肾组织移植对慢性肾功能衰竭大鼠促红细胞生成素的调节作用

目的研究鼠婴肾组织移植于肾包膜下对促红细胞生成素的调节作用,为临床应用治疗肾性贫血提供理论依据。方法以Wistar雄性大鼠建立慢性肾功能衰竭动物模型为受体,将鼠婴肾组织块多点植入受体肾包膜下。治疗期间用EPO酶联免疫(ELISA)试剂盒测定血清EPO水平;观察肾组织病理改变,用免疫组化方法检测EPO在移植物中的表达。结果①60d时D组血清促红细胞生成素(1.768±0.140)mu/mL高于B组(1.160±0.324)mu/mL(P<0.01),与C组(2.329±0.125)mu/mL也有差异(P<0.05)。②移植后60d,移植物的体积由1mm3增至3-4mm3大小,表面血管网丰富,光镜下见肾小球、肾小管结构正常;③移植物EPO免疫组化,发现移植物EPO着色颗粒主要分布于肾皮质的肾小管,明显多于病例对照组大鼠肾组织(P<0.05)。结论通过对移植物的形态观察和功能测定,证明肾组织移植是一种有效的治疗手段,有可能为慢性肾性贫血提供一种新的途径。     

胚胎后肾及其原基同种和异种移植的研究进展

针对目前器官移植所面临的供体严重不足和长期使用免疫抑制剂造成严重并发症的问题，为探索新的供体器官来源，本文就胚胎后肾及其原基同种和异种移植的部位、生长条件、再血管化及功能检测等方面作一综述。     

肾组织活检在移植肾功能损害的诊断与鉴别诊断中的价值

目的 探讨移植肾组织活检在移植肾功能损害的诊断与鉴别诊断中的价值。方法 对158例移植肾组织活检资料进行回顾分析。结果 158例中以急性排斥反应多见,共55例（34．8％）,移植肾改变35例（22．2％）,临界改变32例（20．2％）,慢性排斥反应13例（8．3％）,系膜增生性病变13例（8．3％）,急性肾小管坏死6例（3．8％）,新月体性肾炎、溶血性尿毒综合征和毛细血管内增生性肾炎各1例（0．6％）;血中环孢素A的浓度与急性排斥反应的发生率无明确正相关关系;临床诊断与肾组织活检结果尚存在一些差异。结论 肾组织活检对明确诊断及提高临床诊断的正确率及选择治疗方案有重要价值。     

妊娠对同种移植肾长期功能影响的实验研究

已知在肾功能中度到重度不全的女性患者,妊娠可增加肾功能损害、高血压等并发症,但这并不提示妊娠对移植肾功能正常受者有同样的影响,此外,有关报道结果也不同[1,2]。应用标准的慢性排斥反应动物模型研究肾移植后妊娠对移植肾长期功能的影响,可克服以往临床回顾研究中既存的移植肾功能损害、免疫抑制药物、并发症和移植前疾病的复发对研究的影响,显示在无免疫抑制情形下单纯妊娠对正常功能移植肾脏的长期影响。一、材料与方法1.动物模型:选用雌性Fisher（F344,RT1v1）大鼠作供体,雌性Lewis（LFW,RT1）大鼠作受体,依照标准的移植肾慢性排斥反应大鼠模型要求行左肾     

胎肾细胞移植治疗急性肾功能衰竭的动物实验研究

进行了胎肾细胞移植治疗二氯化汞造成的动物实验。致死量组：细胞移植组平均存活４．２８天，对照组存活３．０２天；重中毒量组：１２０小时细胞移植组平均ＢＵＮ１０．６ｍｍｏｌ／Ｌ，Ｃｒ２２９μｍｏｌ／Ｌ，放射性核素每分钟闪烁计数３３７８ｒ／ｍｉｎ，对照组：ＢＵＮ３２．７ｍｍｏｌ／Ｌ，Ｃｒ８２９μｍｏｌ／Ｌ，ｃｐｍ值１３７３ｒ／ｍｉｎ；中毒量组；细胞移植组ＢＵＮ７．８ｍｍｏｌ／Ｌ，ｃＲ１６７．５μＭＯＬ／ｌ     

同种异体小肠移植的实验研究和临床应用

作者报告了同种异体小肠移植的动物实验结果和国内首例应用情况，以猪为模型，分为无免疫抑制（Ｉ）组，大剂量环孢素（ＣｓＡ）（ＩＩ）组，小剂量ＣｓＡ（Ⅲ）组，雷公藤加小剂量ＣｓＡ（Ⅳ）组，存活１００天后单用雷公藤（Ｖ）组。术后Ｉ，Ⅲ组均发生急性排斥；Ⅱ，Ⅲ组均发生急性排斥；Ⅱ，Ⅳ组未发生急性排斥，但Ⅱ组中有２只猪因严重感染而死亡，Ｖ组中继续服用雷公藤的动物长期存活。一例３１岁女性患者因慢性小肠结肠炎，拓     

供肾重量和受者体表面积与移植肾功能的关系

目的　探讨供肾重量、受者体表面积及二者比值与移植肾功能的关系。　方法　对 5 3例肾移植手术患者供肾重量、受者体表面积及二者的比值与受者术后 2～ 7d血肌酐平均值进行线性相关分析。　结果　供肾重量与术后 2～ 7d血肌酐平均值无明显相关性 (P >0 .0 5 ) ;受者体表面积与术后血肌酐平均值呈正相关 (P <0 .0 1) ;供肾重量及受者体表面积的比值与术后血肌酐平均值呈负相关 (P <0 .0 1)。　结论　受者体表面积、供肾重量及受者体表面积的比值与移植肾功能的关系应引起重视 ,体表面积较大的受者应尽量选择较重的供肾相配。     

SPECT监测移植肾功能

利用单光子发射型计算机断层显象仪监测移植肾功能２５例，计３４例次。观察表明，在肾移植早期，ＳＰＥＣＴ有利于鉴别少层原因，避免冒然切除移植肾；肾移植后期，如有肾功能减退，肾小球滤过率的降低较肌酐升高更敏感，更准确，故ＳＰＥＣＴ监测是了解肾功能及判断预后的最佳方法之一。     

肾组织移植对大鼠促红细胞生成素蛋白表达的实验研究

目的：探讨肾组织移植对大鼠促红细胞生成素（EPO）蛋白表达的影响.方法：以Wistar雄性大鼠建立慢性肾衰竭（CRF）动物模型为受体,将鼠婴肾组织块多点植入受体肾包膜下,在实验过程中监测肾功能及血红蛋白的改变,同时采用Western Blot法和免疫组化方法检测肾组织EPO蛋白的表达情况.结果：模型组、rHu-EPO组及肾移植组中大鼠分别出现死亡现象,且其肾功能均较明显减退,与正常组分别比较差异有统计学意义（P＜0.05）;实验30 ～60 d间期rHu-EPO组、肾移植组的Hb水平比模型组显著升高（P＜0.05）;Western Blot法和免疫组化方法检测肾移植组EPO蛋白表达显著高于模型组（P＜0.05）.结论：肾组织移植可以促进肾组织EPO蛋白表达,从而改善肾性贫血.     

移植肾功能长时间延迟恢复一例治疗体会

肾移植术后肾功能延迟恢复（ＤＧＦ）发生率较高,国外报道高达1０％－６０％;肾移植术后肾功能长时间延迟恢复（ＬＬＤＧＦ） 发生率较少,尚未见较准确的发病率报道。本院１例患者在肾移植术后５８ ｄ才完全恢复肾功能．我们对其病变原因及治疗方法作探讨,报道如下;对象与方法１．对象：患者,女,２４岁、体重4５ ｋｇ,血型Ａ型,ＰＲＡ阴性。供肾为尸体左肾,热缺血时间 ８ｍｉｎ,冷缺血时间 １２ ｈ,采用 ＨＣ－４肾保存液灌洗和保存。ＨＬＡ配型４同２容;原发病为慢性肾小球肾炎,肾移植前维持性血液透析治疗 １年,尿量少于１…     

慢性肾衰患者血红蛋白浓度变化对血清细胞因子活性的影响作用

目的为了探讨贫血与慢性肾衰（ＣＲＦ）免疫功能状态的关系。方法检测了ＣＲＦ患者单纯输血及用红细胞生成素（ＥＰＯ）治疗前后细胞因子白细胞介素２（ＩＬ２）、可溶性白细胞介素２受体（ｓＩＬ２Ｒ）、肿瘤坏死因子（ＴＮＦ）及γ干扰素（γＩＦＮ）水平，并与肾功能正常肾小球肾炎患者（ＧＮ）组及对照组（Ｃ）进行比较分析。结果ＣＲＦ组血清ＩＬ２，ＴＮＦ和γＩＦＮ水平均显著低于ＧＮ组及Ｃ组（Ｐ＜００１），ｓＩＬ２Ｒ水平则较ＧＮ组及Ｃ组明显升高（Ｐ＜００１）。ＣＲＦ组血清ＩＬ２，ＴＮＦ和γＩＦＮ水平与血红蛋白浓度存在直线正相关，而ｓＩＬ２Ｒ水平与血红蛋白浓度呈负相关性，单纯输血或应用ＥＰＯ治疗能改变这些细胞因子活性水平。结论ＣＲＦ免疫功能低下与贫血有关，及时治疗和改善贫血状态可部分纠正这种免疫异常。     

Staghorn calculus in renal allograft presenting as acute renal failure

Background: Urolithiasis is a rare complication in renal transplant recipients. We report a case of a staghorn calculus occurring in renal allograft, presenting as anuric renal failure with Gram-negative sepsis. Methods and Results: A 48-year-old Caucasian female, with end-stage renal disease due to autosomal dominant polycystic kidney disease, underwent cadaveric renal transplantation in 1986. Sixteen years after transplant, she presented with Gram-negative sepsis with Proteus mirabilis and acute anuric renal failure in the allograft. After undergoing an emergency nephrostomy and treatment of sepsis, a staghorn calculus was subsequently removed by percutaneous nephrolithotomy. Based on the stone analysis and history of urinary tract infections with urease splitting bacteria, the calculus was thought to be infection-induced. Conclusion: Although a rare complication, urolithiasis in an allograft can be associated with significant morbidity. Immediate recognition is critical to restore renal allograft function and to treat associated serious infection in an immunocompromised patient.     

Kimura disease in a patient with renal allograft failure secondary to chronic rejection

Recent studies suggest that CD4⁺ T helper 2 (Th2) cell proliferation and overexpression of Th2 cytokines may play an important role in the development of Kimura disease. Chronic rejection of a renal allograft by the indirect allorecognition pathway is also induced by Th2 cytokines. We report a 12-year-old boy who had presented with nephrotic syndrome 10 years previously. He was found to have focal segmental glomerulosclerosis, which was attributed to vesicoureteral reflux, and he underwent renal transplantation at the age of 5 years. Allograft dysfunction secondary to chronic rejection was noted by 2 years post transplant, after which continuous ambulatory peritoneal dialysis was instituted. After discontinuation of immunosuppressive therapy, he progressively developed peripheral eosinophilia and eczema, followed by cervical lymphadenopathy and then epitrochlear lymphadenopathy. Kimura disease was diagnosed on lymph node biopsy. Our patient demonstrated that Kimura disease can occur after renal allograft failure secondary to chronic rejection. Both disorders involve the Th2-dominant immune response, according to previous observations.     

肾衰康延缓慢性肾衰竭进展的实验研究

目的：探讨肾衰康延缓慢性肾衰竭（CRF）进展的疗效及机理。方法：采用5／6肾切除大鼠CRF模型,随机分为模型组、洛汀新组及肾衰康组治疗,观察各组Scr、BUN及尿中细胞外基质成分（ECM）排泄量。结果：洛汀新组及肾衰康组Scr及BUN均显低于模型组（P＜0．01及P＜0．05）,而肾衰康组Scr又低于洛汀新组（P＜0．05）,肾衰康组尿中Ⅳ型胶原（Col-Ⅳ）、纤维连接蛋白（FN）及层粘连蛋白（LN）含量均明显比模型组高（P＜0．01）。结论：肾衰康有延缓CRF进展的作用,其机理可能与促进ECM成分从尿中排泄,从而减轻肾小球内ECM的聚集有关。但肾衰康对ECM是抑制合成还是促进降解尚需进一步探讨。     

Renal function in predialysis children with chronic renal failure treated with erythropoietin

To assess the effect of long-term administration of human recombinant erythropoietin (EPO) on renal function, 11 anemic children aged 1.4 – 17.2 years were followed for 10 – 61 (mean 31) months on treatment. During EPO therapy the mean hemoglobin rose from 8.1 to 11.1 g/dl at the last observation. The final maintenance dose ranged between 70 and 300 U/kg per week. The rate of deterioration of renal function was calculated by comparing the slope of the regression lines of reciprocal serum creatinine values (SCr) derived from a mean of 20 values per patient obtained over 8 – 50 (mean 29) months before and a mean of 24 SCR values during EPO therapy. The individual slopes improved after initiation of EPO therapy in all but 3 patients, but the mean change of slope (from –0.0521 to –0.0299) was not significant. The study suggests that in most children with predialysis chronic renal failure long-term administration of EPO is not associated with accelerated deterioration but rather with delayed deterioration of renal function. Received August 30, 1995; received in revised form November 16, 1995; accepted April 10, 1996     

Chronic renal allograft nephropathy

Chronic rejection/chronic allograft nephropathy is the most prevalent cause of renal graft loss after the first year post-transplant. Chronic rejection/chronic allograft nephropathy is characterized by a slow progressive deterioration of graft function, often in combination with proteinuria and hypertension. Both immunologic and non-immunologic factors play key roles in the pathogenesis of chronic allograft nephropathy. Acute rejection episodes are the most prevalent risk factor for chronic rejection. Many risk factors for chronic allograft nephropathy have been identified, such as delayed graft function, nephron-dosing mismatch, repeated acute rejection episodes, and pathologically severe rejection. However, the precise pathogenesis of chronic allograft nephropathy remains elusive. The differential diagnosis of immunologically mediated chronic rejection and chronic rejection caused by non-immunologic factors is usually not possible using clinical parameters. The histopathologic findings of chronic allograft nephropathy are progressive interstitial fibrosis and remodelling of the vascular wall, and these findings are nonspecific. However, typical chronic transplant glomerulopathy, which affects glomerular tufts, as well as the multilayering of the peritubular capillary basement membrane, are characteristic of immunologic chronic rejection. Furthermore, in long-surviving patient with an allograft treated with a potent immunosuppressive agent, a calcineurin inhibitor, two or more concomitant independent lesions often develop. Therefore, the term "chronic allograft nephropathy" may be clinically preferable to "chronic rejection" to describe the gradual decline in graft function months or years after transplantation, in the absence of a well defined mechanism of graft dysfunction. The most effective way to prevent chronic allograft nephropathy is to avoid any kind of graft damage via either immunologic or non-immunologic mechanisms. Received: April 1, 2000 / Accepted: May 2, 2000     

Reversible renal failure due to the use of captopril in a renal allograft recipient treated with cyclosporin

Angiotensin-converting enzyme (ACE) inhibitors are widely used for the treatment of hypertension, but caution is advised because these drugs may induce reversible acute renal failure. Although this has been ascribed in some cases to nephrotoxicity, hypotension, a hypersensitivity reaction, and interstitial nephritis, most cases have been associated with stenosis of the renal arteries or arterioles occurring in either native or transplanted kidneys. We describe a case of reversible acute renal failure due to the use of captopril in a renal allograft recipient who had no evidence of any of these conditions, but who was also receiving cyclosporin therapy.     

Early prognostic factors of infants with chronic renal failure caused by renal dysplasia

Renal dysplasia (RD) is a common cause of chronic renal failure (CRF) in children. The evolution towards end-stage renal failure is unpredictable due to the paucity of early prognostic factors. In order to identify early prognostic clinical criteria, we have retrospectively analyzed renal function and growth in 11 infants with RD and CRF from birth up to 4 years of age. Children with obstructive RD were not included. Glomerular filtration rate (GFR) was estimated from Schwartz formula. In infants with a GFR below 15 ml/min per 1.73 m² at 6 months of age (group A, n=5), kidney function did not further improve; 4 reached end-stage renal failure between 8 months and 6 years of age. In contrast, infants with a GFR above 15 ml/min per 1.73 m² at 6 months of age (group B, n=6) experienced a significant improvement in renal function during follow-up, and none required renal replacement therapy. During the first 3 months of life all infants with RD and CRF developed severe growth retardation. Between 6 months and 4 years of age, children from group B grew significantly better than those from group A. In conclusion, our experience suggests that GFR, estimated from Schwartz formula at 6 months of age, is a useful prognostic factor in infants with RD and CRF. Infants with a GFR below 15 ml/min per 1.73 m² are at risk of severe growth delay and the need for early renal replacement therapy, whereas those with a GFR above 15 ml/min per 1.73 m² have a relatively favorable long-term prognosis. Received: 4 October 1999 / Revised: 26 October 2000 / Accepted: 26 October 2000     

Connective tissue metabolism in children with chronic renal failure

To assess the characteristics of connective tissue metabolism in chronic renal failure (CRF), urinary excretion of glycosaminoglycan (GAG) fractions and hydroxyproline (HYP) was determined in ten patients with CRF and in ten age-matched healthy children. CRF was found to be associated with elevated free HYP (19.9±6.1 vs 9.8±3.6 mol/day,P<0.05) and depressed peptide HYP excretion (33.1±13.5 vs 225.2±17.7 mol/day,P<0.01), a low rate of total GAG excretion (7.0±2.4 vs 16.1±1.9 mol uronic acid/day,P<0.05) with low chondroitin 4 — sulphate + chondroitin 6 — sulphate (Ch-Ss) (14.0±9.9 vs 65.0±22.1%) and a high proportion of non-sulphated or under-sulphated fractions, i.e. hyaluronic acid + chondroitin + heparan sulphate (HA+Ch+HS) (75.3±11.4 vs 31.5±5.7%). Urinary 3-methyl-histidine (3-met-HIS) excretion and plasma essential free amino acids did not differ in the two groups. In response to haemodialysis no consistent change occurred in urinary excretion of 3-met-HIS, peptide-bound HYP, total GAG or percentage distribution of individual GAG fractions. After haemodialysis all plasma amino acids decreased significantly, and there was a significant increase in urinary excretion of free HYP (P<0.05). We conclude that the alterations in urinary excretion of total and individual GAGs observed in CRF may reflect disturbed connective tissue metabolism which does not appear to be accounted for by protein malnutrition or enhanced protein breakdown and remains uninfluenced by haemodialysis therapy.