Suppr超能文献

肾病综合征中的25-羟基维生素D

25-hydroxy-vitamin-D in nephrotic syndrome.

作者信息

Schmidt-Gayk H, Grawunder C, Tschöpe W, Schmitt W, Ritz E, Pietsch V, Andrassay K, Bouillon R

出版信息

Lancet. 1977 Jul 16;2(8029):105-8. doi: 10.1016/s0140-6736(77)90118-0.

Abstract

Serum-25-hydroxy-vitamin-D (25-OHD) nephrotic syndrome (N.S.) without renal insufficiency (urinary protein excretion greater than 3-5 g/24 h/1-73 m2; glomerular filtration-rate greater than 80 ml/min/1-73 m2). Serum-25-OHD levels were low in patients with N.S. (mean 19 nmol/1, range 4-41 nmol/1), compared with a normal range of 25-200 nmol/1. Serum-concentrations of Gc-globulin--the binding protein for vitamin D and its metabolites (D.B.P.)--were significantly (P less than 0-001) lower in patients with N.S. (mean 340 mg/1, range 190-480 mg/1) than in non-proteinuric controls (mean 440 mg/1, range 376-510 mg/1, measured by radial immunodiffusion). In contrast to non-proteinuric urine, urine of all N.S. patients contained a large amount of 25-OHD-binding capacity; D.B.P. could be detected in all N.S. urines after concentration. Scatchard analysis of the urine demonstrated the presence of a low-affinity and a high-affinity binding protein (tentatively identified as albumin and D.B.P.). These results suggest an acquired deficiency of circulating 25-OHD in N.S. secondary to urinary loss of protein-bound 25-OHD. The biological relevance of the low 25-OHD levels is unknown. There was no clinical evidence of osteomalacia (X-ray, serum-alkaline-phosphatase); however, slightly elevated serum-parathyroid-hormone (P.T.H.) levels would be compatible with borderline vitamin-D depletion.

摘要

血清25-羟维生素D(25-OHD)与无肾功能不全的肾病综合征(NS)(尿蛋白排泄大于3 - 5g/24小时/1.73m²;肾小球滤过率大于80ml/分钟/1.73m²)。与正常范围25 - 200nmol/1相比,NS患者的血清25-OHD水平较低(平均19nmol/1,范围4 - 41nmol/1)。维生素D及其代谢产物的结合蛋白(DBP)——Gc球蛋白的血清浓度,NS患者(平均340mg/1,范围190 - 480mg/1)显著低于非蛋白尿对照组(平均440mg/1,范围376 - 510mg/1,通过放射免疫扩散法测量)(P小于0.001)。与非蛋白尿尿液不同,所有NS患者的尿液都含有大量的25-OHD结合能力;浓缩后在所有NS患者尿液中都能检测到DBP。对尿液进行Scatchard分析表明存在低亲和力和高亲和力结合蛋白(初步鉴定为白蛋白和DBP)。这些结果表明,NS患者循环中25-OHD的缺乏是后天性的,继发于蛋白结合的25-OHD的尿流失。低25-OHD水平的生物学意义尚不清楚。没有骨软化症的临床证据(X线、血清碱性磷酸酶);然而,血清甲状旁腺激素(PTH)水平略有升高与边缘性维生素D缺乏相符。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验