原发性高草酸尿症导致移植肾功能丧失

患者为男性,34岁。因原发性高草酸尿症导致肾功能衰竭,于2003年7月在我院接受同种异体肾移植术,手术顺利,移植肾开放血流后3min即有尿液分泌。术后予以甲泼尼龙冲击4d,并给予霉酚酸酯、环孢素A预防排斥反应。术后第1d,24h尿量为7500ml,术后第4d血肌酐降至223.7μmol/L,第6d出现     

鱼油抑制实验鼠草酸钙结晶形成

目的 了解鱼油在尿石形成中的作用。方法 ６０只大鼠随机分４组,饮用１％乙二醇（ＥＧ）水,同时喂饲不同剂量的鱼油。４周后检测各组大鼠肾功能、草酸钙结晶、２４小时尿钙和尿草酸。结果 加服鱼油组鼠肾积水、组织水肿减轻,肾组织内草酸钙结晶数及含钙量明显减少,２４小时尿钙排出减少;尿尿素氮、肌酐排出明显增加,而血中尿素氮、肌酐浓度显著低于成石组。结论 鱼油能抑制实验性高草酸尿症大鼠体内草酸钙结晶形成,减少尿     

尿石清冲剂预防草酸钙结石的临床研究

我们选择既是食品（或食品添加剂）又是药品的中西药物组方配成尿石清冲剂进行临床观察，３０例患者口服尿石清冲剂５天，２４小时尿钙、磷和草酸含量明显下降，尿量、尿枸橼酸、尿镁和ｐＨ值显著升高。认为尿石清冲剂能明显降低草酸钙结石的形成，是一种有希望的防石药物。     

肠道食草酸杆菌与草酸钙尿石的关系

对３０例尿石及４５例正常人的肠道食草酸杆菌分离培养并对其生物学特性及形态作初步观察。证实尿石病人粪便的肠道食草酸酐菌，显著低于正常对照组，，提出肠道食草酸杆菌浓度过低可能是形成草酸钙结石的和重要原因。     

尿石抑制因子作用机理的体外实验研究

采用体外籽晶——亚稳过饱和溶液晶体生长抑制实验法证实:柠檬酸、焦磷酸对一水草酸钙晶体生长有强烈的抑制作用。对其作用机理作了初步探讨。由于镁竞争性结合柠檬酸,降低了柠檬酸增加草酸钙溶解度的作用。因此,在防治尿结石时,不宜同时使用柠檬酸钾和镁剂。     

草酸钙尿石患者VKDC结构域基因突变的研究

泌尿系结石以草酸钙结石最为常见。现已发现尿液中存在一些大分子蛋白质与尿石形成相关，越来越多的研究证实尿凝血酶原片段1（UPTF1）是正常人尿草酸钙结晶的主要抑制因子之一。     

中药泽泻提取物对尿草酸钙结石形成影响的实验研究

目的　探讨中药泽泻对尿草酸钙结石形成的影响。　方法　采用种晶技术检测泽泻水溶性提取物 (C1、C2 组 )、5 0 %甲醇提取物 (D1、D2 组 )和 10 0 %甲醇提取物 (E1、E2 组 )对体外一水草酸钙晶体生长的抑制指数 (I .I)。 80只Wistar大鼠随机分为 8组 ,对照组 (A组 )、成石组 (B组 )、泽泻水溶性提取物组 (CL、CH 组 )、5 0 %甲醇提取物组 (DL、DH 组 )、10 0 %甲醇提取物组 (EL、EH 组 ) ,分别予不同浓度的泽泻水溶性提取物和甲醇提取物。饲养 4周后 ,检测各组大鼠血生化 ,2 4h尿草酸(Ox)、Ca2 + 、Mg2 + 分泌量和肾组织Ca2 + 、Mg2 + 含量。镜下观察肾组织切片中草酸钙结晶及肾小管扩张情况。　结果　C1、C2 、D1、D2 、E1、E2 组I.I分别为 90 .5 6 %、76 .4 7%、74 .38%、86 .4 1%、6 1.17%和 11.89%。动物实验A组血BUN、Cr明显低于其他各组 ,差异有显著性意义 (P <0 .0 5 ) ;各组间血Ca2 + 、P浓度无显著性差异 ;2 4h尿Ox、Ca2 + 和Mg2 + 分泌量各泽泻实验组与B组差异无显著性意义(P >0 .0 5 ) ;CH、DL、DH 组肾组织Ca2 + 含量明显低于B组 ,差异有显著性意义 (P <0 .0 5 ) ,各组间肾组织Mg2 + 含量差异无显著性 (P均 >0 .0 5 )。A组肾小管正常 ,B组肾小管腔可见大量成片草酸钙结晶存在 ,管腔明显扩张     

离子色谱法测定尿草酸的研究

目的　建立一种直接测定尿草酸的方法———离子色谱法 ,评价此方法在实验室和临床研究中的价值。方法　搜集 2 4h尿液用浓盐酸酸化保存 ,取 0 .1ml尿液 ,用 0 .3mmol/L的硼酸溶液稀释 ,通过 0 .2 μm的微孔滤膜过滤而注入离子色谱仪 ,检测出尿草酸浓度。 结果　对尿草酸的最小检测限为 0 .2 5 μmol/L ,批内变异系数CV =3 .8% ,日间CV =4.2 %。尿样回收率 96.5 %～10 5 .2 % ,CV =3 .1% ,此法与比色法显著相关 (r =0 .996,P <0 .0 5 )。结论　此方法简单、准确而快速 ,适于实验室及临床尿草酸分析     

Conductivometric determination of urinary oxalate with oxalate decarboxylase

Summary An enzymatic method for determination of urinary oxalate is described: the acidified urine samples are extracted with chloroform. This manipulation improves the blank values considerably. 1 ml of extracted urine is incubated with oxalate decarboxylase. The CO₂ released from the medium is absorbed by Sr(OH)₂. The change in conductivity measured in the Sr(OH)₂ solution is linearly proportional to the oxalate concentration in urine and the method is specific for oxalate. The mean recovery is 93.2±2.5%. The coefficient of variation calculated from 28 determinations is 12.6%. The detection limit is 35 nmol. 1 ml of urine is usually sufficient for determination. The mean 24 h urine oxalate excretion of 11 healthy men and 16 women was 240±20 mol.     

The impact of dietary oxalate on kidney stone formation

The role of dietary oxalate in calcium oxalate kidney stone formation remains unclear. However, due to the risk for stone disease that is associated with a low calcium intake, dietary oxalate is believed to be an important contributing factor. In this review, we have examined the available evidence related to the ingestion of dietary oxalate, its intestinal absorption, and its handling by the kidney. The only difference identified to date between normal individuals and those who form stones is in the intestinal absorption of oxalate. Differences in dietary oxalate intake and in renal oxalate excretion are two other parameters that are likely to receive close scrutiny in the near future, because the research tools required for these investigations are now available. Such research, together with more extensive examinations of intestinal oxalate absorption, should help clarify the role of dietary oxalate in stone formation.     

Increased protein intake on controlled oxalate diets does not increase urinary oxalate excretion

High animal protein intake is a risk factor for calcium oxalate stone disease. The effect of dietary protein on the urinary excretion of calcium, acid and citrate is well established. However, its effect on oxalate excretion is unclear, due in part to an inadequate control of dietary oxalate intake in previous studies. This relationship warrants clarification due to the proposed important role of the metabolism of amino acids in endogenous oxalate synthesis. In this study, 11 normal subjects consumed controlled oxalate diets containing 0.6, 1.2 and 1.8 g protein/kg body weight/day. The analysis of 24 h urine collections confirmed that as protein intake increased, urinary calcium and glycolate increased and urinary pH and citrate decreased. The increased glycolate excretion was due in part to an increased hydroxyproline, but not glycolate consumption. Total daily urinary oxalate excretion did not change. When indexed to creatinine there was a small but significant decrease in oxalate excretion. This is most likely due to hyperfiltration. These results indicate that as dietary protein intake increases, the catabolism of diet-derived amino acids is not associated with an increased endogenous oxalate synthesis in normal subjects.     

Intestinal oxalate absorption in patients with continent urinary diversion

The objective of the study is to evaluate the post-operative effect of an orthotopic ileal neobladder or a Mainz pouch I bladder replacement on the extent of intestinal oxalate absorption. Gastrointestinal oxalate absorption was measured in six patients with an orthotopic ileal neobladder and in six patients with a Mainz pouch I bladder replacement. The function test applied was the [¹³C₂]oxalate absorption test. With a range of 5.1–12.4%, the oxalate absorption of these patients was well within the reference range for healthy volunteers. The results from our small study indicate that such continent urinary diversions present no hazard for oxalate hyperabsorption and subsequent calcium oxalate urolithiasis.     

Calcium oxalate monohydrate binding protein: a diagnostic biomarker for calcium oxalate kidney stone formers

Urinary oxalate is a biomarker for calcium oxalate kidney stone disease; however, its assay is insensitive and nonspecific. Calcium oxalate monohydrate (COM) binding protein (45 kDa) is a promoter of calcium oxalate kidney disease, which is markedly upregulated by oxalate induced oxidative stress. The current study was carried out to evaluate whether COM binding protein can serve as a diagnostic marker for calcium oxalate kidney stone formers. COM binding protein was isolated, purified and antibody was raised against it in rabbits. Urine samples (24 h) were collected from patients suffering from various kidney diseases such as acute nephritis, chronic nephritis, nephrotic syndrome, calcium oxalate (CaOx) stone formers, uric acid stone formers, struvite stone formers and calcium phosphate stone formers. This COM binding protein was quantified by an in house ELISA method and the excretion was found to lie between 2 and 3 mg in control samples, while in CaOx stone formers it was detected between 11 and 19 mg. Urinary risk factors were assayed. We conclude that COM binding protein can serve as a diagnostic marker for CaOx stone formers.     

腹腔镜胃癌手术对胃癌细胞腹腔种植转移影响的临床研究

目的探讨腹腔镜胃癌手术和开腹胃癌手术对胃癌细胞种植转移的影响。方法收集2006年4月至2006年11月间腹腔镜胃癌手术中的45例和开腹胃癌手术中的41例患者术前、术后腹腔冲洗液各100ml,进行腹腔脱落肿瘤细胞学检查。腹腔镜组,气腹后通过套管针侧孔引出CO2气体,经过100ml生理盐水的滤过后,收集过滤液进行肿瘤细胞学检查。腹腔镜组术后用100ml生理盐水冲洗腹腔镜手术器械,进行腹腔镜器械冲洗液肿瘤细胞学检查。所有液体离心取沉淀,涂片固定HE染色,光镜下观察肿瘤细胞。结果腹腔镜气腹CO2气体滤过液中未观察到肿瘤细胞;腹腔镜器械冲洗液发现3例阳性(6.7%);两组术前腹腔冲洗液中肿瘤细胞的阳性率分别为60.0%和60.9%,术后肿瘤细胞阳性率分别为53.3%和56.1%,两种手术方式术前、术后腹腔冲洗液肿瘤细胞无明显差异。腹腔冲洗液与胃癌TNM分期有关,两组肿瘤细胞Ⅲ期阳性率均显著高于Ⅱ期,具有非常显著统计学差异(P0.01),即两组中胃癌细胞阳性检出率在肿瘤的病理分期越晚,阳性率越高。结论 CO2气腹不会引起肿瘤细胞的播散。腹腔镜术中器械污染是引起切口转移的主要原因之一。腹腔镜手术不增加肿瘤细胞播散种植的机会。     

胃癌淋巴结转移规律的探讨

目的探讨胃癌淋巴结转移的规律。方法回顾我院1994年1月至2003年5月间608例胃癌术后病理资料,分析各组淋巴结的转移率,并用二值Logistic回归似然比法分析与第7～9组淋巴结转移相关的因素。结果本组608例中,第3组淋巴结转移率最高,为444%,其次为第15组的432%。第7、8、9组淋巴结转移率分别为372%、248%和207%,3组综合转移率为375%。与第7～9组淋巴结综合转移密切相关的因素有第1～6组淋巴结综合转移情况和肿瘤的浸润程度(P<005)。第7～9组淋巴结有转移时,预测第1～6组淋巴结有转移的准确率为822%,假阳性率为15%;第7～9组淋巴结无转移时,预测第10～16组淋巴结无转移的准确率为593%,假阳性率为127%。结论第7～9组淋巴结有类似前哨淋巴结的作用,术中病理活检有利于指导胃癌术式的选择。胃下部癌第7～9淋巴结有转移时宜常规清扫第15组淋巴结。     

Continuous infusion of oxalate by minipumps induces calcium oxalate nephrocalcinosis

It is hypothesized that oxalate plays an active role in calcium oxalate (CaOx) nephrocalcinosis and oxalate driven nephrolithiasis by interacting with the kidney. We developed an adjustable, nonprecursor, continuous infusion model of hyperoxaluria and CaOx nephrocalcinosis to investigate this hypothesis. Minipumps containing PBS or KOx (60–360 μmol/day; n=5–7/dose) were implanted subcutaneously in male Sprague–Dawley rats on D0 and D6. Rats were killed on D13. Oxalate excretion and CaOx crystalluria were monitored by 20+4 h urine collections. Localization and content of intrarenal crystals were determined on frozen sections using polarization and μFTIR. Oxalate excretion was significantly elevated in all KOx rats (P≤0.005). CaOx crystalluria was most persistent in the 240–360 μmol/day KOx rats, but even 60 μmol/day KOx rats showed sporadic crystalluria. One hundred percent of KOx rats had CaOx nephrocalcinosis as confirmed by μFTIR. Most crystals were localized to the lumens of the corticomedullary collecting ducts. A few crystals are localized just under the papillar urothelium. The minipump model is the first model of hyperoxaluria to provide continuous infusion of oxalate. It permits control of the levels of hyperoxaluria, crystalluria and CaOx nephrocalcinosis. The level of sustained hyperoxaluria and CaOx nephrocalcinosis induced by treatment with 360 μmol/day KOx for 13D models the conditions frequently observed in jejunoileal bypass patients. Adjustments in the length of treatment and level of hyperoxaluria may allow this model to also be used to study the oxalate driven CaOx-nephrolithiasis common in patients with hyperoxaluria due to other causes.     

西梅汁预防大鼠草酸钙肾结石的实验研究

目的 研究西梅汁对乙二醇诱导的大鼠草酸钙肾结石形成的影响及其量效关系.方法 40只wistar大鼠随机分为8组:A空白对照组、B单纯乙二醇诱石组、C～E为西梅汁干预组[分别灌喂西梅汁2、4、8 mL· (kg·d)-1],每组8只.除空白对照组外,余皆用含1％乙二醇去离子水作为大鼠的唯一饮用水源并自由饮用,以诱导生成草酸钙肾结石.分别于实验前日和实验第4周末,检测大鼠尿钙、镁、草酸及枸橼酸浓度;血钙、镁、肌酐和尿素氮浓度;肾脏组织丙二醛(MDA)含量及总超氧化物歧化酶(T-SOD)活性;偏光显微镜观察HE染色肾脏组织草酸钙结晶形成情况;TUNEL法检测肾小管上皮细胞凋亡,以此分析西梅汁及西梅干预防肾结石的量效关系.结果 所用三种剂量的西梅汁均能明显减轻乙二醇所致的各项血尿生化指标和肾小管上皮细胞凋亡指数的改变,大幅增加尿镁浓度,明显减少乙二醇诱导的大鼠草酸钙肾结石的生成,且效果呈剂量依赖性.结论 所用的三种剂量的西梅汁均可明显干预乙二醇诱导的大鼠草酸钙肾结石的生成,且呈正相关的量效关系.     

胃癌根治术后复发与转移的区域及规律分析

目的通过CT诊断,分析胃癌根治术后复发与转移的区域及规律。方法选取2009年6月至2014年6月胃癌患者共81例,均行胃癌根治性手术,随访期间CT发现存在局部区域复发或转移。分析术后复发与转移的区域及规律。用SPSS 19.0软件分析数据,以%表示计数资料,Logistic回归分析检验术后复发时间和临床病理特征和治疗之间的关系;P0.05,差异具有统计学意义。结果在81例术后复发患者中,局部区域复发率最高(37.04%),在18例伴有术后区域淋巴结转移的患者中,Ⅰ区10例,Ⅲ区3例,Ⅳ区1例,Ⅵ区4例。术后7~12个月复发率最高(41.98%)。截止至2015年9月30日,在胃癌根治术后复发的81例患者中,中位总生存时间(OS)为33.18个月,中位复发时间为19.94个月,复发后中位生存期为7.19个月。其中发生腹膜种植后,中位生存期最短,仅为4.24个月。单因素分析结果显示,与OS相关的临床病理因素包括年龄(P=0.024),Borrmann分型(P=0.017)、TNM分期(P=0.009)、淋巴结检出总数(P=0.022)、阳性淋巴结数(P=0.002)、治疗方式(P=0.026)和治疗依从性(P=0.035);与局部无复发生存期(LRFS)相关的临床病理因素包括淋巴结检出总数(P=0.012)、阳性淋巴结数(P=0.008)、治疗方式(P=0.034)和治疗依从性(P=0.016)。结论局部区域复发,特别是区域淋巴结转移是胃癌根治术后复发的主要形式,术后通过CT划分淋巴结转移区域对于放疗靶区确定具有一定指导意义。