排石汤对草酸钙泌尿系结石患者尿液成分的影响

目的探讨排石汤对经尿道输尿管镜碎石术(URL)后草酸钙泌尿系结石患者尿骨桥蛋白(OPN)、尿钙、尿草酸钙的影响。方法选取2018年6月至2022年6月在本院收治的80例草酸钙泌尿系结石患者, 随机分为对照组(40例)和观察组(40例)。观察组服用排石汤, 连用3个疗程;对照组给予同等量安慰剂(5%排石汤及食用色素组成)。分别检测两组患者术前、术后第1、7、14、21、28天的尿OPN、尿钙、尿草酸钙含量。结果与术前比较, 术后第7、14、21、28天两组的尿OPN含量均呈上升趋势, 尿钙、尿草酸钙含量均呈下降趋势, 差异均有统计学意义(均P<0.05);但术后第1天与术前比较, 两组的尿OPN、尿钙、尿草酸钙含量比较, 差异均无统计学意义(均P>0.05);而术后第7、14、21、28天, 观察组的尿OPN含量均高于对照组, 尿钙、尿草酸钙含量均低于对照组(均P<0.05)。结论草酸钙泌尿系结石患者URL术后应用排石汤, 对提高尿OPN含量及降低尿钙、尿草酸钙含量有明显帮助。     

尿凝血酶原片断1在肾结石模型大鼠肾组织的表达及其意义

目的　研究尿液中尿凝血酶原片段 1(UPTF1)的来源和UPTF1在肾结石模型大鼠肾组织的表达 ,探讨尿结石形成对肾组织UPTF1表达的影响及其在尿结石形成中的意义。方法用乙二醇和 1α 羟基维生素D3 灌胃制作大鼠肾草酸钙结石模型。采用半定量逆转录聚合酶链反应(RT PCR)检测UPTF1mRNA在结石模型大鼠和正常对照大鼠肾组织中的表达及水平变化。结果　偏光显微镜下结石模型大鼠肾乳头和肾皮质内布满草酸钙晶体 ,肾钙含量、2 4h尿草酸和尿钙分泌量分别为 13 8.3 9mg/g、82 .89μmol和97.3 5 μmol;对照组肾钙含量、2 4h尿草酸和尿钙分泌量分别为 1.5 4mg/g、2 4.2 2 μmol和3 .14 μmol,组间差异均有统计学意义(P <0 .0 1)。UPTF1mRNA在所有大鼠肾组织和肝组织中都有表达 ,但在正常大鼠和肾结石大鼠肾组织中的相对表达量分别为 1.73± 0 .2 5、1.86± 0 .19,两组差异无统计学意义意义 (P >0 .0 5 )。结论　尿液中的UPTF1来源于大鼠肾组织的生物合成 ,可能是草酸钙结石形成的生理性抑制因子 ,从而可以借助实验动物模型为研究UPTF1在尿结石形成中的作用提供了依据。     

药用醋膏预防大鼠泌尿系结石形成及其机制的初步研究

目的:通过应用药用醋膏喂养泌尿系结石模型大鼠,观察大鼠肾组织病理变化及测定肾组织草酸和钙离子含量,观察醋酸预防泌尿系结石的效果,进一步探讨其机制。方法:将适宜体重的健康Wister大鼠随机分为空白组、1%乙二醇+2%氯化铵诱石液造模对照组、30g/100ml高剂量醋膏+1%乙二醇+2%氯化铵诱石液组、10g/100ml低剂量醋膏+1%乙二醇+2%氯化铵诱石液组,喂养28天后处死,取肾组织HE染色,观察草酸钙结晶面积分布情况,测定各组大鼠肾组织中草酸与钙离子含量。结果:空白组与其它三组比较,肾组织草酸钙结晶面积分布及草酸和钙离子含量差异均有统计学意义(均P0.05);造模对照组与高剂量醋膏组比较,肾组织草酸钙结晶面积分布及草酸和钙离子含量差异均有统计学意义(P0.05),而与低剂量醋膏组比较,肾组织结晶面积分布及草酸和钙离子含量差异均无统计学意义(P0.05);高剂量醋膏组与低剂量醋膏组比较,肾组织草酸和钙离子含量差异有统计学意义(P0.05),肾组织草酸钙结晶面积分布差异无统计学意义(P0.05)。结论:在正常食用剂量范围内,高剂量醋膏对大鼠泌尿系结石的形成有预防作用,可降低肾组织中草酸及钙离子含量。     

最大限度雄激素阻断治疗前列腺癌对患者骨密度的影响

目的:探讨最大限度雄激素阻断(MAB)治疗对前列腺癌患者骨密度的影响。方法:对40例因前列腺癌行MAB治疗的患者进行调查,治疗时间7～12个月,分别于治疗前后检测血清前列腺特异性抗原(PSA)、睾酮及血钙、血磷、24 h尿钙、尿磷、碱性磷酸酶、甲状旁腺激素、血常规及肝肾功能,双能X线吸收法测定腰椎、股骨颈骨密度,并进行疼痛评分,比较MAB治疗前后各项指标差异。结果:前列腺癌患者治疗前5例(12.5%)腰椎骨量减少,8例(20.0%)腰椎骨质疏松;13例(32.5%)左股骨颈骨量减少,15例(37.5%)左股骨颈骨质疏松。MAB治疗前患者血清PSA为(52.9±69.9)μg/L,睾酮为(18.9±6.5)nmol/L,治疗后PSA为(1.5±1.6)μg/L,睾酮为(1.9±1.3)nmol/L,与治疗前比较均显著下降(P<0.05)。治疗前血钙为(2.5±0.2)mmol/L,血磷为(1.2±0.2)mmol/L,尿钙为(3.1±1.4)mmol/L,尿磷为(11.5±8.1)mmol/L,治疗后血钙为(2.5±0.1)mmol/L,血磷为(1.2±0.1)mmol/L,尿钙为(2.8±1.2)mmol/L,尿磷为(9.9±4.0)mmol/L,两者比较差异均无统计学意义(P>0.05)。治疗前后碱性磷酸酶、甲状旁腺激素、血常规、肝肾功能差异均无统计学意义(P>0.05)。治疗前腰椎和股骨颈骨密度分别为(1.1±0.1)g/cm2和(0.8±0.2)g/cm2,疼痛评分为(0.6±0.2)分,治疗后腰椎和股骨颈骨密度分别为(1.1±0.2)g/cm2和(0.8±0.1)g/cm2,疼痛评分为(0.7±0.1)分,与治疗前比较差异均无统计学意义(P>0.05)。结论:7～12个月MAB治疗对前列腺癌患者骨密度无明显影响,安全有效,但治疗前应注意监测患者骨密度。     

苄丙酮香豆素对实验性大鼠肾草酸钙结石形成的影响

目的：探讨Vit．K拮抗剂苄丙酮香豆素(商品名华法令)对大鼠肾草酸钙结石形成的影响。方法：采用乙二醇饮水和氯化铵灌胃作成石剂，30只Wistar大鼠随机分为对照组(A组)、成石组(B组)、华法令组(C组)。饲养4周后，检测大鼠肾组织钙含量和草酸钙晶体形成、24h尿钙、尿草酸含量及血生化指标。结果：成石组和华法令组肾组织中钙、镁含量，24h尿草酸及尿钙、镁排泄量差异无显著性意义；镜下观察发现：华法令组大鼠肾脏草酸钙结晶形成多于成石组，但组间比较差异无显著性意义。结论：苄丙酮香豆素对大鼠肾草酸钙结石的形成无显著影响。     

金钱草及广金钱草对大鼠肾草酸钙结石相关代谢产物作用的研究

目的对比金钱草与广金钱草抑制大鼠肾草酸钙结石的具体机制与作用效果。方法54只SPF级SD雄性大鼠适应性喂养1周至体重180~200 g,使用乙二醇灌胃法建立SD大鼠肾草酸钙结石模型,而后将大鼠按照随机数字表法分为9组处理并进行对照,分别为健康对照组(A组),阳性对照组(建模组,B组),金钱草低、中、高剂量组(C1、C2、C3组,共3组),广金钱草低、中、高剂量组(D1、D2、D3组,共3组),疗效对照组(枸橼酸氢钾钠组,E组),每组各6只。4周后收集标本测定各组大鼠血尿生化指标,并行Von Kossa染色检测肾草酸钙晶体,在偏振光显微镜下观察大鼠肾组织草酸钙结晶沉积情况,利用测算照片中阳性面积百分比与相关血尿生化指标判断两者药效差异。计量资料以均数±标准差(x±s)表示,组间比较采用单因素方差分析,两组间比较采用SNK-q检验;结晶形成情况组间比较采用Kruskal-Wallis检验。结果与阳性对照组相比,高剂量的广金钱草相对金钱草能显著降低肾草酸钙结石大鼠血肌酐水平,应用金钱草后血肌酐水平为(86.70±11.49)μmol/L,应用广金钱草后血肌酐水平为(70.72±9.08)μmol/L,两者差异有统计学意义(P<0.01);高剂量金钱草、广金钱草均能显著升高尿镁水平,降低血尿素水平,两者相比差异无统计学意义(P>0.05);与阳性对照组相比,给予高剂量金钱草(P<0.0001)与高剂量广金钱草(P<0.0001)均能显著抑制大鼠肾草酸钙晶体形成,保护大鼠肾脏,两者作用效果相比差异无统计学意义(P>0.05);给予金钱草与广金钱草均未能观察到显著升高尿pH值与显著降低尿钙、尿草酸、24 h尿量、血钙、血磷、血镁、血尿酸和肾草酸含量的效果。结论广金钱草抑制大鼠肾草酸钙结石发生的功效优于金钱草,对肾功能具有更好的保护作用。     

B超引导下经皮肾镜联合碎石、清石系统治疗复杂性肾结石

目的探讨提高复杂性肾结石临床疗效的方法。方法对2003年2月至2004年12月间收治的52例复杂性肾结石患者,采用B超引导下经皮肾镜(percutaneousnephrolithotomy,PCNL)联合碎石、清石系统进行治疗,并设定为实验组;前期采用经皮微造瘘气压弹道碎石治疗34例肾结石患者设定为对照组,将两组临床疗效进行比较。结果实验组手术时间(67±28)min,术中出血量(84±53)mL,结石残留率为5.8%;对照组手术时间(105±36)min,术中出血量(76±47)mL,结石残留率为17.6%。两组术中出血量无明显差异(P>0.05),手术时间、结石残留实验组明显低于对照组(P<0.05)。结论B超引导下经皮肾镜联合碎石、清石系统治疗复杂性肾结石具有碎石效率高,结石残留少等优点,大大提高了治疗效果,具有推广价值。     

酒石酸钾预防草酸钙肾结石形成的研究

体外实验证明酒石酸钾对一水草酸钙晶体的生长和聚集有抑制作用。动物实验发现酒石酸钾能够降低鼠肾组织中钙及草酸的沉积。２７例患者口服酒石酸钾期间，２４小时尿钙、磷和草酸明显下降，尿枸橼酸和尿ＰＨ显著上升，实验证明，酒石酸钾能够抑制草酸钙肾结石的形成，是一种有希望的防石药物。     

广金钱草颗粒对结石患者尿液的影响

目的探讨广金钱草颗粒对结石患者尿液尿酸、尿钙、pH值、尿量、草酸钙结晶的影响。方法 20例结石患者,男12例,女8例,平均年龄37岁(20～55岁)。予广金钱草颗粒30 g,口服,2次/d,于服药前及服药后3 d收集患者晨尿及24 h尿,观察治疗前后患者晨尿pH值、尿酸、尿钙、草酸钙结晶及24 h尿量、尿酸、尿钙的变化。结果晨尿尿酸浓度增加(P<0.05),pH值降低(P<0.05),24 h尿量、尿酸、尿钙及晨尿尿钙、草酸钙结晶无明显变化(P>0.05)。结论单味广金钱草颗粒防治结石,需配合其他药物(如碱化尿液),饮水要昼夜兼顾。     

胃吸收草酸的研究

目的　探讨胃在外源性草酸吸收中的作用。方法　观察健康成人 (n =10 )和无胃者(胃全切除n =8)摄入 40 0 g菠菜泥前后尿草酸排泄 (mg/min)的动态变化 ,计算食入菠菜草酸的生物利用率并与无胃者进行比较。结果　摄入菠菜中草酸含量为 2 5 67～ 2 670mg ,健康成人摄入菠菜后 2 0min尿草酸排泄 (mg/min)较摄入菠菜前的基础水平明显增加 ;7/10参试者约在 40min出现第 1吸收峰 ,60min时尿草酸排泄 (mg/min)为 0 .0 73 2± 0 .0 2 94,较基础水平 0 .0 3 3 1± 0 .0 2 0 3高出 1倍 (P <0 .0 1) ,3h左右出现第 2吸收峰 ;无胃者草酸负荷后 60min的食物草酸生物利用率(0 .0 63± 0 .0 62 ) %较健康成人 (0 .0 98± 0 .0 71) %低 5 0 % (P <0 .0 1) ,且不出现第 1吸收峰。结论　胃在正常生理状况下是强有力的草酸吸收器官 ,胃的功能异常与草酸钙尿石形成的关系有待深入研究     

Effect of diphosphonate on crystallization of calcium oxalate in vitro.

Reliable techniques for the calculation of activity product (state of saturation), formation product (limit of metastability) and crystal growth of calcium oxalate were devised. The activity product at saturation was 2.53 times 10 minus 9 M2, and was independent of duration of incubation, solid-to-solution ratio, pH, calcium concentration or ionic strength. These tehcniques were utilized to assess the effect of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) on crystallization of calcium oxalate in an aqueous salt solution in vitro. EHDP increased the formation product of calcium oxalate, indicating an inhibition of nucleation of calcium oxalate. Further, it inhibited the crystal growth of calcium oxalate.     

Impact of various modifiers on calcium oxalate crystallization

OBJECTIVE: This work focuses on the behavior of in vitro calcium oxalate crystallization. The effects of several compounds on the kinetics of calcium oxalate crystallization were examined. METHODS: Rates of nucleation and aggregation of calcium oxalate crystals were derived from 30-min time-course measurements of optic density at 620 nm after mixing solutions containing calcium chloride and sodium oxalate at 37 degrees C, pH 5.7. The maximum increase of optic density with time, termed S(N), mainly reflects maximum rate of formation of new particles and thus crystal nucleation. After equilibrium has been reached, optic density decreases. No new particles were formed due to crystal aggregation. S(A) (the maximum slope of decrease of optic density at 620 nm with time, representing crystal aggregation) is derived from the maximum decrease in optic density. RESULTS: Among the modifiers studied, citrate decreased both S(N) and S(A) (P < 0.001). Magnesium was also found to inhibit the rate of nucleation and crystal aggregation, but it appeared in a non-concentrated manner. Nucleation and aggregation inhibition ratios were related inversely to concentration of albumin (P < 0.001). CONCLUSION: The growth and agglomeration of calcium oxalate crystals are differently modulated by various compounds. The treatments aiming at inhibiting crystallization of calcium oxalate can be better defined by these findings. And new treatment modalities can be developed.     

肾结石大鼠肾组织bikunin mRNA的表达

目的 :研究bikunin在实验性肾草酸钙结石大鼠肾组织的表达及意义。方法 :采用乙二醇和氯化铵诱导大鼠肾草酸钙结石模型形成 ,检测各组大鼠肾功能、肾组织Ca2 + 含量和草酸钙晶体沉积、尿生化指标 ,并用逆转录聚合酶链反应 (RT PCR)检测bikuninmRNA在肾组织的表达情况。结果 :模型组大鼠的血清Cr、BUN、肾Ca2 + 含量、2 4h尿Ca2 + 、草酸 (Ox)分泌量和肾组织bikuninmRNA的表达均明显高于正常组 (P <0 .0 5 )。结论 :高草酸尿和草酸钙结晶的沉积能促使大鼠肾脏通过合成更多的bikunin来抑制大鼠肾组织草酸钙晶体的形成。     

Concentrated urine and diluted urine: the effects of citrate and magnesium on the crystallization of calcium oxalate induced in vitro by an oxalate load

Supplementation of certain calcium crystallization inhibitors, such as citrate and magnesium, and the dilution of urine with water are now considered consolidated practice for the prevention of calcium kidney stones. The aim of this study is to verify, using tried and true in vitro methods, whether the effect of these inhibitors can manifest itself in different ways depending on whether the urine is concentrated or diluted. Calcium oxalate crystallization was studied on 4-h urine of 20 male idiopathic calcium oxalate stone formers, first under low hydration conditions (non-diluted urine) and then under high hydration conditions (diluted urine). Both the diluted and the non-diluted urine samples were subjected to three types of load: (a) an oxalate concentration increment of 1.3 mmol/l only; (b) an oxalate concentration increment of 1.3 mmol/l with a citrate concentration increment of 1.56 mmol/l; (c) an oxalate concentration increment of 1.3 mmol/l with a magnesium concentration increment of 2.08 mmol/l. In non-diluted urine, the addition of the citrate and magnesium did not modify the crystallization parameters under study. In contrast, in the diluted urine the addition of the citrate and magnesium led to a reduction in the total quantity of crystals (equivalent to 35–45%) and their aggregates (equivalent to 30–40%); at the same time, there was an increase in the diameter of the monohydrate calcium oxalate crystals, which also underwent a morphological change. In conclusion, the inhibitory effects of citrate and magnesium on the crystallization of calcium oxalate do not manifest themselves in highly concentrated urine.     

Effects of sodium urate and uric acid crystals on the crystallization of calcium oxalate

Summary Crystallization of calcium oxalate in the presence of uric acid and sodium urate crystals was analyzed in a metastable crystallization system containing calcium chloride and sodium oxalate (A), in urine highly supersaturated with respect to calcium oxalate (B), and in urine with a high level of metastable supersaturations (C). In system A uric acid crystals in concentrations up to 11.4 mMol/l did not affect calcium oxalate crystallization, neither did sodium urate during the first 6 h in concentrations below 5 mMol/l. In system B neither uric acid nor sodium urate crystals affected calcium oxalate crystallization. However, an increased rate of crystallization was observed with both uric acid and sodium urate in system C, but the effect was less pronounced than with calcium oxalate seed. Urine pre-treated with sodium urate and subsequently analyzed in system A in a concentration of 2%, gave a slightly lower inhibition of calcium oxalate crystal growth. Concerning the crystal size distribution in the same system, larger crystals were observed in several urines pre-treated with uric acid and sodium urate.     

正常人和草酸钙结石病人尿草酸钙晶体基质

以改良Ｍｏｒｓｅ和Ｒｅｓｎｉｃｋ法提取１０例上尿路草酸钙结石病人和１１例正常人的尿草酸钙晶体基璺，用双向聚丙烯酰胺凝胶电泳对晶体基质及结晶前后大分子物的蛋白质组成进行了比较分析。     

月见草油抑制草酸钙结晶形成的实验研究

目的了解月见草油在草酸钙结石形成中的作用,为临床治疗提供新的方法与思路。方法雄性SD大鼠60只,随机分为4组,各组15只。C组和D组以月见草油（含γ-亚麻酸9.2%）或葵花籽油（含亚油酸70%）10g/kg灌胃4周后,用诱石剂1%乙二醇（EG）加2%氯化氨喂饮,同时继续以月见草油或葵花籽油灌胃4周,8周后检测各组大鼠肾功能、24h血尿生化指标和肾草酸钙结晶情况;仅饲普通饲料（A组,空白组）和普通饲料加1%乙二醇（EG）加2%氯化氨喂饮（B组,成石组）大鼠作为对照。结果月见草油组肾组织水肿较轻,肾内草酸钙结晶数及肾成石率低于成石组（P〈0.05）,尿枸橼酸较成石组高（P〈0.01）,24h尿钙、尿草酸排泄均低于成石组（P〈0.01）,血尿素氮（P〈0.01）、血肌酐（P〈0.05）低于成石组。结论γ-亚麻酸能有效改善肾功能,减少尿钙及草酸的排泄,抑制实验鼠肾草酸钙结晶形成,在尿石症防治方面可能有一定应用价值。     

Characterization of Tamm-Horsfall protein in a rat nephrolithiasis model

PURPOSE: The role of Tamm-Horsfall protein in calcium oxalate stone formation is controversial. It is unclear whether Tamm-Horsfall protein has a role in crystallization. If it does, does it act as an inhibitor or promoter of crystallization? To elucidate the nature of its involvement we characterized Tamm-Horsfall protein in a rat model of calcium oxalate nephrolithiasis by in vivo and in vitro techniques. MATERIALS AND METHODS: Calcium oxalate nephrolithiasis was induced in male Sprague-Dawley rats. The amino acid and carbohydrate composition of Tamm-Horsfall protein from normal rats and those with nephrolithiasis was determined. The Tamm-Horsfall protein gene and protein expression in the kidneys were examined by in situ hybridization and immunohistochemistry. Furthermore, the interaction of Tamm-Horsfall protein and calcium oxalate crystals was assessed by an in vitro crystal aggregation assay. RESULTS: Tamm-Horsfall protein from rats with nephrolithiasis was biochemically similar to that from normal rats. Although Tamm-Horsfall protein was associated with crystal deposits in the renal papillae of rats with nephrolithiasis, Tamm-Horsfall protein messenger RNA expression in the kidneys remained unchanged. In each group Tamm-Horsfall protein inhibited calcium oxalate crystal aggregation by 47%, indicating no change in functional capabilities. CONCLUSIONS: The results of this study indicate that urinary excretion, and the biochemical nature and functional capabilities of Tamm-Horsfall protein remain unchanged during experimental calcium oxalate nephrolithiasis. Although staining for Tamm-Horsfall protein was evident in the papillae of rats with nephrolithiasis, the site of Tamm-Horsfall protein synthesis remained cells of the thick ascending limbs of the loop of Henle.     

Ascorbic acid in idiopathic recurrent calcium urolithiasis in humans – does it have an abettor role in oxalate, and calcium oxalate crystallization?

The role of ascorbic acid (ASC) in the pathophysiology of renal calcium stones is not clear. We evaluated ASC in blood and urine of fasting male patients with idiopathic calcium urolithiasis (ICU) and healthy volunteers. Using smaller subgroups, we also evaluated their response to exogenous ASC [either intravenous or oral ASC (5 mg/kg bodyweight)] administered together with an oxalate-free test meal. The influence of ASC on calcium oxalate crystallization, the morphology of crystals at urinary pH 5, 6 and 7, and the effect of increasing duration of urine incubation on urinary oxalate at these pHs, without and with addition of ASC, were studied too. In normo- and hypercalciuric ICU, blood and urinary ASC from fasting patients remained unchanged, but the slope of the regression line of urinary ASC versus urinary oxalate was steeper than in the controls; the plasma ASC half-life did not differ between controls, normo- and hypercalciuric ICU; the ASC-supplemented meal caused an increase in the integrated plasma oxalate in the normocalciuric subgroup versus controls. In normo- and hypercalciuric ICU urinary oxalate, the oxalate/glycolate ratio, and calcium oxalate supersaturation were increased, but urinary glycolate was unchanged. In the controls, oral ASC did not affect calcium oxalate crystallization, while in ICU, ASC inhibited crystal growth. In control urine calcium oxalate dihydrate and calcium oxalate monohydrate develops, while in ICU urine only the former crystal type develops. In vitro oxalate neoformation from ASC did not occur. It was concluded that (1) under normal conditions an abettor role of ASC for renal stones is not recognizable, (2) in ICU, urinary oxalate excess unrelated to degradation of exogenous ASC is exhibited, and that this is most likely unrelated to an initial increase in oxalate biosynthesis, and (3) ASC appears to modulate directly calcium oxalate crystallization in ICU, although the true mode of action is still not known. Received: 24 September 1999 / Accepted: 16 December 1999     

不同浓度TH黏蛋白对草酸钙成核、生长、聚集的影响

目的 观察不同浓度TH黏蛋白(THM)对体外成石系统内一水草酸钙(COM)的成核、生长和聚集的影响.方法 盐析法提取THM,利用原子分光光度计测定0、10、50、100 mg/LTHM人工尿体外成核和种籽晶溶液内Ca~(2+)变化,偏光显微镜计数COM数目.结果 THM为0、10、50、100mg/L时,Ca~(2+)减少量0.81、0.57、0.51、0.96mmol/L;成核数3.20×10~4、2.32×10~4、1.83 × 10~4、2.85×10~4;生长率53.9%、48.7%、34.6%、19.8%;聚集率33.2%、11.7%、9.4%、66.2%,差异均有统计学意义(P<0.01).结论 在生理浓度范围内,THM可以抑制尿结石的形成,且随浓度增加其抑制作用逐渐增强,但超过一定浓度时,其转为结石促进剂.