Docci D, Turci F, Baldrati L
Nephron. 1985;41(3):241-5. doi: 10.1159/000183590.
The possible relationship between red blood cell (RBC) osmotic fragility and secondary hyperparathyroidism (HPT) in chronic renal failure was examined in 23 uremic patients on conservative therapy and in 42 patients on maintenance hemodialysis. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations (X-ray films of the hand skeleton). This study showed increased RBC osmotic fragility in uremic patients when compared with controls, with no difference between those on conservative therapy and those on maintenance hemodialysis. No correlation between RBC osmotic fragility and the hematochemical changes associated with secondary HPT was found. No difference in RBC osmotic fragility was observed with regard to the activity (alkaline phosphatase) and the severity (X-ray findings) of secondary HPT. Effective treatment of secondary HPT by either pharmacological means (1,25-dihydroxycholecalciferol) or surgical removal was not associated with consequent improvement in RBC osmotic fragility. It is concluded that secondary HPT is probably not a major factor influencing RBC osmotic fragility in chronic renal failure.
对23例接受保守治疗的尿毒症患者和42例维持性血液透析患者，研究了慢性肾衰竭时红细胞（RBC）渗透脆性与继发性甲状旁腺功能亢进（HPT）之间的可能关系。通过血清生化检查（甲状旁腺激素、钙、磷和碱性磷酸酶）及影像学检查（手部骨骼X线片）评估继发性HPT。本研究显示，与对照组相比，尿毒症患者的RBC渗透脆性增加，接受保守治疗的患者与维持性血液透析的患者之间无差异。未发现RBC渗透脆性与继发性HPT相关的血液化学变化之间存在相关性。在继发性HPT的活性（碱性磷酸酶）和严重程度（X线表现）方面，未观察到RBC渗透脆性有差异。通过药物治疗（1,25 - 二羟胆钙化醇）或手术切除对继发性HPT进行有效治疗后，RBC渗透脆性并未随之改善。得出的结论是，继发性HPT可能不是影响慢性肾衰竭患者RBC渗透脆性的主要因素。
