紧密连接蛋白claudin-2在急性肾损伤患儿肾组织中的表达及意义

目的 研究紧密连接蛋白claudin-2在急性肾损伤（AKI）患儿肾组织中的表达变化,探讨claudin-2与肾脏病理损害及肾功能损害程度的关系。方法 2009年12月至2011年12月确诊为AKI并完善肾活检的24例患儿,依据病情严重程度分为轻症组（n=7）及重症组（n=17）。对照组为12例肾小球轻微病变的孤立性血尿患儿。采用全自动生化分析仪比色法检测血清肌酐水平;采用肾脏病理计量评分法对肾小管间质损害程度进行分析;免疫组织化学方法 检测肾组织claudin-2的表达;Pearson相关分析评估claudin-2与患儿肾脏病理评分及血肌酐水平间的关系。结果 AKI轻症组（190±68 μmol/L）与AKI重症组（477±128 μmol/L）血清肌酐水平均高于对照组（29±7 μmol/L）（均PPPPPr=-0.809、-0.903,均P结论 AKI患儿肾组织claudin-2的表达水平发生变化,且claudin-2的表达水平与肾脏病理损害程度及肾功能损害程度密切相关。     

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。     

促红细胞生成素对大鼠肾间质纤维化发动蛋白-1表达影响

目的 探讨促红细胞生成素(EPO)对大鼠肾间质纤维化发动蛋白-1（Drp-1）表达的影响。方法 81只SD大鼠,分为假手术组、对照组和EPO组,每组各27只。EPO组、对照组采用单侧输尿管结扎并剪断建立肾间质纤维化模型,假手术组仅游离输尿管而不结扎和剪断;EPO组予EPO皮下注射;假手术组和对照组给予等量生理盐水皮下注射。各组于术后7、14和21 d取动脉血分离血清检测血肌酐和尿素氮水平。取梗阻侧肾组织行苏木精-伊红和Masson染色,观察肾脏病理学变化。用免疫组化方法检测肾组织Drp-1的表达。结果 ①EPO组各时点血清肌酐和尿素氮水平显著低于对照组（P<0.01）,但高于假手术组（P<0.05）。②EPO组各时点肾组织病理改变较对照组明显减轻,肾小管间质损伤评分和肾间质纤维化相对面积均低于对照组（P均<0.05）,但高于假手术组（P<0.05）。③EPO组肾组织的Drp-1表达显著低于对照组（P<0.05）,但高于假手术组（P<0.05）。结论 Drp-1在大鼠肾间质纤维化肾组织中表达增加,参与肾脏纤维化过程;EPO可以通过抑制Drp-1表达,从而延缓肾间质纤维化的进展。     

紫癜性肾炎患儿肾间质血管损害与临床的关系

目的探讨紫癜性肾炎患儿肾间质血管损害与肾脏病理及临床的关系。方法对肾穿刺活检确诊的39例紫癜性肾炎患儿进行肾间质血管损害、肾脏病理积分,并探讨其与临床的关系。结果1.肾脏病理检查中有不同程度肾间质血管损害者36例,占92.3%。其中轻度血管损害15例(38.4%);中度血管损害18例(46.2%);重度血管损害3例(7.7%)。2.肾间质血管中度与轻度损害组相比其血清清蛋白水平明显下降。3.肾间质血管病变积分与肾小球病变、肾间质纤维化、肾小管间质病变、肾脏总的病理损害积分均呈正相关。结论肾间质血管损害在绝大多数紫癜性肾炎患儿中存在,且与肾小球、肾小管间质病变呈正相关关系。     

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目的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±...     

促红细胞生成素对单侧输尿管部分梗阻幼鼠肾脏水通道蛋白2表达的影响

目的 探讨促红细胞生成素(EPO)对单侧输尿管部分梗阻(PUUO)幼鼠肾脏水通道蛋白2(AQP2)表达的影响.方法 SD幼鼠24只,随机分为PUUO组、PUUO+ EPO组和假手术组,各8只.PUUO组和PUUO+EPO组幼鼠采用输尿管腰大肌埋植法建立左侧输尿管部分梗阻模型,PUUO+ EPO组术后给予EPO腹腔注射(500 U/kg),首次于术后1h给予,其余隔天1次,共4次;PUUO组给予同等剂量9g/L盐水.假手术组仅分离输尿管,不包埋.术后1周处死大鼠,取左侧肾脏标本,采用荧光定量PCR、免疫组织化学及Western blot检测各组肾脏组织中AQP2 mRNA及蛋白表达水平.结果 免疫组织化学结果显示PUUO组内髓集合管AQP2阳性染色弱于PUUO+ EPO组和假手术组,经Western blot进一步验证,PUUO组AQP2蛋白表达水平低于PUUO+ EPO组和假手术组(分别为0.290±0.016、0.640 ±0.106和0.840 ±0.134,P＜0.05).经荧光定量PCR检测,3组幼鼠肾脏组织中AQP2 mRNA表达水平差异有统计学意义,假手术组表达最多,PUUO+ EPO组次之,PUUO组表达最少(3组△Ct值分别为-7.60 ±0.18、-9.70 ±0.54和-10.80±0.31,P＜0.05).结论 EPO有阻止PUUO幼鼠肾脏AQP2 mRNA及蛋白表达下调的功能.     

IgA肾病患者肾组织单核细胞趋化蛋白-1表达的意义

目的 探讨原发性IgA肾病(IgAN)患者肾组织单核细胞趋化蛋白-1(MCP-1)的表达变化.方法 选择经皮肾组织穿刺活检确诊为IgAN的患者40例.根据肾脏病理Lee氏分级(Ⅰ～Ⅴ级)将纳入研究的患者分为2组:A组20例,病理分级为Ⅰ～Ⅲ级;B组20例,病理分级为Ⅳ～Ⅴ级.对照组20例标本选取手术切除的肾肿瘤、肾囊肿患者远离病变组织的正常肾组织.同时将肾组织的肾小管和肾间质按照Katafuchi标准分为无间质病变组21例,轻度间质病变组8例,中度间质病变组19例和重度间质病变组12例.均采用免疫组织化学方法测定其肾组织中MCP-1的表达(以灰度值反映),观察其肾组织切片的染色强度及染色透光度,灰度值大则MCP-1表达少,反之则表达多.结果 根据肾脏病理Lee分级分组,各组灰度值比较:B组灰度值(68.08±2.37)与A组灰度值(74.50±3.27)比较、B组与对照组灰度值(81.98±3.21)比较、A 组与对照组比较,差异均有统计学意义(Pa<0.01);根据Katafuchi标准分组,无间质病变组、轻度间质病变组、中度间质病变组及重度间质病变组灰度值分别为82.03±3.13、76.44±2.01、71.49±1.69、66.54±1.23,各组比较差异均有统计学意义(Pa<0.01).结论 MCP-1可反映原发性IgAN患者肾组织的病理损害程度,且表达水平与肾组织损害程度有关.     

不同时机应用促红细胞生成素对感染所致新生大鼠脑损伤的保护作用

目的 探讨促红细胞生成素(EPO)对感染致新生大鼠脑损伤保护作用的最佳应用时机及其相关机制.方法 2日龄(P2)新生SD大鼠按随机数字表法分为4组,分别为对照组(A组)、脂多糖(LPS)感染组(B组)、早期EPO干预组(C组)、晚期EPO干预组(D组).A、B、C组P2新生大鼠连续5d(P2-P6)分别腹腔注射相应药物:等容积9 g/L盐水+等容积EPO空白对照品、0.6 mg/kg LPS+等容积EPO空白对照品、0.6mg/kg LPS+5 000 IU/kg EPO;D组P2新生大鼠连续5d(P2-P6)腹腔注射0.6 mg/kg LPS,P7开始连续腹腔注射5 000 IU/kg EPO 5 d(即P7-P11).A、B2组分别于P2(腹腔注射第1次药物后6h)、P7、P12,各随机数字表法抽取10只新生大鼠取脑,以矢状缝为标志分为左右半脑,右侧脑应用酶联免疫吸附法检测脑组织EPO受体(EPOR)水平,左侧脑应用反转录-聚合酶链反应(RT-PCR)方法检测EPOR mRNA水平;A、B、C3组于P7随机数字表法选取10只新生大鼠灌注取脑,余续养,4组均于P12灌注取脑,应用免疫组织化学方法检测髓鞘碱性蛋白(MBP)、胶质纤维酸性蛋白(GFAP)及EPOR的表达,采用HE染色观察各组大鼠脑组织的病理改变.结果 1.HE染色示B组海马锥体细胞界限不清、层次紊乱,细胞数目减少,脑室扩张,周围白质有囊性软化区域形成;EPO干预组较B组病理改变减轻,早期干预组更明显.2.B组较A组EPOR蛋白及mRNA表达增加,随日龄的增加EPOR与EPOR mRNA表达有下降趋势.3.B组MBP表达(107.46±3.65)较A组(146.78±3.13)明显减少(P＜0.05),EPO干预组较B组表达增加,且C组(126.25±4.42)较D组(117.35±3.42)增加更明显(P＜0.05).4.B组GFAP表达(P7、P12分别为141.46±11.92、149.48±13.59)较A组(P7、P12分别为120.63±13.32、119.74±12.48)增加(P＜0.05),P12时EPO干预组表达较B组降低,C组(134.59±12.19)与D组(137.27±13.87)差异无统计学意义(P＞0.05).结论 EPO对出生后感染所致的脑白质损伤有保护作用,且甲期应用优于晚期,其机制可能与感染可使新生大鼠脑组织EPOR表达增加及EPOR表达随日龄增加而降低有关.     

促红细胞生成素对窒息新生儿血清诱导人肾小管细胞TLR4/MyD88表达的影响

目的 研究促红细胞生成素(erythropoietin,EPO)对新生儿窒息后血清诱导人肾小管上皮细胞(HK-2)TLR4/MyD88(Toll-like receptors 4/myeloid differentiation factor 88)表达的影响.方法 将HK-2分为对照组、窒息组、EPO组,每组12份,分别检测TLR4和MyD88表达情况.对照组加入DMEM/F12培养液,窒息组加入含200 ml/L新生儿窒息后血清的DMEM/F12培养液,EPO组加入含50 IU/ml的EPO培养液预处理后再加入含200 ml/L新生儿窒息后血清的DMEM/F12培养液.其余培养条件3个实验组完全相同,即在37℃、50 ml/L CO2培养箱中培养24 h后,应用倒置相差显微镜观察细胞形态变化;流式细胞仪(flow cytometry,FCM)检测各组细胞TLR4特异性荧光抗体阳性结合率;免疫组织化学法(SP法)检测各组细胞MyD88表达情况.结果 与对照组比较,窒息组细胞形态变化显著,TLR4特异性荧光抗体阳性结合率和MyD88的表达明显增加;与窒息组比较,EPO组细胞形态明显改善,TLR4特异性荧光抗体阳性结合率和MyD88的表达明显减少,差异具有统计学意义(P<0.05).结论 EPO可减少新生儿窒息后血清诱导的人肾小管上皮细胞TLR4/MyD88的表达.     

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     

Treatment of renal anemia by subcutaneous erythropoietin in children with preterminal chronic renal failure

Eleven children aged 0.6–17 years with preterminal chronic renal failure and anemia (mean serum creatinine concentration 4.8 mg/dl; mcan hemoglobin concentration 7.9 g/dl) were treated with sc injections of recombinant human crythropoictin (EPO, initial dose 150 U/kg/week) over a mean period of 13 months. When a target hemoglobin concentration of 11.5–13.5 g/dl was reachcd, the dose was adapted. Iron deficiency was corrected. Hemoglobin concentration increased by > 2 g/dl in all patients within 14–119 (mean 45) days. The last maintenance dose ranged between 75 and 300 (mean 133) U/kg/ wcek. No major adverse effects were observed, except for hypertension which occurred in about half of the patients and necessitated interruption of EPO in one child with advanced renal failure. Additional antihypertensive drugs were given to five patients. Body height increascd in two patients by 0.6 and 1.3 SDS/year, respectively. In six patients with a mean observation period of 14 months before and 16 months after the start of EPO, the mean slope of the reciprocal serum creatinine concentration curve improved slightly ( p = 0.05 ). The proposed schedule appears to be safe for the treatment of renal anemia in most pre-dialysis paticnts. Frequent monitoring of hemoglobin, blood pressure, serum crcatinine and ferritin is required.     

Epidemiology and outcome of acute kidney injury in New Zealand children

Objectives: To determine the aetiology, incidence and short‐term outcomes of New Zealand children with acute kidney injury (AKI) requiring renal replacement therapy (RRT) over a 6‐year period. Methods: A retrospective chart review of all children requiring RRT for AKI from January 2001 to December 2006 at Starship Children's Hospital, Auckland, New Zealand was conducted. The primary outcome was survival to discharge. Results: A total of 226 children required RRT for AKI over the 6‐year study period. The annual incidence was 4.0 per 100 000 total population under 15 years of age. The commonest causes of AKI were post cardiac surgery (58%), haemolytic uraemic syndrome (17%), sepsis (13%) and glomerulonephritis (4%). The survival rate to hospital discharge was 89%. A total of 40% of all surviving children had one or more abnormalities at the time of discharge suggestive of ongoing renal dysfunction (hypertension, continuing need for antihypertensive medication, reduced estimated glomerular filtration rate or abnormal urinalysis). More Maori and Pacific Island children were treated for AKI than would be expected from population data (P < 0.0001). Sepsis and glomerulonephritis were seen more commonly as causes of AKI in Maori and Pacific Island children compared with New Zealand European children. Conclusion: In our study, 40% of surviving children had evidence of short‐term renal dysfunction at discharge following AKI. This suggests that all children should undergo a period of follow‐up after any episode of AKI to look for resolution or further development of signs of renal injury.     

肾脏疾病患儿急性肾损伤的临床分析

目的 了解儿童肾脏疾病中是否存在急性肾损伤(AKI),儿童肾脏疾病基础上AKI的发生率和病因构成,探讨AKI与肾脏疾病患儿住院时间、住院费用和短期预后的关系.方法 对我科住院的部分肾脏疾病患儿进行前瞻性的临床研究.病例入选标准:①确诊(原发性)肾病综合征(NS)、紫癜性肾炎(HSPN)和狼疮性肾炎(LN)的2～18岁住院患儿;②发病或复发≤3个月.AKI的诊断采用成人的AKI诊断标准.结果 共有95例患儿入选本研究,包括原发性NS 65例、HSPN 15例和LN 15例,其中33例(34.7%)符合AKI的诊断标准.LN、HSPN患儿伴发的AKI,100%表现为血肌酐升高;NS伴发的AKI中,65.4%的患儿表现为尿量减少,其中只有19.2%的患儿同时伴有血肌酐升高.AKI的病因:①NS基础上发生的AKI中,只有少数存在明确病因(26.9%),且多由肾外因素导致(15.4%),包括环孢素A的副作用、低血容量和肾小管间质损害;②LN和HSPN基础上发生的AKI,均由基础肾小球疾病导致.AKI组的住院时间和住院费用显著高于非AKI组[住院时间分别为28(6～94)、21(7～100)d;Z=-1.971,P=0.049;住院费用分别为12 035.7(1561.7～94 783.1)、8594.3(1390.1～98 876.5)元;Z=-1.993,P=0.046];随访6个月和12个月时,AKI组和非AKI组的血肌酐水平差异无统计学意义[随访6个月时分别为(60.4±91.8)、(42.8±12.2)μmol/L,t=0.937,P=0.358;随访12个月时分别为(48.7±18.1)、(47.7±14.2)μ,mol/L,t=0.197,P=0.845].结论 在儿童肾脏病急性期,34.7%的病例发生AKI;原发性NS中,非肾性因素是导致AKI发生的主要原因,而在LN和HSPN中,AKI的常见病因为基础肾小球疾病.AKI组的住院时间和住院费用高于非AKI组,但6个月和12个月随访时的血肌酐水平与非AKI组的患儿相比无显著差异.

Abstract：

Objective Acute kidney injury (AKI) was recently proposed for early recognition of renal function impairment and prompt interventions. Previous study revealed that AKI was highly associated with the prognosis. However, there was rare report of AKI in renal diseases, especially in children cohorts.Therefore, we performed the prospective clinical research in children with renal diseases in our hospital,aiming to study the prevalence, the clinical characteristics and the short-term prognosis of AKI. Method The study was designed as a prospective, single-center observational study. Inclusion criteria: ① the primary diagnosis was primary nephrotic syndrome (NS), Henoch-Schoenlein purpura nephritis (HSPN) or lupus nephritis ( LN), ② the duration from the onset of the renal diseases to the admission was less than 3 months. The serum creatinine and urine output of the subjects would be prospectively monitored. AKI was defined by the adult criteria and stratified by Acute Kidney Injury Network (AKIN) criteria. The patients were followed up at 6 months and 12 months after enrollment. Result Between October 2007 and April 2009, a total of 95 children were included, including 65 cases with NS, 15 HSPN and 15 LN. Mean age was (8. 9 ±3. 9) years (range 2-16 years). Thirty-three of the 95 patients (34. 7% ) fulfilled the AKI criteria,13 patients (13.7%) were diagnosed as acute renal failure (ARF). All the AKI in children with LN and HSPN presented with serum creatinine elevation. However, 65.4% of AKI in NS presented with decreasing urine output, only 19. 2% accompanied with increasing creatinine, with higher stages of urine output.Regarding the etiology, only 26.9% of AKI in NS had definite cause, most of which resulted from side-effect of cyclosporine, hypowlemia or tubule-interstitial damage, independent of glomerular diseases. In contrast,the AKI in LN and HSPN were exclusively caused by glomerular diseases. The length and costs of hospitalization of AKI group were significantly higher than non-AKI[length of hospitalization ( d), 28 (6 to 94) vs. 21 ( 7 to 100 ), Z = - 1. 971, P = 0. 049; cost of hospitalization ( yuan), 12 035.7 ( 1561.7 to 94 783.1) vs. 8594.3 (1390.1 to 98 876.5), Z= - 1.993, P=0.046]. There was no significant difference in the serum creatinine at 6-month and 12-month follow-up between AKI group and non-AKI[6-month, (60.4 ±91.8) μmol/L vs. (42. 8 ± 12. 2) μmol/L, t =0. 937, P =0. 358; 12-month, (48. 7 ±18.1) μmol/L vs. (47.7±14.2) μmoL/L, t=0.197, P=0.845]. Conclusion Theprevalence of AKI (34.7%) was higher than that of ARF ( 13.7% ) in children with renal diseases. Most of the AKI in NS resulted from non-glomerular diseases. In contraat, most AKI in LN and HSPN were caused by underlying glomerular diseases. The length and costs of hospitalization were significantly higher in AKI group.However, there was no significant difference in serum creatinine between AKI and non-AKI group in the follow-up at 6 months and 12 months. Further investigations on criteria for the diagnosis of AKI in children with renal diseases are still needed.     

Pharmacokinetics and pharmacodynamics of intravenous epoetin alfa in children with cancer

BACKGROUND: Epoetin alfa (EPO, PROCRIT) pharmacokinetics and pharmacodynamics were evaluated in children with malignant solid tumors receiving chemotherapy. PROCEDURE: Children initially received IV EPO 600 IU/kg (max dose 40,000 IU) or placebo once weekly for 16 weeks. Dose was increased to 900 IU/kg (max dose 60,000 IU) for patients not achieving a 1 g/dl increase in hemoglobin by study week 3 or 4. Serial PK samples were collected for 24 hr after the first study dose, and after the 10th or 11th dose. Serum EPO concentrations were analyzed using an ELISA assay, and pharmacokinetics were evaluated using compartmental methods. RESULTS: Twelve children participated; six (median age 15.2 years; range 9.3-18.6 years) were randomized to receive EPO. All children required dosage increases to 900 IU/kg due to no response. The median (range) apparent EPO AUC0-24 and clearance (CL) were 67.1 IU/ml.hr (13.8-102.6) and 0.26 L/hr/m2 (0.19-1.08), respectively. After the 10th or 11th EPO dose in four of these six EPO patients, the median (range) apparent AUC0-24 and CL of EPO was 126.5 IU/ml.hr (107.3-161.1) and 0.21 L/hr/m2 (0.15-0.25), respectively. No significant correlations were observed between pharmacokinetic parameters and pharmacodynamic effects. CONCLUSIONS: EPO disposition in our patients was similar to other pediatric patient populations or adults receiving IV EPO. Interesting but insignificant trends were noted in pharmacodynamic effects.     

Erythropoietin concentrations and erythropoiesis in newborns suffering from renal agenesis and congenital kidney diseases

We studied serum concentrations of erythropoietin (EPO) in the cord blood of 31 newborns. In patients with renal agenesis (n=6), the EPO levels were 68.2 (23–177) mU/ml (median, range). These values are clearly above EPO levels in the reference groups (median/range: <30 weeks 11.0 (5.5–17.5) mU/ml; 30–32 weeks 18.1 (5.5–136) mU/ml; 33–34 weeks 17.7 (8.3–423) mU/ml; 35–37 weeks 17.3 (5.5–272) mU/ml; 38 weeks 17.8 (8.7–40.3) mU/ml). Neonates with polycystic kidney diseases (n=12, EPO 23.5 (9.7–491) mU/ml) and with severe bilateral hydronephrosis due to obstructive uropathy (n=13, 18.6 (7.5–30.7) mU/ml) showed no difference to the reference groups. In all groups there were only slight differences in haemoglobin/haematocrit values.Conclusion In spite of renal agenesis and severe congenital kidney diseases, erythropoiesis is sufficiently maintained during fetal life. The liver of congenitally kidney-damaged fetuses is sufficiently able to compensate the reduction in — or lack of — renal EPO production.     

促红细胞生成素通过早产儿血脑脊液屏障的观察

目的研究外源性重组人促红细胞生成素(rhu—EPO)能否通过早产儿血脑脊液屏障。方法将胎龄28-35周、体质量<2500g的早产儿随机分为治疗组20例,对照组16例。治疗组给予rhu-EPO750IU/(kg·周).3次/周,隔日1次,疗程2周;对照组按早产儿常规治疗。用酶联免疫法测两组早产儿治疗前后血清、脑脊液EPO浓度。结果1.治疗组治疗2周后血清、脑脊液EPO浓度均明显高于对照组(P均<0.01)。2.治疗组治疗前后血清、脑脊液EPO浓度相比,治疗后明显高于治疗前(P<0.01)。3.对照组血清、脑脊液EPO浓度在2周后同出生时相比均有所降低,但无显著差异(P>0.05)。结论外源性应用rhu—EPO能通过早产儿血脑脊液屏障。     

1型糖尿病伴糖尿病酮症酸中毒患儿发生急性肾损伤的临床研究北大核心CSCD

目的评估1型糖尿病伴糖尿病酮症酸中毒(diabetic ketoacidosis,DKA)患儿发生急性肾损伤(acute kidney injury,AKI)的情况,探讨导致DKA患儿发生AKI的可能潜在因素。方法回顾性将2018年1月1日至2020年12月31日在南京医科大学附属儿童医院就诊的45例1型糖尿病伴DKA患儿,按照入院时是否合并AKI分为无AKI组(n=37)和合并AKI组(n=8)。收集两组患儿社会人口学资料,入院时的体检数据,包括身高、体重、血压和心率等,采用化学发光微粒免疫分析法测定患儿入院及出院时血肌酐和尿素氮等指标水平。采用多因素logistic回归模型分析1型糖尿病伴DKA患儿发生AKI的影响因素。结果45例患儿确诊中位年龄为9.2岁,8例(18%)入院时合并AKI的患儿中,6例为1期AKI,2例为3期AKI。血校正钠水平升高与1型糖尿病伴DKA患儿发生AKI密切相关(P<0.05),而入院时较高的胰岛素水平则不易发生AKI(P<0.05)。结论1型糖尿病伴DKA患儿AKI的发生率较高,临床上应积极纠正DKA,尽快控制血糖,并定期对这部分儿童病例进行肾功能复查和随访。[中国当代儿科杂志,2022,24(8):858-862]     

Omi/HtrA2在缺氧复氧后人近曲肾小管上皮细胞中的表达及促红细胞生成素对其表达的影响

目的 探讨缺氧复氧(H/R)后人近曲肾小管上皮细胞内Omi/HtrA2的表达变化及促红细胞生成素(EPO)干预的影响.方法 以人近曲肾小管上皮细胞株(HK-2细胞)为研究对象,将其分为对照组、H/R组及EPO干预组.对照组常规培养;H/R组缺氧24h后复氧6 h;EPO干预组在H/R前加入5 000 U·L-1EPO预处理.倒置显微镜观察细胞形态,四甲基偶氮唑蓝(MTT)法检测细胞活力,流式细胞仪检测细胞凋亡,免疫组织化学检测细胞内Omi/HtrA2表达变化.结果 与对照组比较,H/R组细胞数量减少,细胞形态发生改变,细胞活力下降,细胞凋亡率显著增加,细胞内Omi/HtrA2表达增强,差异均有统计学意义(Pa＜0.05);而与H/R组相比,EPO干预组细胞数量增多,细胞形态明显改善,细胞活力增加,细胞凋亡率下降,Omi/HtrA2表达减弱,差异均有统计学意义(Pa＜0.05).但各指标均未恢复至对照组水平.结论.H/R可通过上调Omi/HtrA2表达而促进肾小管上皮细胞凋亡,EPO对H/R肾小管上皮细胞具有保护作用,其机制可能与抑制Omi/HtrA2表达、减少细胞凋亡有关.     

急性肾损伤269例

目的 探讨儿童急性肾损伤(AKI)的病因、临床特点及治疗方法,以助于早期诊断及制定合理的治疗方案.方法 回顾性分析269例AKI患儿的临床资料.分析儿童AKI的病因分布.并探讨其病史、临床表现、实验窒检查、肾损伤分期与预后的相关关系.结果 AKI患儿平均年龄6.06岁.肾前性AKI 34例(占12.6%,依次为腹泻50.0%,新生儿HIE 23.5%,烧伤11.8%),肾实质性AKI 165例(占61.3%,依次为肾病综合征21.8%,非链球菌感染后肾炎14.5%,感染13.9%,SLE 12.1%),肾后性AKI 70例(占26.0%,依次为结石81.4%,膀胱输尿管返流28.6%,肿瘤梗阻7.1%,肾盂输尿管连接处梗阻5.7%,细菌栓塞及后尿道瓣膜各1.4%).死亡2例(肾实质性AKI),未愈48例,好转142例,治愈77例.不同年龄段患儿的病因分布差异有统计学意义(P=0.000),新生儿AKI主要为肾前性原因(65.4%),婴幼儿期以肾后性AKI(58.3%)为主,学龄前及学龄儿主要为肾性AKI(61.9%,86.2%).其预后与原发肾脏疾病类型、AKI分期、病史长短及是否伴有少尿、蛋白尿相关(P<,a><0.05).结论 新生儿AKI主要为肾前性AKI,婴幼儿期主要为肾后性AKI,学龄前及学龄儿主要为肾性AKI.预后主要取决于原发肾脏疾病类型、病情分级、病史长短及是否伴有少尿、蛋白尿.早期诊断、早期冶疗有助于改善预后,提高生存率.     

紫癜性肾炎患儿合并急性肾损伤危险因素的病例对照研究

背景 肾功能损害是紫癜性肾炎(HSPN)预后不良的危险因素,但目前关于HSPN伴急性肾损伤(AKI)患儿的临床和病理特征报道较少.目的 探讨儿童HSPN合并AKI的病理特征及其危险因素.设计病例对照研究.方法 纳入2016年1月至2020年12月贵州省贵阳市妇幼保健院经肾活检确诊的HSPN连续病例,根据是否合并AKI分...