophy, separate from osteomalacia, appearing when bone resistance to PTH develops, probably a transient stage to more hyperparathyroid histological classes with increasing severity of chronic renal failure.
与透析患者相比,肾性骨营养不良在透析前患者中的研究较少。对于肾功能不全从中度到重度自然演变过程中的不同类型或组织学模式,我们仅了解一部分,尤其是关于骨再生障碍和它与骨软化症的关系。
我们对76例未经过挑选、接受保守治疗、肾功能不全严重程度各异的慢性肾衰竭患者进行了一项横断面回顾性研究。所有患者均接受了骨活检以进行组织学和组织形态计量学评估。这些患者年龄在18至72岁之间,血清肌酐为1.2 - 11.4mg/dl,共44名男性和32名女性,未接触过含铝药物,也从未接受过维生素D或骨化三醇治疗。
10例患者骨正常,9例被诊断为骨再生障碍,26例为轻度混合性骨营养不良,7例以骨软化症为主,22例为晚期混合性骨营养不良,2例以甲状旁腺功能亢进为主。骨再生障碍患者的慢性肾衰竭程度比其他病理亚组轻,完整甲状旁腺激素高于正常上限,血钙正常,血清骨钙素降低,与骨表面矿化面积/骨小梁表面积显著降低一致。骨软化症出现在慢性肾衰竭更晚期,伴有相对低钙血症和更严重的代谢性酸中毒。肌酐清除率20ml/min是该组织学组与骨再生障碍之间的明确分界线。
据推测,骨再生障碍是肾性骨营养不良的一种形式,与骨软化症不同,当骨骼对甲状旁腺激素产生抵抗时出现,可能是随着慢性肾衰竭严重程度增加向甲状旁腺功能亢进组织学类型发展的一个过渡阶段。