期刊文献+

终末期肾脏病患者钙磷代谢及甲状旁腺激素水平的临床分析 被引量:63

Study of calcium-phosphorous metabolism and intact parathyroid hormone levels in end stage renal disease patients
下载PDF
导出
摘要 目的: 了解终末期肾脏病(ESRD)患者的钙磷代谢情况及全段甲状旁腺激素(iPTH)水平,分析其临床特征,为合理治疗提供依据。方法: 对 2000年 1月至 2003年 7月在我院准备进行透析治疗的 100例ESRD患者的临床资料进行回顾性分析。结果: (1)在 100例患者中,经白蛋白校正过的血清总钙分布为:低钙血症患者占 15%;其余患者血钙正常或偏高(其中高钙血症的患者占 27% ),这些患者中有 31. 8 %使用了含钙的磷结合剂和 /或活性维生素D。比较未经干预治疗的 14例血钙低的患者和 58例血钙不低的患者,发现低血钙患者的二氧化碳结合力水平明显降低(P<0. 05);两组在年龄、血磷、血肌酐及iPTH水平方面差异无统计学意义。(2)在 100例患者中, 81%存在高磷血症; (3)iPTH<100ng/L的患者占 18%,iPTH>300ng/L的患者占 46%,前者的主要病因是慢性肾小管间质病变,后者的主要病因是慢性肾小球肾炎(除去使用含钙的磷结合剂和 /或活性维生素D的患者 )。两组在年龄、血钙、血磷及酸中毒方面差异无统计学意义。多因素回归分析显示校正后血钙水平与iPTH水平呈负相关 (r=-0. 275,P=0. 006)。结论: ESRD患者高血磷表现突出,近 50%的患者伴发继发性甲状旁腺功能亢进。血钙水平除了受应用含钙的磷结合剂和 /或活性维生素D影响外,还与酸中毒有关? Objective: To investigate the state of calcium-phosphorus metabolism and serum intact parathyroid hormone (iPTH) levels in end stage renal disease (ESRD) patients, to analyze clinical characters, and to provide scientific basis for clinical treatment. Methods: The data of 100 ESRD patients who received hemodialysis in Peking University First Hospital from January 2000 to July 2003 were analyzed retrospectively. Results: (1) The levels of serum total calcium were adjusted by serum albumin. There were 15 patients with hypocalcemia and 85 patients with normocalcemia or hypercalcemia. 31.8% of the latter took calcium-containing phosphate binders or/and vitamin D. In the 14 patients with hypocalcemia and 58 patients without low serum calcium who did not take calcium-containing phosphate binders or/and vitamin D, we found the levels of carbon dioxide combining power (CO 2CP) were lower in the group of hypocalcemia (P<0.05), at the same time, there were no significant differences in age and the levels of serum phosphorous, creatinine and iPTH between the two groups. (2) Hyperphosphataemia occurred in 81 patients (81%). (3) The levels of serum iPTH were lower than 100 ng/L in 18 patients (18%) and higher than 300 ng/L in 46 patients (46%), the most common cause of the former was chronic tubular-interstitial nephropathy and that of the latter was chronic glomerulonephritis, excluding the patients who took calcium-containing phosphate binders or/and vitamin D.There were no significant differences in age and the levels of serum calcium, phosphorous and CO 2CP between the two groups. Multiple regression analyses indicated the levels of serum calcium were in negative correlation with the levels of serum iPTH (r= -0.275, P=0.006). Conclusion: Hyperphosphataemia is one of the outstanding characters in ESRD patients and nearly 50% of all the patients develop secondary hyperparathyroidism. The serum calcium levels are correlative with acidosis besides calcium-containing phosphate binders or/and vitamin D.
出处 《北京大学学报(医学版)》 CAS CSCD 北大核心 2005年第2期147-150,共4页 Journal of Peking University:Health Sciences
  • 相关文献

参考文献18

  • 1Johnson WJ. Optimum dialysate calcium concentration maintenance hemodialysis[J]. Nephron, 1976, 17:241-258
  • 2Mactier RA, Van Stone J, Cox A, et al. Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia[J]. Clin Nephrol, 1987, 28:222-226
  • 3Andress DL, Norris KC, Coburn JW, et al. Intravenous calcitriol in the treatment of refractory osteitis fibrosa of chronic renal failure[J]. N Engl J Med, 1989, 321:274-279
  • 4Goodman WG, Goldin J, Kuizon BD, et al. Coronary artery calcification in young adults with end-stage renal disease who are undergoing dialysis[J]. N Engl J Med, 2000, 342:1478-1483
  • 5Block GA, Port FK. Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients: recommendations for a change in management[J]. Am J Kidney Dis, 2000, 35: 1226-1237
  • 6Francesco L, Jorge-B CA, Tilman BD, et al. Management of disturbance of calcium and phosphate metabolism in chronic renal insufficiency with emphasis on the control of hyperphosphataemia[J]. Nephrol Dial Transplant, 2002, 17:723-731
  • 7Lemann JJ, Litzow JR, Lennon EJ. The effect of chronic acid loads in normal man: Further evidence against chronic metabolic acidosis[J]. J Clin Invest, 1966, 45:1608-1614
  • 8Lemann JJ, Litzow JR, Lennon EJ. Studies of the mechanism by which chronic metabolic acidosis augment urinary calcium excretion in man[J]. J Clin Invest, 1967, 46:1318-1328
  • 9Craig BL. Calcitriol metabolism during chronic metabolic acidosis[J]. Semin Nephrol, 1989, 9:65-71
  • 10Kurz P, Monier Faugere MC, Bognar B, et al. Evidence for abnormal calcium homeostasis in patients with adynamic bone disease[J]. Kidney Int, 1994, 46:855-861

同被引文献592

引证文献63

二级引证文献506

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部