维持性血液透析患者甲状旁腺增生的影响因素

目的 探讨维持性血液透析患者甲状旁腺增生的影响因素.方法 对北京安贞医院肾内科维持性血液透析治疗1年以上的71例患者进行甲状旁腺超声检查,根据患者是否存在甲状旁腺增生分为甲状旁腺增生组(33例)和甲状旁腺非增生组(38例).统计分析甲状旁腺增生与患者年龄、透析时间及血钙(校正钙)、血磷、全段甲状旁腺激素(iPTH)、总碱性磷酸酶(ALP)、25-羟维生素D等指标之间的关系.结果 有71例患者接受甲状旁腺的超声检查,其中甲状旁腺增生组的患者占46.5％(33/71),非增生组患者占53.5％(38/71),2组间透析时间、血磷、iPTH水平差异有统计学意义[(64±40)个月比(44 ±33)个月,(2.2±0.5) mmol/L比(2.0±0.5) mmol/L,600(505,1 060) ng/L比299(191,433) ng/L](P＜0.05或P＜0.01).对年龄、透析时间及血钙、血磷、ALP、iPTH、25-羟维生素D水平的单因素分析结果显示,甲状旁腺增生与透析时间、血磷、iPTH、ALP呈正相关(r=0.293,r=0.533,r=0.269,r=0.308,P＜0.05);对上述指标进行Logistic回归分析显示仅iPTH与甲状旁腺增生存在独立相关性(P＜0.05).受试者工作特征曲线分析表明iPTH水平能高度提示甲状旁腺增生,曲线下面积及95％置信区间为0.852(0.757 ～0.946),对应界定值为513 ng/L,相对应的敏感度为75.8％,特异性为86.8％.结论 维持性血液透析患者的透析时间、血磷是甲状旁腺增生的影响因素,而iPTH大于513 ng/L提示存在甲状旁腺增生.     

口服活性碳对尿毒症患者血液透析治疗过程中血清钙、磷及甲状旁腺激素浓度的影响

目的探讨尿毒症患者血液透析治疗过程中口服活性碳对改善血清钙、磷及甲状旁腺激素浓度的影响效果。方法观察对象为2012年1月~2014年12月间80例尿毒症患者,所有患者采用维持性血液透析治疗1年以上,40例患者入选对照组,采用血液透析组,观察组入选患者40例,采用血液透析联合口服碳片治疗,治疗6个月后比较两组患者血清钙、磷及甲状旁腺激素浓度变化。结果全部患者血透治疗后血钙浓度均有所升高,但组间差异无统计学意义(P0.05);观察组患者治疗后血磷浓度低于治疗前[(1.88±0.43)mmol/m L vs(2.68±0.56)mmol/m L],PTH低于治疗前[(310.13±147.21)pg/m L vs(611.58±145.37)pg/m L],组内差异有统计学意义(P0.05);观察组治疗后血磷及甲状旁腺激素浓度低于对照组,组间差异均有统计学意义(P0.05)。结论血透同时口服活性碳对改善尿毒症患者的钙、磷代谢及纠正甲状旁腺激素紊乱具有较好治疗的作用。     

尿毒清颗粒对慢性肾脏病患者钙磷代谢的影响

目的:观察尿毒清颗粒对慢性肾脏病(CKD)患者钙磷代谢的影响.方法:113例CKD患者按肾小球滤过率(GFR)分为A组(CKD 3～4期)42例、B组(CKD 5期,尿量>400 mL/d)33例和C组(CKD 5期,尿量<400 mL/d)38例;30例健康体检者为D组(对照组).所有CKD患者(CKD5期患者常规血透治疗)均口服尿毒清颗粒5 g,3次/天,疗程6个月,2例(A组和C组各有1例)因严重腹泻而停止治疗,检测各组治疗前后血钙、血磷及甲状旁腺素(PTH)等临床指标的变化.结果:A组血钙(2.15±O.67)mmol/L低于D组(2.43±0.88)mmol/L,但无统计学意义,B组血钙(1.78±0.69)mmol/L和C组(1.69±0.71)mmol/L均显著低于D组;A组(1.85±0.31)mmol/L,B组(2.19±0.65)mmol/L,和C组(2.22±0.75)mmol/L血磷及PTH均显著高于D组(1.27±0.59)mmol/L.经口服尿毒清颗粒治疗6个月后B组血钙(2.10±0.72)mmol/L显著升高,A组(1.33±0.31)mmol/L和B组(1.67±0.45)mmol/L血磷及PTH均显著下降,但C组血钙、血磷和PTH均无显著变化.结论:CKD患者存在钙磷代谢紊乱,尿毒清颗粒能纠正CKD尿量>400 mL/d及钙磷代谢紊乱.     

低蛋白饮食联合复方α-酮酸对维持性血液透析患者钙磷代谢的影响

目的 观察低蛋白饮食联合复方α-酮酸对维持性血液透析(MHD)患者钙磷代谢紊乱的影响.方法 MHD患者80例随机均分为两组:治疗组给予低蛋白饮食联合复方α-酮酸;对照组给予正常蛋白饮食.检测治疗前和治疗1、3个月血清钙、磷、甲状旁腺激素(iPTH)、白蛋白(Alb)和前白蛋白(PA).结果 治疗组治疗1、3个月后的血磷分别为(1.81±0.12) mmol/L和(1.79±0.13) mmol/L,明显低于治疗前的(2.27±0.14) mmol/L和对照组的(2.31±0.09) mmol/L和(2.28±0.12) mmol/L(P＜0.05);治疗3个月,治疗组血清iPTH为(174.1±71.2) pg/ml,明显低于治疗前的(411.2±98.3)pg/ml(P＜0.05).结论 低蛋白饮食联合复方α-酮酸可有效降低MHD患者的血磷和血清iPTH.     

原发性高血压患者血清维生素D水平及相关性研究

目的 了解原发性高血压患者血清维生素D的变化,并探讨维生素D对原发性高血压发展的影响.方法 按危险因素将140例原发性高血压患者分为低危组(1级高血压且无其他危险因素,56例)、中危组(2级高血压或1级高血压伴1～2个危险因素,53例)和高危组(3级高血压或1～2级高血压伴≥3个危险因素或任何一级高血压伴1项靶器官损害或1种临床疾患,31例),并设立对照组(体检健康者,33例),检测4组的血清钙、磷、25-羟基维生素D3[25(OH)D3]、甲状旁腺激素(PTH).结果 低危、中危、高危组25(OH)D3分别为(27±6)、(27±5)、(21±5)μg/L,对照组为(32±8)μg/L,低危组与中危组之间差异无统计学意义(P＞0.05),其余各组之间差异有统计学意义(P＜0.05).25(OH)D3与收缩压、舒张压存在负相关(r值分别为-0.412、-0.377,均P＜0.01),与PTH、钙、磷、年龄无明显相关性.结论 原发性高血压患者血清维生素D水平降低,尤其是伴有高危因素的患者血清维生素D水平降低更明显.     

尿毒症继发性甲状旁腺功能亢进症患者应用甲状旁腺全切除加自体移植术5年随访资料分析

目的:观察慢性肾脏病(5D期)患者因继发性甲状旁腺功能亢进症(SHPT)行甲状旁腺全切除加自体移植术(TPTX+AT)的远期临床疗效。方法:回顾性分析2011年3月—2014年12月慢性肾脏病(5D期)患者因继发性甲状旁腺功能亢进症行TPTX+AT的41例患者的临床资料(随访至2019年12月),收集患者术前、术后全段甲状旁腺激素及血清钙、磷、碱性磷酸酶等变化情况,临床症状改善情况,复发和死亡情况,判断临床疗效。结果:共41例患者,年龄(47.0±9.0)岁,透析(76.0±38.9)个月。患者术后1周、1个月、6个月各时间点血全段甲状旁腺素(iPTH)、血清磷、血清钙均较术前显著下降(P<0.001)。术后早期甲状旁腺功能亢进持续状态2例,术后第1年复发5例,其中3例共行5次移植物切除手术。随访期满共有27例存活,血清钙(2.17±0.26)mmol/L,血清磷(2.16±0.47)mmol/L,iPTH达标率70.4%(19/27)。结论:甲状旁腺全切除加自体移植术,能安全、有效治疗尿毒症难治性SHPT,可以改善SHPT患者远期预后。     

预防性应用VitD、钙剂对糖皮质激素治疗儿童肾病综合征骨密度的影响

目的:观察维生素D(VitD)、钙剂对应用泼尼松治疗肾病综合征(NS)患儿骨密度(BMD)的作用,探讨其变化对NS患儿骨代谢的影响及意义。方法:以本院2009年1月至2011年5月临床资料完整的激素敏感型NS患儿90例为对象,男52例,女38例,55例为初发,35例为复发病例,平均年龄(5.33±2.86)岁,随机分为A、B、C三组,每组30例。A组单用激素治疗,口服泼尼松1.5～2 mg/(kg.d),最大剂量80 mg/d,并逐渐减量,疗程9～12个月;B组在A组治疗基础上加用VitD;C组在B组治疗基础上加用钙剂治疗。所有患儿在激素治疗前、激素治疗后1个月及6个月分别测量血清钙、BMD。结果:三组患儿治疗1个月、6个月后与治疗前比较,BMD降低(P<0.01),治疗1个月后A、B组BMD下降更明显,与C组比较差异有统计学意义(P<0.05);治疗6个月后A组BMD由(0.751±0.042)g/cm2降至(0.639±0.035)g/cm2(P<0.01),B组由(0.750±0.040)g/cm2降至(0.640±0.025)g/cm2(P<0.01),较C组由(0.748±0.041)g/cm2降至(0.665±0.038)g/cm2(P<0.01)下降更明显(P<0.01);血清钙值A组由(1.940±0.068)mmol/L降至(1.742±0.048)mmol/L,B组由(1.932±0.085)mmol/L升至(2.158±0.131)mmol/L,C组由(1.921±0.083)mmol/L升至(2.338±0.081)mmol/L,差异有统计学意义(P<0.01)。结论:糖皮质激素治疗NS患儿可降低BMD,加用适当剂量VitD和钙剂可减轻但并不能完全阻止骨质疏松,未发现其他不良反应。     

高通量血液透析对维持性血液透析患者钙磷代谢的影响分析

目的探究高通量血液透析对维持性血液透析(MHD)患者钙磷代谢的影响。方法84例MHD患者作为研究对象,依据双色球法分为研究组与对照组,各42例。对照组给予低通量血液透析,研究组给予高通量血液透析。比较两组透析前、透析6个月后的钙磷代谢情况。结果透析6个月后,研究组甲状旁腺激素(261.33±25.21)pg/L、钙磷乘积(34.64±3.12)mg²/dl²、血磷(1.56±0.20)mmol/L、血钙(2.11±0.55)mmol/L,均优于对照组的(398.37±27.63)pg/L、(47.23±4.24)mg²/dl²、(1.81±0.31)mmol/L、(1.79±0.62)mmol/L,差异有统计学意义(P<0.05)。结论MHD患者在血液透析过程中使用高通量血液透析,可有效改善患者钙磷代谢水平,利于患者疾病治疗,值得在患者血液透析过程中推广使用。     

2型糖尿病患者血清25-羟维生素D及甲状旁腺激素水平与高血压的相关性分析

目的探讨2型糖尿病患者血清25-羟维生素D、甲状旁腺激素水平与高血压的相关性。方法选取厦门大学附属第一医院思明院区2018年2月至2020年8月收治的2型糖尿病患者100例为研究对象, 根据患者高血压、血清25-羟维生素D水平进行分组, 分析不同水平血清25-羟维生素D、甲状旁腺激素与高血压的相关性。结果 100例2型糖尿病患者中, 高血压1级25例、2级30例、3级45例, 血清25-羟维生素D水平充足5例(5%)、不足10例(10%), 缺乏85例(85%)。1级、2级、3级高血压患者的血清25-羟维生素D分别为(12.18±2.52)μg/L、(12.45±2.39)μg/L、(10.33±1.26)μg/L, 甲状旁腺激素分别为(36.48±0.25)ng/L、(41.15±0.39)ng/L、(47.52±1.44)ng/L, 随着血压的升高, 患者血清25-羟维生素D水平呈先增后降趋势, 而甲状旁腺激素水平则呈逐渐增加趋势, 但不同高血压分级与患者血清25-羟维生素D、甲状旁腺激素水平差异均无统计学意义(F=0.96、1.93, 均P > 0.05)。logistic...     

甲状旁腺次全切除并射频消融术后持续性低血钙1例

1病历摘要患者女性,54岁,10年前因确诊为尿毒症,行腹膜透析治疗。4年前因感染性腹膜炎改为维持性血液透析治疗。2年前查甲状旁腺激素(PTH)为1142pg/ml,予以骨化三醇胶丸(罗钙全)10粒,每周2次,口服1个月,改为1粒,每日1次,口服5个月。一年半前,查PTH为2222pg/ml,血钙2.05mmol/L,血磷1.92mmol/L,血镁1.05mmol/L。患者在上级医院行甲状旁腺次全切除术。术后1周PTH为1989pg/ml,血钙1.98mmol/L,血磷1.88mmol/L,血     

假性甲状旁腺功能减退症 12 例诊治分析

目的：研究并探讨假性甲状旁腺功能减退症的临床特点、诊断及临床治疗情况。方法对2002年3月-2012年3月12例假性甲状旁腺功能减退症（ PHP）的临床诊治资料进行回顾分析。结果本组患者男女比例为1∶2,发病年龄（22.5±8．6）岁;所有患者的血钙、尿钙、血镁以及尿磷比正常人低,甲状旁腺素（ PTH）、血磷、骨碱性磷酸酶（ BALP）比正常人高;较为常见的临床症状为手足抽搐10例、癫痫样发作7例、肢端麻木5例;3例合并遗传性骨营养不良;2例合并甲状腺功能减退;所有患者均行颅脑CT检查,其中10例发现颅内钙化;病症误诊5例,主要误诊为缺钙、原发性癫痫及脑膜炎后遗症。结论假性甲状旁腺功能减退症发病患者多为儿童,临床诊断易被误诊为原发性癫痫。为了降低临床误诊率,临床医生应该注意低钙血症的临床表现。假性甲状旁腺功能减退症主要采用钙剂联合维生素D或是其衍生物进行治疗。对于同时合并甲状腺功能减退的患者应同时给予相应治疗。     

Effect of bendrofluazide on calcium reabsorption in hypoparathyroidism

Summary In hypoparathyroidism the absence of parathyroid hormone leads to a reduction in the absorption of calcium by renal tubular cells. In spite of treatment with vitamin D, hypercalciuria persists and normocalcaemia can only be maintained by providing the kidney with a large load of calcium. Thiazide diuretics enhance tubular calcium reabsorption and it has been suggested that they can be used as an alternative to vitamin D. Bendrofluazide in a dose of 10 mg daily was given to 9 patients with severe hypoparathyroidism in addition to their usual treatment with calcium and vitamin D. Following the introduction of Bendrofluazide the calculated renal threshold for calcium reabsorption (TmCa/GFR) increased by a mean value of 0.14 mmol/l, and the mean rise in serum calcium was 0.13 mmol/l. This increase was due to a direct effect of the drug and was not caused by salt restriction or changes in glomerular filtration rate. The rise in serum calcium is modest compared to the rise following the introduction of vitamin D and except for patients with mild hypoparathyroidism, thiazides are not an alternative to vitamin D. They may however reduce the oral calcium load required to maintain normocalcaemia.     

Aspirin inhibition of 1 alpha-hydroxyvitamin D3 or parathyroid hormone induced hypercalcemia in vivo in rats. A mechanism independent of prostaglandin biosynthesis inhibition

The interactions of calcium-regulating hormones, active forms of vitamin D and parathyroid hormone, and aspirin were studied in rats. Aspirin, a prostaglandin biosynthesis inhibitor, abolished the hypercalcemia induced by 1 alpha-hydroxyvitamin D3 at 20, 50 and 100 mg/kg p.o. in parathyroidectomized or thyroparathyroidectomized rats with or without vitamin D deficiency, and in thyroparathyroidectomized plus nephrectomized rats. Aspirin did not affect the stimulation of intestinal calcium absorption by 1 alpha-hydroxyvitamin D3. By contrast, indomethacin, another prostaglandin biosynthesis inhibitor, did not affect hypercalcemia or stimulation of intestinal calcium absorption by 1 alpha-hydroxyvitamin D3. Aspirin also abolished the hypercalcemic action of parathyroid hormone in rats with or without intact thyroparathyroid glands. Moreover, aspirin alone caused hypocalcemia in rats with intact thyroparathyroid glands. Indomethacin had no effect in either of these systems. These data suggest that aspirin may inhibit bone resorption by the active form of vitamin D or parathyroid hormone via a mechanism independent of prostaglandin biosynthesis inhibition.     

Drug safety evaluation of parathyroid hormone for hypocalcemia in patients with hypoparathyroidism

Introduction: Hypoparathyroidism is a rare disorder characterized by low serum calcium levels and high serum phosphate levels, and low or inappropriately normal levels of parathyroid hormone (PTH). This disease is commonly treated with calcium supplements and active vitamin D metabolites or analogues, but large doses of these supplements are often utilized to relieve the symptoms caused by hypocalcemia, without guarantee of a physiological normalization of calcium-phosphate homeostasis.

Areas covered: Several studies have investigated replacement therapy with recombinant human PTH [rhPTH (1-84) and rhPTH (1-34)] for subjects with hypoparathyroidism. In 2015, The Food and Drug Administration (FDA) approved, in the United States, rhPTH (1–84), named Natpara®, a bioenginerred rhPTH, for the management of chronic hypoparathyroidism not well controlled with conventional therapy. This article evaluates the safety and tolerability of rhPTH (1–84) in patients with chronic hypoparathyroidism, and also describes the studies conducted so far on rhPTH (1-34) used for chronic hypoparathyroidism.

Expert opinion: The research done in this field has shown that replacement treatment with rhPTH is an attractive option for subjects with hypoparathyroidism who are unable to maintain stable and safe serum and urinary calcium levels. However, since therapy with rhPTH is a long-term management option in hypoparathyroidism, more long-term safety data are needed.     

甲状腺术中甲状旁腺损伤临床分析

目的对甲状腺术中甲状旁腺损伤开展研究。方法对本院收治的10例甲状腺术中甲状旁腺损伤患者资料开展分析。结果患者均确诊,经过针对性治疗,未造成永久性甲状旁腺功能低下。结论甲状腺术中要注重对甲状旁腺血供保护,甲状旁腺开展分离时防止出现误切以及操作挫伤,预防术后甲状旁腺功能低下,术后甲状旁腺功能低下患者采用口服钙片和肌注维生素D治疗。     

The interaction between burn injury and vitamin D metabolism and consequences for the patient

The stress and inflammatory responses to burn injury are associated with bone loss. The stress response entails production of large amounts of endogenous glucocorticoids that decrease osteoblasts on the mineralization surface of bone and decreases differentiation of marrow stromal cells into osteoblasts, thereby decreasing the amount of bone formation. Deficiency of osteoblasts also blocks osteoclastogenesis thus leading to low bone turnover and bone loss. The inflammatory response generates cytokines such as interleukin 1-beta and interleukin-6, which normally increase osteoclastogenic bone resorption via stimulation of osteoblast production of RANK ligand. However, in the absence of osteoblasts as a target we postulate that they attack the parathyroid gland chief cells and up-regulate the calcium-sensing receptor. The consequence of this upregulation is the lowering of the circulating calcium necessary to suppress parathyroid hormone production and the development of hypocalcemia and urinary calcium wasting. It is the parathyroid hormone suppression that causes us to postulate acute deficiency of 1,25-dihydroxyvitamin D and the consequence of this for post-burn metabolism could include derepression of the gene that controls renin production, leading to elevated levels of angiotensin II, which can contribute to insulin resistance, as can vitamin D deficiency itself. Moreover, the skin from burned patients cannot synthesize vitamin D normally. Thus vitamin D supplementation is the only means by which to ensure vitamin D sufficiency for burn victims. The proper requirement for vitamin D in acutely burned patients remains unknown.     

Pharmacological and clinical trial data on a novel phosphate-binding polymer (sevelamer hydrochloride), a medicine for hyperphosphatemia in hemodialysis patients

Hyperphosphatemia is one of the major complications of hemodialysis patients and plays a key role in the pathogenesis of cardiovascular calcification and secondary hyperparathyroidism. Dietary phosphate restriction and removal of phosphate by dialysis are insufficient to control hyperphosphatemia. Therefore, almost all patients undergoing hemodialysis should take oral phosphate binders. Sevelamer hydrochloride (sevelamer) is a novel phosphate-binding polymer that contains neither aluminum nor calcium, and it is not absorbed from the gastrointestinal tract. In rat models with progressive chronic renal insufficiency, in addition to lowering effects on serum levels of phosphorus, calcium x phosphorus product, and parathyroid hormone, dietary treatment of sevelamer can prevent parathyroid hyperplasia, vascular calcification, high turnover bone lesion, and renal functional deterioration. In clinical studies with hemodialysis patients, sevelamer lowers serum phosphorus and calcium x phosphorus product without any incidence of hypercalcemia. Switching calcium-containing phosphate binders to sevelamer can decrease the percentage of hypoparathyroidism and hyperparathyroidism by negative calcium balance and increased dosage of vitamin D, respectively. Sevelamer also decreases serum low-density lipoprotein cholesterol levels by its bile acid-binding capacity. A long-term clinical study has demonstrated that the progression of coronary and aortic calcification in hemodialysis patients is attenuated by sevelamer. Thus, sevelamer offers the promise of impacting cardiac calcification and thereby reducing morbidity and mortality of hemodialysis patients.     

甲状旁腺全切除加上臂移植术治疗尿毒症继发性甲状旁腺功能亢进

目的 研究尿毒症患者因继发性甲状旁腺功能亢进（SHPT）行甲状旁腺全切除加自体上臂移植术（TPTX＋AT）的临床疗效.方法 回顾分析我院30例因慢性肾脏病长期接受规律性透析的患者发生难治性SPTH,予行甲状旁腺全切除加自体上臂移植术,比较患者术前、术后全段甲状旁腺激素（iPTH）、血清钙、磷及碱性磷酸酶（ALP）、血红蛋白（Hb）的变化情况、临床症状改善情况,从而判断疗效.结果 30例患者中,无一例死亡;2例患者发生喉返神经损伤,发生率为6.67％.术后低钙发生率高（79.5％,25/30）,均经积极静脉补钙后有效控制.患者术后各时间点（1天、1周、1、3、6个月）血iPTH、血清磷、血清钙均较术前显著下降（P＜0.01）.术后3、6个月血清ALP较术前显著下降（P＜0.01）,而Hb较术前明显升高（P＜0.05）.术后患者骨痛、皮肤瘙痒、肌无力、失眠、不宁腿、贫血等得到明显改善,全身营养状态好转.结论 甲状旁腺全切除加自体上臂移植术能安全、有效治疗尿毒症难治性SHPT.     

Paricalcitol capsules for the control of secondary hyperparathyroidism in chronic kidney disease

Secondary hyperparathyroidism is a common complication of patients with chronic kidney disease. Treatment with calcitriol, the active form of vitamin D, reduces parathyroid hormone levels, but may result in elevations in serum calcium and phosphorus. New vitamin D analogues have been developed to reduce parathyroid hormone secretion without concomitant hypercalcaemia and hyperphosphataemia. Recent data from studies with paricalcitol capsules, the oral formulation of 19-nor-1,25(OH)2D2, show a significant reduction in parathyroid hormone levels with no change in calcium and phosphorus levels when compared with placebo. Paricalcitol also compares favourably to other oral vitamin D analogues, effectively decreasing parathyroid secretion with less hypercalcaemia and hypercalciuria than other agents.     

Pathogenesis and treatment of secondary hyperparathyroidism in dialysis patients: the role of paricalcitol

Hemodialysis (HD) patients are commonly affected by secondary hyperparathyroidism (SHPT), in which 3 well-known factors are usually involved: hypocalcemia, hyperphosphatemia and calcitriol deficiency. Classically, high parathyroid hormone (PTH) levels cause bone-associated diseases, such as osteitis fibrosa and renal osteodystrophy, but more recently it has been demonstrated the link between SHPT and a systemic toxicity, with a major role in determining cardio-vascular disease, including arterial calcification, endocrine disturbances, compromised immune system, neurobehavioral changes, and altered erythropoiesis. Treatment with calcitriol (CT), the active form of vitamin D, reduces parathyroid hormone (PTH) levels, but may result in elevations in serum calcium (Ca) and phosphorus (P), increasing the risk of cardio-vascular calcification in the HD population. Several new vitamin D analogs have been developed and investigated with the rationale to treat SHPT with a reduced risk of hypercalcemia and hyperphosphatemia in HD patients. Paricalcitol (1,25-dihydroxy-19-nor-vitamin D(2), 19-Nor-D(2)) is a vitamin D analog that suppresses PTH secretion with minimal increases on serum calcium and phosphate levels. It was demonstrated that paricalcitol prevents vascular calcification in experimental models of renal failure, compared with calcitriol. Furthermore, 19-Nor-D(2) is the first analog approved for use in HD patients and is available for i.v. and oral administration, commonly 3 times weekly after HD. The purpose of the present review is to analyze the pathogenesis and treatment of SHPT in HD patients, and the role of paricalcitol in the prevention of arterial calcification.