激素耐药性肾病综合征肾小管上皮细胞-间充质转化临床意义研究

探讨肾小管上皮细胞-间充质转化（EMT）与肾脏病理进展及原发性肾病综合征（INS）糖皮质激素（GC）耐药的关系。方法　2005年9月至2007年12月在中南大学湘雅二医院儿科住院行肾穿刺活检的INS患儿40例,分为激素耐药性肾病综合征（SRNS）组（20例）和激素敏感性肾病综合征（SSNS）组（20例）。免疫组化双染法检测INS患儿和5例正常对照组儿童肾组织中细胞角蛋白（CK）和波形蛋白（vimentin）的表达,肾脏病理评分半定量评价肾组织病理损害程度。结果　SRNS组肾小管-间质病理评分显著高于SSNS组（P < 0.05）;正常对照组肾小管上皮细胞内只表达CK,不表达vimentin;INS肾小管上皮细胞均不同程度表达vimentin;SRNS组肾组织CK表达较SSNS组显著降低[分别为（66.25±12.13）%和（76.64±7.64）%,P < 0.05],vimentin表达较SSNS组显著增高[分别为（11.51±7.48）%和（4.98±2.27）%,P < 0.05];不同肾小管-间质病变（轻、中、重度）组肾小管上皮细胞内CK和vimentin表达量的差异均有统计学意义[CK表达量分别为（79.97±3.70）%、（65.47±7.93）%和（48.47±5.98）%,P < 0.05];vimentin表达量分别为（4.74±1.84）%、（9.65±5.10）%、（23.60±7.72）%,P < 0.05];肾小管-间质病理评分与肾小管上皮细胞CK表达呈负相关（r = -0.887,P < 0.01）,与vimentin的表达呈正相关（r = 0.868,P < 0.01）。结论 　肾病综合征肾组织的肾小管上皮细胞存在不同程度的肾小管上皮细胞-间充质细胞转化（EMT）现象,尤以SRNS为甚;检测肾组织EMT水平可能有助于判断INS的预后。     

肾病综合征患儿肾组织中AP-1及TGF-β1的表达与激素疗效关系的探讨

目的探讨原发性肾病综合征(PNS)患儿肾组织激活蛋白_1(AP_1)、转化生长因子_β1(TGF_β1)的表达与激素耐药、肾脏病理损害的相关性,以期阐明PNS激素耐药的可能机制。方法应用非生物素免疫组化ElivisionTMplus法检测48例PNS(SSNS8例,SRNS20例,SDNS20例)患儿肾组织中AP_1亚基c_Jun和TGF_β1的表达水平,用计分法半定量评价肾脏的病理损害程度。结果①肾小球内和肾小管间质内AP_1和TGF_β1的表达,均为SRNS>SDNS>SSNS(P<0.01)。②SSNS、SDNS、SRNS3组肾小球的病理损害分数分别为4.25±1.49,5.25±1.65,8.10±2.57(SRNS与SDRS比较P<0.01,SDRS与SSNS比较P>0.05);SSNS、SDNS、SRNS3组肾小管间质的病理损害分数分别为4.13±0.99,6.90±1.55,11.10±2.94(P<0.01)。③肾组织中AP_1和TGF_β1的表达与肾小球和肾小管间质病理损害的程度呈正相关(相关系数分别为:0.463,0.352;0.547,0.646,P均<0.05)。结论SRNS患儿肾组织中AP_1和TGF_β1的表达增强,并与肾脏病理损害程度密切相关。     

肾病综合征患儿肾组织原位血管紧张素转换酶mRNA表达与激素疗效关系的研究

目的　探讨肾病综合征 (NS)患儿肾脏局部肾素 血管紧张素系统 (RAS)、激素耐药、肾脏病理损害程度之间的关系 ,阐述激素耐药的部分机制。方法　 85例原发性NS患儿按激素敏感型NS(SSNS)、激素依赖型NS(SDNS)、激素耐药型NS(SRNS)分成 3组 ,选 6例行肾切除的肾肿瘤患儿的正常肾组织作为对照组。采用原位杂交的方法检测 4组患儿肾脏原位血管紧张素转换酶 (ACE)mRNA的表达水平 ;评分法半定量评估肾脏的病理损害程度。分析NS患儿肾组织ACEmRNA表达水平、激素反应性、肾脏的病理损害程度间的关系。结果　①在肾小球和小管间质区域的ACEmRNA表达水平均为SRNS组 >SSNS组 >对照组 (P <0 0 1)。②SRNS、SDNS、SSNS肾小球病理损害的评分分别为 :6 6 7± 2 4 3,4 6 8± 2 30 ,4 4 2± 2 87(P <0 0 1) ;小管间质病理损害评分分别为 :10 4 8± 3 77,7 2 0± 2 79,4 2 5± 1 4 8(P <0 0 1)。③肾组织ACEmRNA的表达与肾小球和小管间质病理损害程度呈正相关 ,相关系数分别为 0 4 82 ,0 85。结论　SRNS型NS患儿肾组织ACEmRNA表达增强 ,并且与肾脏的病理损害程度密切相关     

P300在肾病综合征糖皮质激素耐药中的作用

目的观察原发性肾病综合征(PNS)激素敏感与激素耐药组P300表达的差异,探讨P300在肾病综合征糖皮质激素耐药中的作用,为揭示PNS激素耐药发生机制提供理论依据。方法采用免疫组化法检测正常对照组肾组织及40例PNS患儿(激素敏感组20例,激素耐药组20例)肾活检组织中P300表达差异。结果正常肾组织仅偶见肾小管上皮细胞P300呈阳性表达;PNS患儿肾组织均存在不同程度P300表达,主要分布于肾小管上皮细胞,肾小球系膜区表达微弱或未表达,其他肾固有细胞未见P300表达;激素敏感组肾小管上皮细胞P300表达较激素耐药组明显增多(P<0.01),P300表达密集部位的肾小管形态正常,结构完整;肾小管上皮细胞P300阳性表达与肾小管间质病理积分呈负相关(P<0.01)。结论P300蛋白主要通过肾小管上皮细胞促进GC效应发挥;PNS患儿肾小管上皮细胞P300表达下降,可能是导致GC耐药及增加GC对肾小管上皮细胞损伤的机制之一。     

肾病综合征患儿肾组织P-糖蛋白170表达的研究

目的检测P-糖蛋白170(P-gp170)mRNA及蛋白在糖皮质激素(GC)敏感和耐药型肾病综合征(NS)患儿肾组织中的分布、表达变化,初探NS患儿肾组织P-gp170表达在GC耐药中的作用。方法2005-09—2006-04在中南大学湘雅二医院住院的初发特发性肾病(INS)患儿34例,按照GC对患儿的疗效分为GC敏感组(SSNS)和GC耐药组(SRNS),分别以免疫组织化学和原位杂交方法检测患儿肾组织P-gp170蛋白及mRNA的表达,6例正常肾组织为对照。结果正常对照组肾组织及NS患儿肾组织中均有P-gp170蛋白及mRNA的表达;正常对照组及NS患儿肾小球均无P-gp170蛋白及mRNA的表达,其蛋白及mRNA均主要表达于肾小管及肾间质,肾小管近端表达多于远端(P<0.01);免疫组化和原位杂交结果均显示SSNS阳性信号表达多于对照组,而SRNS又高于SSNS(P均<0.01);P-gp170蛋白与mRNA的表达成显著正相关(r=0.87,P<0.05)。结论肾脏本身即可合成、分泌P-gp170;P-gp170在正常肾小管的表达可能与某些代谢物质的转运有关;NS患儿肾小管P-gp170表达增高可能与NS本身的状态有关,或者是GC通过诱导P-gp170的表达增高而导致GC耐药;P-gp170表达上调可能为GC耐药的机制之一;检测肾组织P-gp170的表达水平有助于预测NS患儿GC反应差异性。     

激素耐药型与激素敏感型肾病综合征儿童尿液双向电泳图谱分析

目的建立激素耐药型原发性肾病综合征(SRNS)儿童与激素敏感型原发性肾病综合征(SSNS)儿童尿液全蛋白双向凝胶电泳(2-DE)图谱,分析差异的蛋白质位点,为研究原发性肾病综合征(INS)糖皮质激素耐药的机制提供依据。方法病例来源于湘雅二医院儿科住院部,收集时间为2005-01-2005-10,入选的INS患儿依据中华医学会儿科学分会肾脏病学组制定的诊断标准,分为3组,每组5例。利用2-DE技术分离SRNS与SSNS(治疗前、后)儿童尿液总蛋白质,Image Master 2D V3.01分析软件进行凝胶图像分析。结果获得了图像清晰、分辨率高的SRNS组、SSNS(治疗前)与SSNS(治疗后)组儿童尿液2-DE图谱,3组点数分别为(206±8)个、(204±5)个、(55±5)个;SRNS组与SSNS组(治疗前)尿液2-DE凝胶共筛选出差异蛋白质点66个;SRNS组与SSNS组(治疗后)尿液2-DE凝胶共筛选出差异蛋白质点33个。结论该研究成功建立了分辨率高且重复性较好的SRNS与SSNS儿童尿液全蛋白的2-DE图谱;通过组间尿液2-DE图谱分析,发现了一些可能与INS激素耐药或敏感有关的蛋白质位点,为进一步运用蛋白质组学技术寻找与INS激素耐药抑或激素敏感相关的蛋白质打下了基础。     

Toll样受体4在原发性肾病综合征患儿肾组织及外周血中表达的意义

目的探讨Toll样受体4(TLR4)在原发性肾病综合征(INS)患儿肾组织及外周血中的表达及意义。方法采集2015年10月至2018年6月在新乡医学院第一附属医院确诊为INS的78例患儿肾活检组织及21例儿童正常肾组织(对照组1),应用免疫组织化学方法检测标本中TLR4表达水平,比较INS不同肾脏病理类型、不同临床分型中TLR4表达水平的差异,分析其与24 h尿蛋白、血清清蛋白的相关性;应用酶联免疫吸附试验(ELISA)检测INS患儿治疗前(活动期)及治疗后(缓解期)和23例健康儿童(对照组2)外周血中TLR4表达水平,比较INS不同肾脏病理类型、不同临床分型患儿血清中TLR4表达水平的差异,分析其与24 h尿蛋白、血清清蛋白的相关性;对INS患儿肾小管中TLR4的表达水平与血清TLR4的表达水平进行相关性分析。结果1.与正常肾组织TLR4水平[(0.93±0.26)%]比较,TLR4在各型INS患儿肾小球及肾间质的表达[系膜增生性肾小球肾炎(MsPNG)型:(0.93±0.21)%、局灶节段性肾小球硬化(FSGS)型:(1.02±0.25)%、膜性肾病(MN)型(1.03±0.09)%、微小病变(MCD)型(1.02±0.27)%]差异无统计学意义(F=0.741,P=0.562);而肾小管TLR4的表达水平明显增高[MCD型:(82.94±4.62)%、MN型:(63.54±1.98)%、MsPGN型:(42.32±2.97)%、FSGS型:(22.60±2.07)%],差异有统计学意义(F=1929.842,P<0.01),其中MCD型INS患儿肾小管TLR4表达水平较MN型、MsPGN型、FSGS型明显增高,差异均有统计学意义(均P<0.01);肾小管TLR4在临床分型为激素敏感型肾病综合征(SSNS型)肾脏组织中表达最高,在激素耐药型肾病综合征(SRNS)型表达最低,差异有统计学意义(F=220.951,P<0.01)。2.活动期INS患儿血清TLR4表达[MsPNG型:(143.36±12.99)ng/L、FSGS型(75.94±7.29)ng/L、MN型(210.22±14.66)ng/L、MCD型(283.93±21.58)ng/L]显著高于缓解期患儿[MsPNG型:(29.51±4.93)ng/L、FSGS型(15.66±3.78)ng/L、MN型(45.40±5.73)ng/L、MCD型(62.29±7.90)ng/L]及对照组2儿童[(0.69±0.33)ng/L],差异均有统计学意义(均P<0.01);且缓解期INS患儿血清TLR4的表达水平高于对照组2儿童,差异有统计学意义(F=286.287,P<0.01)。活动期及缓解期INS患儿血清TLR4的表达水平均以MCD型最高,其次为MN型,而FSGS型最低;血清TLR4在临床分型为SSNS型表达最高,SRNS型表达最低,差异有统计学意义(F=147.438,P<0.01)。3.INS患儿肾小管中TLR4的表达水平[(62.82±20.94)%]与其活动期血清中TLR4的表达水平[(213.26±73.33)ng/L]呈正相关(r=0.852,P<0.05);INS患儿肾小管及活动期血清TLR4的表达水平均与24 h尿蛋白水平[(123.05±33.55)mg/kg]均呈正相关(r=0.401、0.427,均P<0.05),与血清清蛋白水平[(19.54±3.55)g/L]均呈负相关(r=-0.602、-0.617,均P<0.05)。结论TLR4在INS患儿肾小管及血清中表达增高,且表达水平可能与不同肾脏病理类型及临床分型有关,与疾病活动具有相关性。     

应用SELDI-TOF-MS筛选激素耐药型肾病综合征患儿尿液生物标志物

目的应用表面增强激光解吸电离飞行时间质谱(SELDI-TOF-MS)蛋白质芯片技术筛选激素耐药型肾病综合征(SRNS)患儿尿液生物标志物。方法激素敏感型肾病综合征(SSNS)组32例,SRNS组9例,正常对照组45例,应用金芯片检测各组尿液标本。结果SRNS有差异明显的生物标志物4个,相对分子量分别为6703、7212、11820、14356,其中7212、11820、14356差异表达蛋白质在SRNS呈高表达,在SSNS呈低表达,6703差异表达蛋白质在SSNS高表达,在SRNS低表达。4个蛋白质峰[6703、7212、11820、14356质荷比(m/z)]组合构建的诊断模型鉴别SRNS和SSNS,灵敏度为88.89%,特异度93.75%。结论SELDI-TOF-MS蛋白质芯片技术是一种无创、快速、简便易行、用量少和高通量分析方法,能直接筛选出SRNS患儿尿液中的生物标志物,具有较好的临床应用价值。     

原发性肾病综合征患儿肾组织中p18的表达及意义(英文)

目的：肾脏固有细胞的异常增生是肾小球硬化发展的病理基础,细胞增生又受细胞周期调控物质的调节。本研究通过探讨肾病综合征患儿肾组织细胞周期调节蛋白p18的表达水平及其与肾脏固有细胞增生之间的关系,为抑制肾脏固有细胞的异常增生,延缓肾脏病的慢性进展开辟新的途径。方法：以39例原发性肾病综合征患儿［8例微小病变(MCD),15例系膜增生性肾小球肾炎(MsPGN),7例膜增生性肾小球肾炎(MPGN),9例局灶节段性肾小球肾炎(FSGS)］肾活检石蜡包埋肾组织及6例肾肿瘤肾切除病人的正常肾组织作为研究对象,用免疫组织化学方法检测了p18在肾组织的表达水平,分析其与肾病综合征的病理类型及肾组织中增殖细胞核抗原(PCNA)的表达的关系。结果：肾病综合征组肾小球内PCNA阳性细胞百分率(28.6%±3.4%)明显高于对照组(10.8%±3.4%)(P<0.05),p18阳性细胞百分率(35.8%±4.0%)明显高于对照组(6.1%±1.9%)(P<0.05);肾病综合征组肾小管-间质内的PCNA阳性细胞百分率(68.3%±11.6%)明显高于对照组(12.6%±2.6%)(P<0.05)。不同病理类型肾病综合征患儿的肾小球内PCNA阳性细胞百分率存在显著差异,分别为MCD 23.6%±4.6%,MsPGN 40.2%±5.1%,MPGN 27.5%±3.6%,FSGS 34.6%±5.1%(均P<0.05);不同病理类型肾病综合征患儿的肾小球内p18阳性细胞百分率存在显著差异,分别为MCD 25.2%±4.3%,MsPGN35.7%±7.1%,MPGN 37.7%±4.0%,FSGS 40.1±6.4%(均P<0.05)。肾小球内p18的阳性细胞百分率和PCNA阳性细胞百分率成正相关(r=0.6632,P<0.05)。结论：肾病综合征患儿肾组织p18表达水平增加可能起促进异常增生的肾脏固有细胞消退的作用。［中国当代儿科杂志,2004, 6(5): 373-376］     

P-糖蛋白170在原发性肾病综合征患儿糖皮质激素耐药中的作用

目的探讨原发性肾病综合征(PNS)患儿治疗前外周血单个核细胞(PBMC)P-糖蛋白170(P-gp170)与糖皮质激素(GC)耐药的关系。方法采用流式细胞仪(FCM)检测30例PNS患儿PBMCP-gp170的表达,并分析其与复发次数、24h尿蛋白定量(24hUTP)及肾脏病理积分的关系。根据随访结果分成激素耐药型肾病综合征(SRNS)和激素敏感型肾病综合征(SSNS)2组,各15例。10例健康体检儿童作为正常对照组。结果SRNS组患儿PBMCP-gp170的表达量显著高于SSNS组患儿(P均<0.05)。PNS患儿激素治疗前PBMCP-gp170的表达量与复发的次数呈正相关(r=0.399,P<0.05);SRNS患儿激素治疗前PBMCP-gp170的表达量与24h尿蛋白定量(24hUTP)及肾脏病理积分均呈正相关(r=0.576、0.529,P均<0.05)。结论PBMCP-gp170表达增高可能与PNS患儿GC耐药有关,可作为PNS患儿GC耐药的标志之一。PBMCP-gp170表达增高与PNS活动、复发及病理有关,可做为临床判断预后的指标。     

Prospective evaluation of selective criteria for imaging among children with suspected blunt renal trauma

The evaluation of children with suspected blunt renal injury relies mainly on clinical assessment, urinalysis, and imaging studies. Because imaging studies rarely influence management, yet entail both risk and expense, we investigated a protocol to define their appropriate use. During a one-year period, children seen in the emergency department underwent a mandated radiographic evaluation for renal injury only if they had (a) severe injuries or (b) a urinalysis with greater than 20 RBC/hpf. Thirty-two children were enrolled; 16 had imaging studies that detected four abnormalities, ie, three contusions and one incidental finding of renal papillary necrosis. All children with abnormal imaging studies had greater than 20 RBC on urinalysis. None of the 16 children who were not studied radiographically developed complications related to renal trauma during short-term follow-up. Our findings support earlier recommendations for limiting the use of imaging for suspected blunt renal trauma in children with minor to moderate injuries and hematuria of less than or equal to 20 RBC/hpf.     

Statural growth of children with chronic renal failure on conservative treatment

Statural growth was studied in 20 prepubertal children with chronic renal failure on conservative treatment followed-up 1.1 to 8.9 years (average 3.9). Five children reached end-stage renal failure during the follow-up period and underwent dialysis or transplantation. Most patients grew at a normal rate. During the observation period only 1 out of 20 children lost more than 0.5 height standard deviation score whereas 9 gained 0.5 to 3.1. A growth velocity above the 97th percentile for at least 1 year was observed in 6 patients. A normal growth rate and even catch-up growth is possible in children with chronic renal failure regardless of the degree of reduction of glomerular function.     

Statural Growth of Children with Chronic Renal Failure on Conservative Treatment

ABSTRACT. Statural growth was studied in 20 prepubertal children with chronic renal failure on conservative treatment followed-up 1.1 to 8.9 years (average 3.9). Five children reached end-stage renal failure during the follow-up period and underwent dialysis or transplantation. Most patients grew at a normal rate. During the observation period only 1 out of 20 children lost more than 0.5 height standard deviation score whereas 9 gained 0.5 to 3.1. A growth velocity above the 97th percentile for at least 1 year was observed in 6 patients. A normal growth rate and even catch-up growth is possible in children with chronic renal failure regardless of the degree of reduction of glomerular function.     

Evaluation of the delayed skin reaction in chronically ill children

The evaluation of delayed cutaneous hypersensitivity by using a standardized test system offers an assessment of cell-mediated immunity. The number and diameter of positive responses induced by seven antigens result in a score. The study included 21 healthy children, 20 children with bacterial infections as well as 20 patients with chronic renal insufficiency. In addition, 16 children with cystic fibrosis were also studied. No differences in the skin reactions was found in children with bacterial infections, showing a score of 13 +/- 6 mm. But children with cystic fibrosis or with renal insufficiency exhibited a severe impaired cell-mediated immunity. To what extent the alteration of cell-mediated immunity affects the course of the various diseases, has to be investigated by further prospective studies.     

儿童急性肾功能不全临床分析

目的探讨儿童急性肾功能不全的病因、治疗和预后。方法回顾2002~2005年本院34例儿童急性肾功能不全住院患儿的临床资料,对其发病原因、临床表现、治疗和预后行归纳分析,并作进一步探讨。结果急性肾功能不全34例中男19例,女15例;起病年龄16.0 d~15.5岁。因急性肾功能发病占35.3%。药物引起占29.4%。药物致儿童急性肾功能不全死亡率为20%,转为慢性肾功能不全为30%。结论原发性肾小球疾病是儿童急性肾功能不全的最常见原因,药物致儿童急性肾功能不全预后差,应及早干预原发性肾小球疾病防止慢性化,充分重视肾毒性药物的临床应用。     

Dense B cell infiltrates in paediatric renal transplant biopsies are predictive of allograft loss

Abstract:  Recent studies have suggested adverse outcome for renal allograft rejection associated with dense CD20 lymphocytic infiltrates in transplant renal biopsies. We investigated further the relationship between renal allograft survival and CD20+ lymphocytic infiltrates in renal transplant biopsies from children with graft dysfunction. Fifty consecutive unselected renal transplant biopsies were performed for investigation of acute, chronic or acute on chronic renal allograft dysfunction in 48 children aged 1–17 (median 13.1) years, at 0–155 (median 22) months post-transplantation with median follow up of 24 months post-biopsy. Seventeen (35%) graft losses occurred at 1–163 (median 49) months post-transplantation. There was increased graft loss in those with dense (>300 cells/hpf) CD20+ lymphocytic infiltrates present on biopsy (p = 0.043). Dense B-cell infiltrates were also associated with increased glucocorticoid requirement in those with acute cellular rejection (p = 0.0015). There were no significant differences in age, sex, HLA-mismatch, type of transplantation, EBV or CMV serology or baseline immunosuppressive regimens between those with or without dense CD20+ infiltrates. Dense CD20+ lymphocytic infiltrates in renal transplant biopsies are associated with adverse clinical outcome, including increased graft loss. This observation raises the possibility of future studies examining the efficacy of B cell depletion therapy in this clinical context.     

Renal failure in children with hepatic failure undergoing liver transplantation

Over a 3 1/2 year period, 133 children with hepatic failure underwent orthotopic liver transplantation (OLT) at our center. Renal failure (creatinine clearance less than 20 ml/min/1.73 m2) was present in 19 (14.3%) of these children. In seven of the 19 children, renal failure was present before OLT, and in the other 12 after OLT. The causes of renal failure included hepatorenal syndrome in seven, postischemic acute tubular necrosis in five, severe prerenal azotemia in five, and cyclosporine nephrotoxicity in two. Eight other patients died of renal failure while awaiting emergency transplantation. Of the total of 31 deaths among 133 children who underwent OLT, nine occurred in the 19 patients with renal failure. Thus patients with OLT and renal failure had a significantly higher mortality than other patients with transplants (P less than 0.025). Dialysis was not associated with improved survival. The majority of deaths in patients with renal failure were related to severe hemorrhage, thromboembolic events, and systemic fungal infections. Our experience suggests that renal failure is common in children with hepatic failure and is associated with reduced patient survival after OLT.     

Polyomavirus (BK) in pediatric renal transplants: evaluation of viremic patients with and without BK associated nephritis

Polyoma BK virus (BKV) is emerging as a significant complication in renal transplantation, which may lead to renal dysfunction and graft loss caused by BK nephritis (BKN). We report the management and outcome of 20 children who developed BK viremia. Serum polymerase chain reaction (PCR) for BKV DNA was measured monthly for the first year in transplant recipients and every six months thereafter, or for unexplained creatinine elevation. With seroconversion to +PCR, patients were managed with reduction of immunosuppression. Renal biopsy was performed if PCR or creatinine did not improve. From June 2003 to January 2006, 20 children seroconverted for BKV at 23 to 1410 days post-transplant (mean 467 days). Sixteen underwent renal biopsy. Eight displayed BKN, three acute rejection and five were normal. Patients with BKN displayed higher PCR and serum creatinine and presented later than children with viremia without BKN. There were no differences between the two groups for age, gender, donor source or immunosuppression. Seven children with BKN received treatment with cidofovir. Thirteen patients (65%) remained PCR+ after reduction of immunosuppression or treatment with cidofovir. Renal function was stable in 16 children (80%) at 13 +/- 6 months after seroconversion. Four patients with BKN demonstrated progressive loss of renal function. BKV infection in children can occur as an early complication or may develop years after transplantation. Patients with BKN presented later and displayed higher viral loads and serum creatinine than viremic patients without BKN. Children with BKN remained PCR+ despite reduction of immunosuppression or treatment with cidofovir and were at greater risk for loss of renal function.     

The case against screening urinalyses for asymptomatic bacteriuria in children.

Screening children for asymptomatic bacteriuria to prevent pyelonephritis and renal scarring is widely recommended, but its cost-effectiveness has not been established. We reviewed published studies to determine the costs and benefits of screening toilet-trained, asymptomatic children for bacteriuria. Given the sensitivity and specificity of current screening methods (approximately 80% each) and the prevalence of bacteriuria in asymptomatic children (approximately 1% in girls and 0.03% in boys), screening 100,000 children would result in 19,897 (20%) false-positive tests; initial screening and two urine cultures to confirm the diagnosis of asymptomatic bacteriuria would miss 28% of 515 children with true bacteriuria, and cost nearly $2.9 million. There is no evidence that detection and treatment of children with asymptomatic bacteriuria prevents subsequent pyelonephritis or renal scarring. Screening for bacteriuria in asymptomatic children is costly, fails to prevent pyelonephritis or renal scarring, and should be discontinued as a part of routine well-child care.     

Unilateral vesicoureteric reflux: Low prevalence of contralateral renal damage

OBJECTIVE: We assessed the risk for the occurrence of renal damage in children with vesicoureteric reflux (VUR). STUDY DESIGN: We reviewed the records of 187 consecutive children, aged 3.8 +/- (SD) 2.8 years, with unilateral primary VUR diagnosed after urinary tract infection (UTI). Dimercaptosuccinic acid renal scintigraphy was performed 4 to 6 months after the last UTI. Three patterns of renal damage were identified: global reduction (GR) of renal radionuclide uptake (20% to 40% of relative uptake), focal defects (FD) in uptake, and shrunken (relative uptake <20%) kidney (SK). We assumed that in these subjects FD indicated postpyelonephritic damage and that GR indicated congenital renal damage. RESULTS: Scintigraphic renal damage of any type was present in 36.9% of the refluxing and in 3.2% of the nonrefluxing kidneys (odds ratio [OR], 17.6; 95% CI, 7.4 to 41.9). FD were present in 15.5% and 2.7% (OR, 6.7; CI, 2.5-17.6), GR in 19% and 0.5% (OR, 44.3; CI, 6.1 to 327.2), and SK in 6.9% and 0%, respectively. Patients with severe VUR showed a higher probability of renal damage than those with nonsevere VUR. CONCLUSIONS: In children with UTI and VUR, the refluxing kidney is most at risk of both congenital and acquired renal damage, and this risk increases with severity of reflux.