肾移植术后高尿酸血症与痛风的治疗

肾移植术后高尿酸血症与痛风的治疗和一般性患者的高尿酸血症与痛风的治疗有不同之处 ,现就我们所遇 10例高尿酸血症和 6例痛风治疗的经验教训和体会 ,报告如下。1　临床资料1 1　一般资料　本组 16例 ,男 11例 ,女 5例 ,年龄2 4～ 55岁 ,其中伴肢体关节疼痛者 6例 ,血尿酸356 88～ 4 16 36μｍｏｌ/Ｌ者 5例 ,4 75 84～ 594 8μｍｏｌ/Ｌ者 8例 ,654 2 8～ 713 76μｍｏｌ/Ｌ者 3例。术后出现高尿酸血症时间为术后 15ｄ～ 5个月 ,出现痛风的时间为术后 2 0ｄ～ 5个月。1 2　治疗1 2 1　持续卧床至急性发作缓解后约 2～ 3ｄ。1 2 2　严格…     

氯沙坦治疗肾移植术后的高血压和高尿酸血症

目的 探讨氯沙坦治疗肾移植术后高尿酸血症和高血压的有效性和安全性。方法 以环孢素A（CsA）为基础免疫抑制治疗的肾移植患者36例，术后应用氯沙坦或卡托普利，共4周；经过7d洗脱期后，将氯沙坦和卡托普利相互替换治疗患者，共4周。采用双因素随机交叉试验设计，测定血尿酸、尿尿酸、血肌酐、尿肌酐、24h尿蛋白定量、血钾、血红蛋白、血CsA浓度及血压的基础值和药物治疗4周后的改变值。结果 氯沙坦治疗后，36例患者血尿酸较基础值明显下降，差异有统计学意义（P〈0．01），尿尿酸较基础值明显增加（P〈0．05），而卡托普利治疗后，血尿酸及尿尿酸均无明显改变。经过氯沙坦和卡托普利治疗4周后，患者的收缩压和舒张压较基础值均有明显下降，且均达到目标值范围，差异有统计学意义（P〈0．01）。经氯沙坦和卡托普利治疗后，患者的血红蛋白较基础值均明显下降（P〈0．05），血清CsA浓度较基础值均降低（P〈0．05），但CsA浓度仍在目标值范围。结论 氯沙坦不仅可有效控制肾移植术后的高血压，而且可以明显减轻高尿酸血症。     

肾移植术后早期的高尿酸血症与结石形成（附四例报告）

本文报告了４例肾移植患者术后１－３个月出现高尿酸血症并形成了移植肾、输尿管尿酸盐结石，结合复习文献探讨了环孢素Ａ（ＣｓＡ）引起高尿酸血症的可能机制和促成结石形成的因素。通过回顾４例患者成功治疗的体验，讨论了移植肾、输尿管尿酸结石预防及治疗的选择。     

高尿酸血症相关肾损伤机制的研究进展

高尿酸血症（hyperuricemia,HUA）的发病率逐年升高,其与慢性肾脏病的关系越来越受到重视,研究发现两者间存在独立相关性,但其具体机制尚不清楚。本文通过从尿酸的病理生理学和HUA的发病机制等角度出发,对HUA相关肾损伤机制的研究进展进行梳理总结,并对降尿酸治疗对肾脏的影响、尿酸水平与肾损伤的关系进行了讨论。基于此对HUA相关肾损伤的机制及治疗时机等问题提出思考。     

Hyperuricemia and gout following pediatric renal transplantation

Hyperuricemia and gout are common complications in adult renal transplant recipients. In pediatric recipients, however, hyperuricemia seems to be rare, but data are scarce. Thirty-two children (21 males, 11 females) were investigated for a median time of 4.8 years (range: 0.4–11.2 years) following renal transplantation. The median age of this pediatric study group was 13.9 years (range: 5.7–20.3 years), and the calculated glomerular filtration rate (GFR) was 61 ml/min per 1.73 m² (range:12–88 ml/min per 1.73 m²). All patients were given calcineurin inhibitors, with 22 and ten children receiving cyclosporine A (CSA) and tacrolimus (TAC), respectively. The median plasma uric acid was 385 μmol/l (range: 62–929 μmol/l); 15 children (47%) were above the age-related normal range. Only one patient experienced gouty arthritis. There was a significant correlation between plasma uric acid concentration and both time span after transplantation and plasma creatinine, and an inverse correlation to GFR (p<0.05). No significant correlation was found between plasma uric acid and body mass index (BMI). Plasma uric acid concentrations were neither different among CSA- and TAC-treated children, nor did they correlate with drug exposure or blood trough levels of CSA or TAC. Plasma uric acid concentration was not different when compared to children with chronic renal failure (CRF) of a similar degree in native kidneys. We conclude that hyperuricemia is common among pediatric renal transplant recipients and rather a consequence of chronic renal transplant dysfunction than the use of calcineurin inhibitors. Gout, however, is rare.     

肾移植术后妊娠五例六次

目的 探讨肾移植术后妊娠对受者及移植肾的影响.方法 回顾性分析5例6次肾移植术后妊娠的临床资料.结果 受者妊娠时平均年龄为31.1岁,移植至妊娠的时间平均为3.6年.5例6次妊娠中发生先兆子痫2例次,高脂血症1例次.最终成功分娩4例,分别于38周、35周、35周和38周接受剖宫产,新生儿平均体重为3262.5 g,新生儿Apgar评分均为10分.2例次因减少或停用免疫抑制剂,移植肾功能丧失而终止妊娠,其中1例接受再次肾移植后再次妊娠并成功分娩.结论 对于移植肾功能正常的女性受者,在合理应用免疫抑制剂的前提下妊娠和分娩是可行的,但具有较高风险,需要严密监护.     

Hyperuricemia after renal transplantation

Hyperuricemia is common in cyclosporine-treated renal allograft recipients. An increased incidence of gout in patients receiving both diuretics and cyclosporine has been reported, but the effect of hyperuricemia on renal allograft function has not been studied. In a prospective, randomized trial of cyclosporine and prednisone versus azathioprine, prednisone, and antilymphocyte globulin for immunosuppression in renal allograft recipients, 105 of 131 cyclosporine and prednisone-treated patients (80 percent) experienced hyperuricemia (serum uric acid level above 8 mg/dl) and 13 of 131 (10 percent) were severely hyperuricemic (serum uric acid level above 14 mg/dl). In contrast, hyperuricemia developed in 63 of 115 patients (55 percent) treated with azathioprine, prednisone, and antilymphocyte globulin (p less than 0.002). Despite the frequent occurrence of hyperuricemia, gout was rare. Clinical gout developed in six patients in the cyclosporine and prednisone group and in 0 patients in the azathioprine, prednisone, and antilymphocyte globulin group between 1 and 43 months (median 22.5 months) after transplantation. Neither severe hyperuricemia nor diuretic therapy were associated with a significantly increased incidence of gout. The mean serum creatinine concentration of severely hyperuricemic patients (all on cyclosporine and prednisone) was similar to that of normouricemic cyclosporine and prednisone patients (1.8 mg/dl versus 1.6 mg/dl, p greater than 0.2), and the severely hyperuricemic patients had a 4-year graft survival rate of 90 percent. Asymptomatic hyperuricemia after renal transplantation does not adversely affect allograft function, requires no specific therapy, and is not a contraindication to use of diuretics.     

Hyperuricemia after renal transplantation

Background

Hyperuricemia is a common complication after kidney transplantation, and may adversely affect graft survival.

Objective

To assess the prevalence of and predictors for development of hyperuricemia after renal transplantation.

Materials and Methods

Hyperuricemia was defined as a serum uric acid concentration of at least 7.0 mg/dL in men and 6.0 mg/dL in women. From March 2008 to May 2010, uric acid concentration was measured in 12,767 blood samples from 2961 adult renal transplant recipients (64% male and 36% female patients).

Results

Hyperuricemia was observed in 1553 patients (52.4%). The disorder frequently occurred in women (P = .003) and in patients with impaired renal graft function (P = .00). After adjustment for sex, serum creatinine concentration, diabetes mellitus, cyclosporine concentration, and dyslipidemia, only female sex (P = .03) and renal allograft dysfunction (P = .05) were associated with hyperuricemia after kidney transplantation.

Conclusion

Hyperuricemia is a common complication after kidney transplantation, and renal allograft insufficiency predisposes to higher uric acid concentration.     

尿毒症患者肾移植前后血浆同型半胱氨酸浓度的变化及临床意义

目的:观察尿毒症患者肾移植前后血浆同型半胱氨酸(Hcy)浓度的变化,探讨其临床意义。方法:选择40例尿毒症患者,测定肾移植前及术后第3天、第10天、第15天、第30天、第90天血浆Hcy浓度,同时测定肾功能,比较肾移植前后血浆Hcy浓度的变化。结果:在肾移植前,40例患者中有38例血浆Hcy异常。肾移植后,血浆Hcy浓度随着肾功能的好转逐渐下降,在术后15天时基本降到正常水平;以后尽管肾功能稳定,血浆Hcy浓度逐渐上升,在30天时有26例患者血浆Hcy高于正常,90天时有30例患者血浆Hcy高于正常。结论:肾移植后血浆Hcy水平仍高于正常,可能是肾移植患者心血管发病率较高的原因。     

肾移植术后并发卡氏肺孢子虫病的诊断和治疗

目的　探讨肾移植术后并发卡氏肺孢子虫病的早期诊断及治疗。方法　对 6例肾移植术后并发卡氏肺孢子虫病的有关临床资料进行分析和总结。结果　 6例患者确诊为卡氏肺孢子虫病后给予复方磺胺甲卟恶唑 (SMZ 6 0～ 70mg·kg-1·d-1,TMP 12～ 14mg·kg-1·d-1,分 2～ 4次给药 )治疗 3周 ,并调整免疫抑制方案及对症治疗 ,除 1例患者因放弃治疗死亡外 ,其余 5例均治愈 ,移植肾功能正常。结论　卡氏肺孢子虫病的确诊有赖于肺组织活检找到病原体 ,治疗首选复方磺胺甲卟恶唑 ,并适当减少免疫抑制剂用量。     

肾移植术后妊娠对移植肾的影响

目的 探讨肾移植术后妊娠对移植肾的影响。方法 对1978年4月至2002年3月妊娠超过5个月的13例肾移植受者资料进行回顾性分析。结果 免疫抑制方案，4例采用环孢素A（CsA)及泼尼松（Pred)。5例为CsA，霉酚酸酯（MMF）及Pred。4例为他他克莫司（FK506），MMF及Pred。13例中，10例患者妊娠足月，生产，母，婴均存活，移植肾功能稳定；1例产后2周因并发肺部感染，心力衰竭死亡，死亡时移植肾有功能，婴儿存活；2例妊娠中期出现蛋白尿，病理证实移植肾发生慢性排斥反应，终止妊娠，但抗排斥治疗无效，切除移植肾，恢复血液透析，目前11名子女健康，无发育异常。结论 肾移植患者若情况允许，在严重监护下是可以妊娠的。     

肾移植前后妇女的性激素状态

为了解女性尿毒症及肾移植受者性激素状态,作者应用酶联免疫法检测了５０例女性患者肾移植前、后的性激素水平,并以１５例近龄健康妇女对照。结果显示肾移植受者的泌乳素（ＰＲＬ）、促卵泡素（ＦＳＨ）及促黄体素（ＬＨ）较慢性肾功能衰竭（ＣＲＦ）血液透析组明显降低,而雌二醇（Ｅ）和孕酮（Ｐ）值在正常范围。对于ＣＲＦ患者检测发现ＰＲＬ明显升高,而孕酮值显著下降,经给该组闭经患者作克罗米酚刺激试验,结果阳性,说明闭经为下丘脑性功能障碍。作者认为成功肾移植可纠正肾衰患者由于血中肌酐、尿素氮升高造成的下丘脑功能障碍,且能恢复正常月经周期及生育力。透析期间可对症治疗,但不必促排卵,而成功肾移植是最好的治疗方法。     

肾移植术后肝功能异常的临床分析

目的总结肾移植术后肝功能异常的病因及其预防。方法回顾性分析肾移植后发生肝损伤者的临床资料。结果68例患者出现肝损伤，其中21例发展至肝功能衰竭，肝损伤的原因主要有肝炎病毒(乙型肝炎病毒、丙型肝炎病毒)感染、免疫抑制剂肝毒性等。多数患者术后1年内出现肝功能异常临床表现，主要有丙氨酸转氨酶升高、乏力、纳差、黄疸、腹胀、肝性脑病、出血等。结论术前应对肾移植受者的肝脏情况进行严格的综合评估，术后定期进行相关检查，尤其是术前检查有阳性发现者。     

肾移植术后真菌感染的防治

为探讨肾移植术后真菌感染的预防及治疗，对肾移植术后２８例发生真菌感染患者的临床资料和在３２例新移植患者中应用氟康唑预防真菌感染的资料进行分析。结果预防用药的３２例术后均未发生真菌感染；２８例感染者中，２３例治愈，５例死亡。认为对于术后真菌感染，重点在于针对诱发因素进行预防，早期诊断，及时应用氟康唑能有效地治疗真菌感染，移植后常规应用氟康唑可有效预防真菌感染的发生。