泌尿系统疾病(913552～913604)

913552 血清维生素D代谢产物水平与肾脏疾病的关系/薛延…//中华内分泌代谢杂志.-1991,7(2).-84～86 成人慢性肾功能不全28例、儿童肾脏疾患18例的血清25-羟维生素D_3包量均低于健康对照组(健康成人316例,儿童285例),平均下降41.2％(P<0.01),以尿毒症最低。尿毒症和肾病综合征患者血清1,26-二羟维生素D_3分别比对照组降低33.5％和42.4％(P<0.05);而慢性肾功能不全者该指标与BUN呈负相关(P<0.01),与内生肌酐清除率呈正相关(P<0.05),     

甲状旁腺功能减退症、垂体生长素瘤及垂体泌乳素瘤患者血1,25-(OH)_2D_3水平

本文报道用不需高压液相层析的1,25-双羟维生素D[1,25-(OH)_2D_3]放射受体测定法检测甲旁减患者用1α-羟维生素D_3(1α-OHD_3)治疗前后、垂体生长素瘤及垂体泌乳素瘤患者血清1,25-(OH)_2D_3水平的结果,及1,25-(OH)_2D_3与某些激素关系的初步探讨。     

同时限制蛋白和磷对于重度慢性肾衰竭患者1,25-二羟维生素D_3和甲状旁腺素的影响

限制饮食中磷含量可使正常人和中等度慢性肾衰竭(CRF)病人1,25-二羟维生素 D_3[1,25(OH)_(23)]D增高,重度 CRF 患者降低血磷可导致甲状旁腺素(PTH)降低,但血磷下降对1,25(OH)_2D_3的影响尚不了解。本组终末期 CRF 病人,给予蛋白和磷含量极低的饮食,辅以必需氨基酸(EAA)和成酮氨基酸(KAA),以观察重度 CRF 时1,25(OH)_2D_3的调节     

24,25—双羟维生素D_3和1,25(OH)_2D_3对佝偻病鼠镁代谢的影响

已知维生素D及其活性代谢物1,25-双羟维生素D_2(1,25(OH)_2D_3)对钙磷代谢有重要作用,但尚不知其对镁代谢的作用。本文给Vit D缺乏鼠一定量的1,25(OH)_2D_3和24,25—双羟维生素D_3(24,25(OH)_2D_3),观察对鼠镁代谢的影响。 选体重90～100g的雄鼠分别喂养,自由饮水和进食,食物中含(mg/100g)Ca=600,Mg=30,P=100及一种标准的无Vit D的维生素混合物。40天后可见鼠有佝偻病表现。再将鼠分为4组。Ⅰ     

血清1,25-二羟维生素D3水平与哮喘患儿病情以及哮喘控制状况的关系分析

目的探讨血清1,25-二羟维生素D_3水平与哮喘患儿病情以及哮喘控制状况的关系。方法选取2015年5月至2017年5月我院儿科收治的180例哮喘患儿为研究对象,根据病情严重程度分为轻度组、中度组和重度组,每组60例。另选取同期我院体检中心进行健康体检的60例儿童为对照组。所有哮喘患儿均给予哮喘正规治疗,治疗前后分别检测血清1,25-二羟维生素D_3水平。比较轻度组、中度组、重度组患儿和对照组儿童血清1,25-二羟维生素D_3的水平;比较治疗后不同哮喘控制状况患儿血清1,25-二羟维生素D_3的水平。结果哮喘患儿血清1,25-(OH)_2D_3水平显著低于健康儿童(P0.05);患儿哮喘严重程度越重,血清1,25-(OH)_2D_3水平越低,不同严重程度哮喘患儿血清1,25-(OH)_2D_3水平比较差异有统计学意义(P0.05)。治疗后哮喘完全控制组患儿血清1,25-(OH)_2D_3水平最高,哮喘未控制组患儿最低,不同治疗效果(哮喘控制状况)患儿血清1,25-二羟维生素D_3水平比较差异有统计学意义(P0.05)。结论血清1,25-二羟维生素D_3水平与哮喘患儿病情的严重程度以及哮喘控制状况密切相关,可作为判断患儿治疗效果的指标。     

老年原发性高血压患者血清1,25-二羟维生素D_3水平的研究

目的分析老年原发性高血压患者血清1,25-二羟维生素D3水平的变化,探讨1,25-二羟维生素D3水平与高血压的关系。方法选取老年原发性高血压患者98例(高血压组)和健康体检者90例(对照组),检测其血清1,25-二羟维生素D3水平和血浆肾素活性(PRA),并进行比较。结果与对照组比较,高血压组1,25-二羟维生素D3水平明显降低,PRA明显升高(P<0.01)。Pearson相关分析显示,1,25-二羟维生素D3水平与PRA、收缩压、舒张压呈负相关(r=-0.438、r=-0.355、r=-0.655,P<0.05)。logistic回归分析显示,PRA为高血压的危险因素,1,25-二羟维生素D3为高血压的保护因素。结论老年原发性高血压患者血清1,25-二羟维生素D3水平明显低于正常人群。1,25-二羟维生素D3是高血压的保护因素。     

2型糖尿病伴特发性甲状旁腺功能减退症一例

对一例T2DM伴严重低钙血症患者行甲状旁腺素(PTH),降钙素,1,25二羟维生素D_3[1,25(OH)_2D_3],24 h尿钙、磷检测及头颅CT检查。其24 h尿磷偏低,血PTH和1,25(OH)_2D_3下降,头颅CT示小脑和基底节区的双侧多发对称性钙化,明确诊断为特发性甲状旁腺功能减退症,经补充钙剂、骨化三醇、钾镁盐及其他综合治疗,患者症状改善,代谢指标控制良好。     

慢性肾功能衰竭骨软化时维生素D的缺芝

慢性骨软化的组织学损害与缺乏维生素D者相似,也是维生素D代谢异常所致。人体内1,25-双羟基维生素D_3(1,25-(OH)_2D_3)是由肝内25-羟基维生素D_3(26-OHD_3)转变而来,肾脏是利用25-羟基维生素D_3制造1,25-双羟基维生素D_3的唯一部位。慢性肾衰患者,其血浆1,25-(OH)_2D_3水平较低。过去认为这些患者的骨软化是缺乏1,25-(OH)_2D_3的假设不能令人满意。因为在有些没有1,25-(OH)_2D_3的患者(无肾的透析患者及双肾切除的患者),在术后6年仍未     

2型糖尿病肾病患者血清1,25-二羟维生素D3与肾功能指标的相关性研究

目的检测不同严重程度2型糖尿病肾病患者的血清1,25-二羟维生素D3水平,并分析其与肾功能指标的相关性。方法根据尿清蛋白肌酐比值及血肌酐值将48例2型糖尿病肾病患者分为微量蛋白尿组、大量蛋白尿组及肾功能不全组。采用ELISA法测定血清1,25-二羟维生素D3水平,同时常规测定血糖、糖化血红蛋白、肌酐、血钙、血磷等指标,计算肌酐清除率。结果微量蛋白尿组、大量蛋白尿组及肾功能不全组的血清1,25-二羟维生素D3水平逐渐降低,组间比较差异均有统计学意义(P均<0.05)。血清1,25-二羟维生素D3与血肌酐值呈负相关(P<0.05),与肌酐清除率呈正相关(P<0.05)。结论血清1,25-二羟维生素D3水平可能与2型糖尿病肾病相关,并且能够在一定程度上反映其严重程度。     

抗维生素D佝偻病和25-羟基胆钙化醇

虽然低血磷抗维生素D佝偻病患者临床及生化上对25-羟基胆钙化醇(25-OHD_3)和1,25-双羟基胆钙化醇(1,25-(OH)_2D_3)是有反应的,但有些作者建议对有长骨病理骨折的患者应用磷酸盐和维生素D治疗,因25-OHD_3和1,25-(OH)_2D_3不能纠正基本的代谢缺损。本文用25-OHD_3成功地治疗了一例用维生素D和磷酸盐不能使病理骨折愈合的患者。     

Plasma vitamin D metabolite concentrations in chronic renal failure: effect of oral administration of 25-hydroxyvitamin D3

The circulating concentrations of 1,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D are abnormally low in patients with chronic renal failure (CRF). To determine the importance of substrate (25-hydroxyvitamin D) concentration in this phenomenon, five patients with end stage renal disease treated with hemodialysis were given 25-hydroxyvitamin D3 (25-OH-D3) orally for 4 weeks. The serum concentration of 25-OH-D3 increased from a mean (+/- SEM) of 26 +/- 5 ng/ml immediately before therapy to a maximum of 108 +/- 5 ng/ml 4 weeks after beginning administration of 25-OH-D3. The concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), 24,25-dihydroxyvitamin D3 (24,25(OH)2D3), and 25,26-dihydroxyvitamin D3 (25,26(OH)2D3) increased from 6.6 +/- 0.8 pg/ml, 0.29 +/- 0.10 ng/ml, and 0.36 +/- 0.06 ng/ml, respectively, immediately before 25-OH-D3 administration to 21.7 +/- 2.2 pg/ml, 0.48 +/- 0.09 ng/ml; and 0.78 +/- 0.12 ng/ml, respectively, after 4 weeks of administration of 25-OH-D3. These results suggest that substrate availability may be an important determinant of the circulating concentrations of these metabolites in patients with CRF. It seems possible that the therapeutic effects of 25-OH-D3 administration to the CRF patient may be mediated through the normal actions of 1,25-dihydroxyvitamin D3, 24,25-dihydroxyvitamin D3, and perhaps other metabolites rather than through analog effects of 25-OH-D3.     

Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings.

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.     

Serum vitamin D metabolites are not responsible for low turnover osteoporosis in chronic liver disease

We measured the concentrations of vitamin D-binding protein (DBP), total 25-hydroxyvitamin D, total 1,25-dihydroxyvitamin D [1,25-(OH)2D], and free 1,25-(OH)2D in sera of 107 patients with histologically proven chronic liver disease. Bone density measurements and dynamic skeletal histomorphometry were also performed. Osteoporosis, as defined by arbitrary criteria, was found in 42 patients (39%), while no patient had osteomalacia. Serum concentrations of vitamin D-binding protein, 25-hydroxyvitamin D, total 1,25-(OH)2D, and free 1,25-(OH)2D were reduced in patients with cirrhosis, but not in the noncirrhotic patients. Bone formation rates, which were low in 55 patients (51%), were correlated with liver functions, but not with the concentrations of either vitamin D metabolite. A subgroup of 44 patients with low serum 1,25-(OH)2D concentrations and low bone formation rates failed to show an appropriate increase in serum bone Gla protein after 1,25-(OH)2D3 administration even though serum concentrations of 1,25-(OH)2D rose normally. These data suggest that the bone disease in patients with hepatic disorders is not related to the serum concentrations of vitamin D metabolites or the effect of these metabolites on osteoblast function.     

25-hydroxyvitamin D deficiency in renal transplant recipients

CONTEXT: Bone disease after kidney transplantation is a common problem. The serum levels of the active vitamin D metabolite 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D] have been studied extensively. In contrast, there has not been much concern about the serum levels of 25-hydroxyvitamin D(3) [25(OH)D]. However, it is well recognized that serum levels of 1,25(OH)(2)D are often normal in vitamin D-deficient patients. Moreover, inadequate serum 25(OH)D may limit the extrarenal production of 1,25(OH)(2)D that could lead to increased risk of many chronic diseases. OBJECTIVE: We analyzed whether renal transplant patients were at a higher risk of 25(OH)D deficiency because of the consequence of their need to protect themselves from sun exposure. DESIGN, SETTING, AND PATIENTS: We hypothesized that renal transplant recipients are at high risk to develop 25(OH)D deficiency. Serum 25(OH)D levels were analyzed in renal transplant patients with adequate renal function and in an age- and gender-matched control group (n = 31) at the end of winter. All renal transplant patients practiced solar UV-protection after transplantation. 25(OH)D levels were compared using a nonparametrical test (Wilcoxon rank sum test). RESULTS: Serum 25(OH)D levels were significantly lower in renal transplant patients compared with controls (P = 0.007). Geometric mean (with 95% confidence interval) in renal transplant patients was 10.9 ng/ml (8.2-14.3) compared with 20.0 ng/ml (15.7-25.5) in the control group. CONCLUSIONS: Renal transplant recipients are at high risk to develop 25(OH)D deficiency. Treatment with vitamin D is recommended to correct their vitamin D deficiency, which may help protect them from serious vitamin D deficiency-related health problems that include an increased risk for internal malignancies.     

Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure

It has been postulated that hyperparathyroidism in chronic renal failure results from hypocalcemia, occurring, in part, from phosphate retention and/or deficient 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] synthesis. However, many studies have failed to demonstrate hyperphosphatemia or low 1,25-(OH)2D levels in patients with mild renal failure. We measured creatinine clearance (CCr), fractional excretion of phosphorus (FEP), and serum phosphorus, ionized calcium, and plasma N-terminal PTH, and 1,25-(OH)2D concentrations in 21 normal subjects and 51 patients with renal failure. Patients with mild renal failure (Ccr, greater than 40 mL/min.1.73 m2) had normal mean serum phosphorus and ionized calcium and decreased mean 1,25-(OH)2D levels compared with those in normal subjects. In patients with moderate renal failure (CCr, 20-40), the mean ionized calcium level was normal, plasma PTH levels and FEP were elevated, and the decrement in 1,25-(OH)2D was more pronounced. The mean ionized calcium level was decreased only in the group of patients with severe renal failure (CCr, less than 20). The 1,25-(OH)2D values correlated positively with CCr and negatively with the log of plasma PTH and serum phosphorus concentrations. Log of plasma PTH correlated negatively with CCr and positively with FEP. The ionized calcium concentration correlated very weakly with CCr and the log of the plasma PTH level. These data demonstrate the presence of hyperparathyroidism, normocalcemia, and 1,25-(OH)2D deficiency in renal failure and are consistent with a role for 1,25-(OH)2D in the suppression of parathyroid activity through as yet unidentified mechanisms.     

MEASUREMENT OF 1,25-DIHYDROXYCHOLECALCIFEROL IN MAN BY RADIOIMMUNOASSAY

1 alpha, 25-Dihydroxycholecalciferol (1,25-(OH)2D3) has been measured in human serum by radioimmunoassay. The assay uses a high titre antiserum raised in sheep against 1,25-(OH)2D3-25-hemisuccinate, conjugated to bovine serum albumin. The sensitivity of the assay is 10 pg/tube. Other hydroxylated forms of vitamin D3 cross react with the antiserum and are therefore removed from serum extracts by chromatography on Sephadex LH 20 followed by high pressure liquid chromatography. The mean (+/- SEM) serum 1,25-(OH)2D3 concentration for a group of healthy adult subjects was 41 +/- 2.5 pg/ml. None was detected in anephric patients and the concentration was low or undetectable in patients with chronic renal failure.     

系统性红斑狼疮初发患者外周血中维生素D及其受体mRNA的水平和意义

目的 ①检测初发系统性红斑狼疮(SEE)患者外周血中维生素D内分泌系统的水平,探讨维生素D内分泌系统在SLE发病中的作用.②分析维生素D内分泌系统水平与SLE患者骨密度和病情活动程度的关系.方法 选择初发SLE患者43例,健康对照组44名,用酶联免疫吸附试验(ELISA)检测患者外周血浆中25羟基维生素D3(250HD3)和1,25-二羟基D3[1,25(OH)2D3]的水平,利用实时定量反转录-聚合酶链反应(RT-PCR)法检测患者外周血维生素D受体(VDR)表达水平.双能X线分别检测患者腰椎(L1-4)和股骨近端2个部位的骨密度,根据SLE疾病活动指数(SLEDAI)评分评估SLE病情活动程度.采用统计学单因素分析分别检验25OHD3、1,25(OH)2D3和VDR基因mRNA表达水平与SLE患者骨密度和病情活动程度的关系.结果 初发SLE患者25OHD3和1,25(OH)2D3激素水平与健康对照组比较,差异有统计学意义(P均<0.01);初发SLE患者组与健康对照组比较,VDR基因mRNA表达水平的差异有统计学意义(P<0.01);SLE患者2个部位的骨密度均低于健康对照组,且两组间的差异有统计学意义(P<0.05),SLE患者组骨量异常的发生率为35%,骨量异常与骨量健康对照组之间25OHD3、1,25(OH)2D3激素水平及VDR基因mRNA表达水平的差异无统计学意义(P0.05);250HD3、1,25(OH)2D3激素水平和VDR基因mRNA表达水平与SLE患者骨密度的情况不存在相关性(r=0.187,P0.05;r=0.172,P0.05;r=0.287,P0.05),它们与SLE患者的病情活动度之间也不存在相关性(r=0.054,P0.05;r=0.190,P0.05;r=0.046,P0.05).结论 SLE患者维生素D激素的水平及VDR基因的表达异常提示维生素D内分泌系统可能参与了SLE的发病,但与SLE患者骨量异常的发生和SLE病情活动度不存在相关性.     

Hyperphosphatemic tumoral calcinosis: effects of phosphate depletion on vitamin D metabolism, and of acute hypocalcemia on parathyroid hormone secretion and action

In hyperphosphatemic tumoral calcinosis, plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels are inappropriately elevated, suggesting an abnormality in vitamin D metabolism. To define this abnormality further, we measured vitamin D metabolites in two patients and four controls before and after phosphate depletion. The patients showed elevated plasma levels of 1,25(OH)2D in the basal state. Phosphate depletion reduced serum phosphate in patients from a mean of 6.1 to 2.6 mg/dl; this was accompanied by a rise in plasma 25-hydroxyvitamin D from 33.6 to 41.9 ng/dl, and in 1,25(OH)2D from 67.7 to 93.2 pg/ml. The absolute rise in 1,25(OH)2D was similar to that of controls. EDTA infusion produced a normal increase of serum immunoreactive PTH levels and urinary cAMP excretion. In this form of tumoral calcinosis, 1,25(OH)2D levels are elevated despite hyperphosphatemia, normal immunoreactive PTH, and normal serum calcium concentrations, suggesting an abnormality in the regulation of 1,25(OH)2D synthesis or metabolism, or alternatively, another undefined stimulus for 1,25(OH)2D synthesis. These patients appear to have concurrent abnormalities of renal tubular phosphate transport and vitamin D metabolism.     

Vitamin D status affects osteopenia in postmenopausal patients with primary hyperparathyroidism

Controversy still exists about whether vitamin D status is related to the severity of primary hyperparathyroidism (pHPT), although vitamin D insufficiency is frequent in pHPT. The present study was therefore performed to examine the relationships between vitamin D status and various parameters in 30 postmenopausal pHPT patients. BMD values were measured by dual-energy x-ray absorptiometry at the lumbar spine (L(2-4)), femoral neck (FN) and distal one third of the radius (Rad 1/3). Serum levels of 25 hydroxy-vitamin D(3) [25(OH)D] and 1,25-dihydroxy vitamin D(3) [1,25(OH) (2)D(3)] were 15.8 +/- 3.5 microg/l and 69.3 +/- 33.3 ng/l in pHPT patients, respectively. Serum levels of calcium and PTH seemed to be negatively correlated to serum 25(OH)D levels, although the differences were not significant. However, when subjects with the highest serum PTH levels (PTH>1000 pg/ml) were excluded from the analysis, the correlation was significant between serum 25(OH)D levels and PTH, indicating that vitamin D status affects the severity of pHPT when severe cases were excluded. In addition, serum levels of 1,25(OH)(2)D(3) were significantly and negatively correlated to serum 25(OH)D levels. On the other hand, serum levels of 25(OH)D were significantly and positively correlated to BMD (Z-score) at the lumbar spine, but not at the radius and femoral neck; however, serum 25(OH)D levels were not correlated to the levels of any bone metabolic indices measured. Moreover, serum levels of 25(OH)D were not related to urinary calcium and the tubular reabsorption rate of phosphorus, and they were similar in groups with and without renal stones. In conclusion, vitamin D status seemed to be related to the severity of disease in postmenopausal patients with pHPT. In particular, the relationship between serum 25(OH)D level and BMD at the lumbar spine was predominant.     

Reduced 25-hydroxyvitamin D levels in primary Sj?gren's syndrome. Correlations to disease manifestations.

The purpose of this study was to explore the clinical and pathogenic significance of vitamin D metabolites in primary Sj?gren's syndrome (primary SS). We measured blood concentrations of 25-hydroxyvitamin D (25 OH D) and calcitriol (1,25(OH)2D)vc in 41 patients and correlated the results with blood levels of various immune activation products, as well as with patients' clinical status. Levels of 25 OH D were slightly decreased as compared to normal controls and the reduced levels of 25 OH D were stable over the observed period of 2 years. Levels of 25 OH D correlated inversely with levels of soluble interleukin-2 receptor, status indices for global disease, total exocrine disease, surface exocrine disease, internal organ exocrine disease, and mediator-induced disease. Levels of 1,25(OH)2D varied considerably and compared to normal control values. Levels of 1,25(OH)2D did not correlate with clinical/immunopathological status. In conclusion the inverse correlations found between levels of 25 OH D and measures of clinical and immunoinflammatory status support the notion that vitamin D metabolism may be involved in the pathogenesis of primary SS.