小儿肾积水肾盂成形术后尿理化性质和尿水通道蛋白2改变的研究

目的 探讨小儿单侧先天性肾盂输尿管连接处梗阻(pyeloureteric junction obstruction,PUJO)肾积水术后1周内尿理化性质和尿水通道蛋白2(aquaporins-2.AQP2)的变化.方法 选取14例符合Grignon法四、五级标准的小儿单侧先天性PUJO.肾积水患儿;经肾盂成形术后给予严格设定的补液标准,收集术后第一、三、五、七天积水侧肾脏和对侧无积水肾脏24 h尿液,分别测定排尿量、渗透压、Na+和肌酐,并用酶联免疫吸附法(ELISA)测定尿液中AQP2水平.结果 相对于对侧无积水肾脏,积水侧肾脏梗阻解除术后1周内尿液AQP2显著降低.尿量明显增多.尿渗透压显著降低,Na+排泄分数显著增加;同时术后1周内双侧肾脏尿液AQP2、排尿量和尿渗透压有升高趋势,而积水侧肾脏Na+排泄分数有减少的趋势;积水侧.肾脏术后第五、七天的尿液AQP2.排尿量和尿渗透压较第一天均显著增加(P<0.05).对侧无积水肾脏术后第五、七天的尿液AQP2和尿渗透压较第一天也显著增加(P<0.05).其余指标在术后小同天数之间差异无统计学意义(P>0.05).结论小儿单侧先天性PUJO解除术后1周内积水侧.肾脏的尿液AQP2和尿渗透压均较对侧尤积水肾脏尿液显著减少.提示梗阻解除后尿液中AQP2可能和尿液浓缩能力改变有关.     

先天性肾积水肾脏及其尿液中水通道蛋白2表达的相关性研究

目的 探讨先天性肾积水患儿肾脏水通道蛋白2(aquaporin-2,AQP2)表达水平及其尿液AQP2表达水平之间的相关性.方法 选取20例单侧先天性肾盂输尿管连接处梗阻肾积水肾脏,其中轻度和重度积水肾脏各10例,并选取8例正常肾脏作为对照组.应用免疫组织化学方法检测肾脏AQP2表达水平,并采用酶联免疫吸附法(ELISA)检测其尿液中AQP2浓度.结果 AQP2阳性着色位于肾脏集合管主细胞胞膜和胞质.积水肾脏AQP2表达水平下降和其尿液中AQP2表达水平下降及尿渗透压下降相一致.重度积水组显著低于轻度积水组,重度和轻度积水组均显著低于正常对照组(P＜0.05).积水肾脏AQP2表达水平与其尿液AQP2表达水平以及尿渗透压均有显著正相关性(分别为r尿AOY2=0.706,P＜0.05;r尿渗透压=0.810,P＜0.05).结论 随着先天性.肾积水患儿积水程度增加,其肾脏AQP2表达水平和其尿液AQP2浓度及尿渗透压均明显下降.检测尿液AQP2浓度可间接反映肾脏中AQP2的表达情况,为临床评估肾脏浓缩稀释功能损害程度提供依据.     

尿液AQP2在先天性肾积水患儿中的检测和意义

目的研究单侧先天性肾盂输尿管连接处梗阻（pyeloureteric junction obstruction，PUJO）肾积水患儿尿液水通道蛋白2（Aquaporins-2，AQP2）测定在肾脏浓缩功能评价中的意义。方法选取12例正常儿童，26例单侧先天性PUJO肾积水患儿，其中轻度14例，重度12例，均经彩超、静脉。肾盂造影证实，并排除其它泌尿系统疾病；在严格设定条件下，收集正常对照组术前和梗阻解除术后第3天患肾24h尿液，同时收集术中。肾盂尿液，测定尿渗透压，并用酶联免疫吸附法（ELISA）测定尿液中AQP2。结果与正常对照组比较，积水组术中尿液AQP2和尿渗透压明显下降（P〈0．05），且重度积水组术中尿液AQP2与轻度积水组相比，明显降低（P〈0．05），但重度积水组和轻度积水组术中尿渗透压相比无显著差异（P〉0．05）；梗阻解除后，轻、重度积水组术中尿液AQP2与术后第3天相比，无显著差异（P〉0．05），而术后第3天两组尿渗透压却明显下降／P〈0．05），术后第3天重度积水组与轻度积水组尿液AQP2和尿渗透压相比较，显著下降（P〈0．05）；正常对照组与轻、重度积水组术后第3天尿液AQP2和尿渗透压之间存在一定相关性。结论小儿单侧先天性PUJO尿液AQP2和尿渗透压较正常对照组显著降低，且二者之间存在一定相关性。尿液中AQP2下降可能和尿液浓缩功能改变有关。     

幼鼠双侧输尿管梗阻后肾脏钠通道NHE3和TSC的变化

目的探讨幼鼠双侧输尿管梗阻后肾脏3型钠氢交换蛋白（Na^＋-H^＋exchangers，NHE）和钠氯协同转运通道蛋白（thiazide-sensitivesodium cortransporter，TSC）的变化和了解输尿管梗阻解除后利尿现象发生的分子生物学机制。方法24只幼年大白鼠随机分为梗阻组（BUO，n=13）及对照组（n=11），梗阻组行双侧输尿管梗阻24h后再解除梗阻，对照组仅行输尿管游离而不结扎。每日观察体重、饮水量、食量、尿量变化，并留取尿液冰冻待检。4d后抽取动脉血化验，同时取出双侧肾脏，右肾全肾快速放入液氮冰冻备份、左肾分离出外髓内带（ISOM）、外髓外带加肾皮质（OS-OM＋C），行免疫杂交（western blooting）实验，检测NHE3和TSC的变化。结果解除输尿管梗阻后，实验组肾脏功能明显受损，发生明显的梗阻解除后利尿现象，血浆渗透压增高，血液中肌苷和尿素氮明显高于对照组；外髓内带（ISOM）和外髓外带加皮质（OSOM＋C）检查，发现NHE3均明显降低（P〈0．01和P〈0．05）；而TSC在OSOM＋C表达也明显下降（P〈0．01）。结论大白鼠BUO 24h肾近曲小管和Henle’S环的粗升管，NHE3表达明显下降，TSC水平显著降低，提示NHE3和TSC减少可能是形成肾小管性钠吸收障碍、尿量增多的主要原因之一。     

血管紧张素Ⅱ对幼鼠输尿管梗阻后AQP2表达变化的调控

目的 通过观察血管紧张素Ⅱ(angiotensin Ⅱ,ANG Ⅱ受体阻滞剂坎地沙坦对双侧输尿管梗阻(bilateral ureteral obstruction,BUO)幼鼠肾脏水通道蛋白2(aquaporin 2,AQP2)表达的影响,探讨ANG Ⅱ对梗阻肾脏功能和AQP2的调控作用。方法 24只慕尼黑幼鼠随机分为BUO组、坎地沙坦干预组(BUO+ CAN)和对照组(Sham),每组n=8只。BUO组和BUO+ CAN组均行双侧输尿管结扎,并采用微型泵分别给以生理盐水和坎地沙坦,Sham组仅游离输尿管但不结扎,24h后解除梗阻并继续观察48h后收集血液和肾脏标本,采用免疫印记技术检测肾脏AQP2表达水平。结果 梗阻解除后BUO组与Sham组相比尿量显著增高,(92±7)μl·min-1 ·kg-1比(25±3)μl· min-1·kg-1、尿渗透压显著降低,(636±55) mosmol/kgH2O比(1 853±163) mosmol/kgH2O、血浆渗透压和血浆醛固酮均显著增高,分别为(336±10) mosmol/kgH2O比(303±7)mosmol/kgH2O和(4.1±0.2)nmol/L比(1.4±0.1)nmol/L;肾脏AQP2表达下调到Sham组17％各组比较差异有统计学意义,P＜0.05。BUO+ CAN组与BUO组相比尿量显著减少,(55±5)μl·min-1 ·kg-1比(92±7)μl·min-1 ·kg-1,尿渗透压显著增高(783±47) mosmol/kgH2O比(636±55) mosmol/kgH2O,血浆醛固酮含量显著降低(2.8±0.5) nmol/L比(4.1±0.2)nmol/L,肾脏AQP2表达增高,各组比较差异有统计学意义,P＜0.05。结论 ANG Ⅱ受体拮抗剂可通过阻止AQP2下调纠正水代谢紊乱,保护肾功能,提示ANG Ⅱ通过调节肾脏AQP2表达参与输尿管梗阻后肾脏水代谢变化。     

先天性肾积水患儿尿液水通道蛋白1表达的意义

目的研究先天性肾积水患儿尿液水通道蛋白1(AQP1)的表达情况及其临床意义。方法选取26例不同程度肾积水患儿作为试验组。其中轻度组7例,中度组10例,重度组9例。均经彩超、电子计算机X射线断层扫描技术(CT)或MRI证实,并排除其他泌尿系统疾病。对照组选取10例无泌尿系统疾病的儿童。在严格选定条件下,收集试验组患儿术前晨尿、术中肾盂尿液、梗阻解除术后第3、7天患肾晨尿,同时收集对照组患儿晨尿,采用间接ELISA法测定其尿液AQP1水平。结果与对照组比较,中、重度积水组患儿术前尿液中AQP1水平均明显下降(Pa<0.05),且重度积水组尿液AQP1水平与中度积水组比较,明显降低(P<0.05);轻度积水组与对照组比较,差异无统计学意义(P>0.05)。试验组术后第3天尿液AQP1水平与术中比较,差异无统计学意义(P>0.05),术后第7天尿液AQP1水平与术中比较均明显上升,但仍低于对照组(Pa<0.05)。对照组、试验组术前及术后第7天尿液AQP1水平与尿渗透压呈正相关,实验组术中及术后第3天尿液AQP1水平和尿渗透压之间无相关性。结论尿液AQP1水平可能是新型的评价先天性肾积水患儿肾浓缩功能的指标之一。     

水通道蛋白2在脓毒症大鼠肾脏的表达及意义

目的 探讨水通道蛋白2(AQP2)在脓毒症大鼠肾脏的表达及对水代谢调节的意义.方法 将6周龄Wistar大鼠64只,随机分为假手术组和手术组各32只,采用盲肠结扎穿孔法(CLP)复制脓毒症模型.每组分为3、6、12和24 h 4个亚组,各8只,分别留取尿液、血液、肾脏标本.观察尿量、尿渗透压和肾功能,HE染色光镜观察肾脏病理变化,采用实时定量PCR方法检测AQP2 mRNA表达,免疫组织化学方法检测AQP2的蛋白表达.结果 手术组大鼠术后3 h尿量减少、尿渗透压增高,6 h后尿量逐渐增多、尿渗透压降低;血肌酐和尿素6 h开始升高,24 h达高峰;随术后时间延长肾脏病理损害加重,主要表现为肾小管上皮细胞之间间隔消失,细胞核消失;肾小球球襻融合,细胞结构不清;间质可见点灶状炎性细胞侵润.AQP2 mRNA的表达在术后3 h增高,12、24 h明显减低;AQP2蛋白表达在术后12 h下降,24 h最低,较假手术组均有显著性差异(P<0.05).结论 AQP2参与脓毒症时肾脏水代谢的调节,AQP2表达下调导致脓毒症尿浓缩功能障碍的主要病理机制之一.     

先天性肾盂输尿管连接部梗阻患儿积水肾脏中水通道蛋白1-4的表达

目的 观察先天性肾盂输尿管连接部梗阻患儿积水肾脏中水通道蛋白l-4(aquaporin,AQP1-4)的表达及其与积水程度之间的关系.方法 收集22例接受肾盂成形术和肾造瘘术的先天性肾盂输尿管连接部狭窄(pyeloureteral junction obstruction,PUJO)患儿的肾组织标本,并将其按照静脉肾盂造影(intravenous pyelography,IVP)显影时间的长短分为两组.轻度肾积水组(10例;IVP60min内显影)和重度肾积水组(12例,IVP 60min内不显影).8例正常肾组织标本来自于肾母细胞瘤周围正常肾组织.免疫组织化学技术检测AQPl-4在正常肾脏和积水肾脏中的表达与定位.逆转录聚合酶链反应(RT-PCR)检测AQP1-4 mRNA在正常肾脏和积水肾脏中的表达水平.结果 AQP1阳性着色主要分布于肾小球毛细血管内皮细胞、近曲小管的上皮细胞及髓袢降支细段上皮细胞胞质,AQP2阳性着色主要分布于肾脏集合管上皮细胞胞膜和胞质,AQP3阳性着色主要分布于肾脏集合管主细胞的基底侧,AQP4阳性着色主要分布于肾内髓集合管上皮细胞基底侧.而积水肾脏AQP1-4表达均有不同程度下降.RT-PCR显示重度肾积水中AQPl-4的相对表达量显著低于轻度肾积水和正常对照组(AQP1:0.194±0.118比0.598±0.092比0.858±0.122;AQP2:0.247±0.089比0.566±0.105比0.976±0.134;AQP3:0.426±0.126比0.741±0.074比1.006 ±0.084;AQP4:0.171±0.115比0.420±0.081比0.739±0.201;P＜0.01).结论 AQP1-4在先天性PUJO患儿积水肾组织中的表达水平降低,且随着积水程度的加重而下降,表明其在肾积水发展的过程中可能与肾脏浓缩稀释功能的下降有一定的关系.     

幼鼠双侧输尿管梗阻24 h后肾脏水通道蛋白1-4的变化

目的探讨4个月大白鼠双侧输尿管急性梗阻24h后肾脏水通道蛋白1-4的变化。方法14只大白鼠随机分为梗阻组（bilateral ureteral obstruction，BUO，n：7）及对照组（Sham，n=7），梗阻组行双侧输尿管结扎，对照组仅游离输尿管而不结扎，24h后收集动脉血和肾标本，在显微镜下将肾脏分离出内髓（IM）及外髓外带加肾皮质（OSOM＋C）后，分别行免疫杂交实验，检测水通道蛋白。（AQP1-4）的变化。结果BUO24h使血浆渗透压明显增高至（338±3．0）mOsm，原为（300±0．6）mIsm，P〈0．01，血钾显著上升至（5．4±0．2）mmol／L，原为（4．0±0．1）mmol／L，P〈0．01；血浆肌苷（372±5．3）μmol／L，原为（30±2．8）μmol／L，P〈0．01和尿素氮（40．7±1．4）mmol／L，原为（5．8±0．2）mmol／L，P〈0．01明显高于对照组，而血钠低于正常（138．9±0．3）mmol／L，原为（141．0±0．3）mmol／L，P〈0．01。免疫杂交结果发现近端小管上皮细胞AQP，明显降低，下降到对照组的46．6％（P〈0．01）；在肾脏集合管主细胞顶膜上，AQP2的表达明显下降，为对照组的68．1％（P〈0．01）；而基底膜上分布的AQR和AQP4也明显下调，分别为对照组的76．3％和73．2％（P〈0．01）。结论双侧输尿管梗阻24h显著影响肾脏AQP。在近端小管和AQP24。在集合管的表达，使其明显下调。该变化可能对梗阻后水分重吸收障碍并引发低渗性多尿的病理生理过程起重要作用。     

水通道蛋白基因在胎肾中表达的研究

现已发现共有7种水通道蛋白(AQP)1,2,3,4,6,7,8在肾脏中表达,主要集中在近曲小管、亨勒袢降支、集合管等;AQP1-4参与水的重吸收和尿浓缩,AQP6-8的生理与病理意义不明。在成年肾的尿浓缩中发挥重要功能的AQPs,在胎肾发育的早期就有表达,但是其在胎肾中的表达水平很低,直到出生后随着肾脏发育完全而逐渐表达升高,并达到稳定水平,这种现象符合胎儿生长发育的生理需求,即产生足够的稀释尿,作为羊水来源途径的生理需求。     

Urinary aquaporin-2 excretion in preterm and full-term neonates

The study was undertaken to define the role of aquaporin-2 (AQP2) in renal concentrating performance by measuring urinary AQP2 excretion and urine osmolality in healthy preterm and full-term neonates during early postnatal life. Random urine samples were obtained from 9 full-term newborn infants (mean birth weight 3,218 g, mean gestational age 39.2 weeks) at postnatal ages of 1, 3 and 5 days. Five premature infants with a mean birth weight of 1,570 g and mean gestational age of 30.6 weeks were studied at the end of the 1st week and then weekly up to the 6th week. Urine osmolality (Knauer osmometer), creatinine (modified Jaffé's method) and AQP2 concentrations (radioimmunoassay) were measured. In full-term neonates, urinary AQP2 excretion showed no consistent changes over the age period studied, while urine osmolality decreased significantly with advancing age. In premature infants, urinary AQP2 excretion remained practically unchanged during the first 4 weeks followed by an abrupt increase thereafter. Urine osmolality did not follow the developmental pattern of AQP2 excretion; its mean values varied only from 78 +/- 39 to 174 +/- 146 mosm/l during the experimental period. It is concluded that during the early postnatal period, urinary AQP2 excretion does not serve as a direct marker of the renal action of AVP and the renal capacity to concentrate urine.     

Urinary aquaporin-2 excretion during ibuprofen or indomethacin treatment in preterm infants with patent ductus arteriosus

Aim: Water channel AQP2 is the target for vasopressin (AVP) and a major determinant of urinary concentrating capacity. In mature kidneys, prostaglandins counteract the effect of AVP on AQP2 expression at functional sites. We investigated whether disturbances in water homeostasis in infants with patent ductus arteriosus (PDA) treated with prostaglandin inhibitors can be attributed to activation of AQP2. Methods: In 53 infants with symptomatic PDA (gestational age 24–33 weeks), 30 receiving ibuprofen and 23 indomethacin starting at 2–15 days of life, clinical and biochemical data were collected before treatment and after each dose of the drugs. Urinary AQP2 was determined by dot immunoblotting. Results: Urinary AQP2 level and osmolality were decreased in both groups. Urinary osmolality was overall low and correlated inversely with fluid uptake. In ibuprofen group, there was no correlation of AQP2 level with urinary osmolality. Conclusion: There was no AQP2 upregulation in the infants. The low urinary osmolality and dissociation between urinary osmolality and urinary AQP2 level indicate that the fluid retention sometimes observed in PDA infants treated with prostaglandin inhibitors is not caused by increased levels of functional AQP2. Thus, knowledge about the renal physiology of the adult cannot always be transferred to the infant kidney.     

Perinatal management of a preterm neonate affected by hyperprostaglandin E2 syndrome (HPS)

BACKGROUND: Neonates affected by hyperprostaglandin E(2) syndrome (HPS) present with severe polyuria. Both urinary losses as well as prostaglandin synthesis inhibitors may precipitate acute renal failure (ARF). AIM: Our goal was to maintain euvolaemia by replacement of urinary losses. PATIENT: Our patient was born prematurely with a family history typical of HPS. Urinary salt and water losses and PGE(2) excretion were determined in 2- to 4-h intervals. Salt and water were replaced accordingly. RESULTS: Within the first 48 h, urinary losses and PGE(2) increased continuously to 50 ml/kg/h and 374 ng/h/1.73 m(2), respectively. Following exposure to 0.05-0.5 mg/kg/d indomethacin, urinary output decreased steadily to 10-15/ml/kg/h.CONCLUSION: In euvolaemic preterm neonates with HPS and the need for excessive replacement of salt and water, inhibition of renal PGE(2) excretion with indomethacin effectively reduces polyuria and natriuresis without acutely compromising renal function.     

改良UW灌注液治疗新生猪急性肾小管坏死的实验研究

目的 通过改良UW(University of Wisconsin solution)肾保存液在体肾动脉灌注,探讨改良UW肾保存液对新生猪急性肾小管坏死的治疗作用.方法 出生1周无特殊病原体幼猪10只,通过夹闭肾动脉制作急性肾小管坏死动物模型,将其分为模型组和改良UW灌注治疗组,每组5只,另设5只为假手术组.分别记录术后各组幼猪12 h、1 d、2 d、3 d、7 d的尿量并进行尿蛋白定量及静脉血中尿素氮(BUN)和肌酐(Cr)含量的检测,同时于术后12 h、24 h及7 d行肾脏病理学检查.结果 10只幼猪经肾脏病理和血生化检查证实建模成功,术后12 h模型组和灌注治疗组BUN和Cr含量明显高于假手术组,差异有统计学意义(P＜0.05),其含量在第2天达到峰值,第7天均显著降低,以灌注治疗组最为显著,并恢复至假手术组水平.尿蛋白定量模型组和灌注治疗组与假手术组比较各时间段均明显升高,差异有统计学意义(P＜0.05或P＜0.01),1 d后达到峰值,后缓慢下降,灌注治疗组下降尤为明显.尿量在模型组各时间段均较假手术组显著减少(P＜0.05或P＜0.01);而灌注治疗组只在12 h、1 d、2 d减少,差异有统计学意义(P＜0.05),在3 d、7d则无统计学意义.肾脏病理学检查提示:与模型组相比灌注治疗组的病理学改变较模型组明显减轻.结论 肾动脉灌注改良UW肾保存液可能具有缓解新生猪急性肾小管坏死程度的作用.

Abstract：

Objective To determine the effect of the modified UW (University of Wisconsin)solution in the treatment of acute renal tubular necrosis in newborn swine. Methods Ten one-week-old newborn swine were used to establish the animal model of acute renal tubular necrosis by clamping their renal arteries,and were divided into two groups: the model group( n = 5 ) and the treatment group ( n = 5 ) in which fructose diphosphate sodium UW solution was used. Sham surgery was performed on other five swine, which were used as the sham group. At 12 h,l d,2 d,3 d and 7 d after the operation,the urine volume,urine protein,blood urea nitrogen(BUN) and creatinine(Cr) were determined. At 12 h ,24 h and 7 d after the operation ,renal pathological examination was conducted. Results The renal pathological examination and the blood biochemistry tests showed that the animal model was successful. BUN and Cr in the model group and the treatment group were significantly higher than those in the sham group at 12 h after operation(P ＜0. 05) ,and they arrived at their peak values at 2 d after operation,showed remarkable decline at 7 d,especially in treatment group,and returned to the level of the sham group. The urine protein in the model group and treatment group were higher than those in the sham group at various times(P ＜0.05 or P ＜0.01) and it peaked at 1 d after operation,then declining gradually,especially in the treatment group. Compared with the sham group,there were a significant decrease in the urine volume at various times in the model group(P ＜0. 05 or P ＜0. 01 ) ,while in the treatment group,the decrease in the urine volume were significant only at 12 h, 1 d and 2 d( P ＜ 0. 05 ) ,and turned insignificant at 3 d and 7 d. The pathological examination showed that the pathological changes in the treatment group were significantly milder than those in the model group. Conclusion The modified UW solution is effective in reducing the acute renal tubular necrosis in newborn swine.     

三聚氰胺致大鼠泌尿系结石肾脏损害及病理改变的实验研究

目的 建立三聚氰胺泌尿系结石大鼠模型,观察肾脏病理改变,初步探讨三聚氰胺亚慢性肾脏毒性的可能机制。方法 将3周龄刚断乳雄性Wistar大鼠60只按随机数字表法分为实验组2组（A、B组）和对照组（C组）,每组20只,A、B、C组分别给予三聚氰胺质量分数为1％、2％、0的饲料。比较大鼠体重、摄食量、血清尿素氮和肌酐水平。15周时（用药期末）3组各随机选取半数处死,剩余半数停药继续喂养4周后（停药期末）处死,均行肾脏重量、系数比较并观察病理改变。采用高效液相色谱-质谱联用法检测血清和结石中三聚氰胺、三聚氰酸和尿酸含量。结果 用药期末,A、B组血清尿素氮水平分别为( 13.23 ±5.10)、( 18.30 ±5.90) mmol/L,均高于C组(8.23 ±2.30) mmol/L(P＜0.01);B组肌酐水平(19.90 ±2.90) mmoL/L高于C组(10.04±1.73) mmol/L(P＜0.01);A、B组左右肾系数均高于C组(P＜0.01);肾脏中可见结晶形成,结晶所在肾小管扩张明显,肾小管周围肾间质淋巴细胞浸润及间质纤维化,B组最为显著。停药期末,A、B组血清尿素氮水平分别为(17.96±2.04)、(19.20±3.36) mmol/L,均高于C组的（8.30±1.79）mmol/L(均P＜0.01);B组肌酐水平(24.20±5.28) mmol/L高于C组(9.87 ±2.71) mmol/L(P ＜0.01),且分别较用药期水平升高（分别为P＜0.01,P＜0.05）;两实验组肾脏系数较前下降;肾脏仍有结晶未排出,间质改变较停药前未见减轻。结论(1)饲喂3周龄刚断乳雄性Wistar大鼠含三聚氰胺质量分数为2％的饲料15周能够建立三聚氰胺泌尿系结石模型。饲喂含三聚氰胺质量分数为1％的饲料15周,仅少数大鼠可形成肉眼可见的肾脏结石,部分形成镜下结晶。结石成分主要为三聚氰胺(＞90％)、少量尿酸及极少量三聚氰酸。(2)三聚氰胺可导致大鼠肾功能受损,镜下可见肾小管结晶形成、肾小管扩张、炎症、纤维化等病理表现,并具有剂量依赖性。三聚氰胺的肾脏损害与结晶、结石梗阻有一定相关性。(3)停止摄入三聚氰胺后,肾功能及肾脏炎症、纤维化等改变短期内未见好转,结晶自行排出的过程较为缓慢,如结晶持续存在可能会造成进一步的或不可逆转的肾脏损伤。     

过敏性紫癜患儿早期肾损害的实验室检查及干预

目的 探讨过敏性紫癜( Henoch-Schonlein purpura,HSP)患儿早期肾损害诊断的实验室指标及早期干预的临床疗效.方法 对143例多次尿常规检查正常的HSP患儿进一步检测尿微量蛋白[免疫球蛋白G(IgG)、微量白蛋白(MA)、转铁蛋白(TRF)、a1-微球蛋白(α1-MG)、β2-微球蛋白(β2-MG)]以及尿酶[N-乙酰-β-D氨基葡萄糖苷酶(NAG),y-谷氨酰转肽酶(y-GT)]的含量.采用对比研究方法,将131例检查异常的HSP患儿随机分成两组(对照组65例、干预组66例).两组均给予甲氰咪胍、氯雷他定、钙剂等综合治疗,干预组66例在综合治疗的基础上加用小剂量肝素微量泵持续定时静脉滴注及甘利欣口服治疗,对照组65例未给予其他治疗.结果 143例尿常规检查正常的HSP患儿中尿微量蛋白和尿酶异常131例(91.61％),干预组治疗2个月、4个月尿微量蛋白、尿酶各项指标均较治j前降低,差异有统计学意义(P＜0.01).对照组治疗2个月仅尿β2-MG、NAG、y-GT 3项指标降低,差异有统计学意义(P＜0.01),治疗4个月尿微量蛋白、尿酶各项指标均较治疗前降低,差异有统计学意义(P＜0.01).干预组治疗2个月、4个月尿微量蛋白、尿酶各项指标均较对照组低,差异有统计学意义(P ＜0.05或P＜0.01).尿IgG、MA、TRF 、NAG恢复较快,干预组治疗4个月时已基本接近正常,而尿α1-MG、β2-MG、γ-GT恢复较慢,干预组治疗4个月时仍有轻重不一的异常.两组治疗4个月时,对照组尿常规异常率高于干预组(36.92％ vs 6.10％),差异有统计学意义(P＜0.05).结论 尿微量蛋白及尿酶7项指标的联合检测是早期诊断HSP肾损害的良好指标.应用肝素钠、甘利欣对其进行早期干预,能有效预防肾损害,延缓疾病进展.对HSP肾损害须强调早期诊断及早期干预.