腹部大器官联合移植围手术期护理重点

[目的]探讨腹部大器官联合移植治疗腹部多器官功能衰竭的效果及围手术期的护理重点。[方法]对2例1型糖尿病并发尿毒症病人施行改良式胰液肠腔引流、胰十二指肠及肾一期联合移植；1例高龄酒精性肝硬化终末期并慢性肾功能不全尿毒症病人施行一期肝肾联合移植；1例慢性乙型病毒性肝炎、肝硬化、原发性肝细胞癌合并胰岛素依赖型糖尿病病人施行同期原位肝-异位胰十二指肠联合移植的围手术期实施护理。[结果]2例胰肾联合移植病人术后第5天肾功能恢复正常，术后第10天停用胰岛素，2例均分别于术后20d、22d出现消化道出血，经止血治疗后痊愈。肝肾联合移植病人术后第3天移植肝肾功能正常，术后第10天移植肝发生急性排斥反应，抗排斥治疗后逆转。肝胰联合移植病人术后5d停用胰岛素，移植肝功能恢复正常。4例病人分别随访6个月～29个月，移植物功能均正常。[结论]腹部大器官联合移植是腹部多器官功能衰竭的有效治疗方法。良好的术前准备、细致的移植物功能观察、排斥反应监测以及术后并发症的观察护理有助于移植手术成功。     

腹部大器官联合移植围手术期护理重点

[目的 ]探讨腹部大器官联合移植治疗腹部多器官功能衰竭的效果及围手术期的护理重点。 [方法 ]对 2例 1型糖尿病并发尿毒症病人施行改良式胰液肠腔引流、胰十二指肠及肾一期联合移植 ;1例高龄酒精性肝硬化终末期并慢性肾功能不全尿毒症病人施行一期肝肾联合移植 ;1例慢性乙型病毒性肝炎、肝硬化、原发性肝细胞癌合并胰岛素依赖型糖尿病病人施行同期原位肝 -异位胰十二指肠联合移植的围手术期实施护理。 [结果 ] 2例胰肾联合移植病人术后第 5天肾功能恢复正常 ,术后第 10天停用胰岛素 ,2例均分别于术后 2 0d、2 2d出现消化道出血 ,经止血治疗后痊愈。肝肾联合移植病人术后第 3天移植肝肾功能正常 ,术后第 10天移植肝发生急性排斥反应 ,抗排斥治疗后逆转。肝胰联合移植病人术后 5d停用胰岛素 ,移植肝功能恢复正常。 4例病人分别随访 6个月～ 2 9个月 ,移植物功能均正常。 [结论 ]腹部大器官联合移植是腹部多器官功能衰竭的有效治疗方法。良好的术前准备、细致的移植物功能观察、排斥反应监测以及术后并发症的观察护理有助于移植手术成功     

胰液膀胱引流式胰肾联合移植长期存活15例随访

背景：胰肾联合移植是治疗1型糖尿病合并终末期肾病的首选疗法,但由于移植风险高,并发症多,国内开展并不广泛。目的：总结胰液膀胱引流式胰肾联合移植长期存活的临床经验,观察其远期效果并分析影响因素。方法：对15例患者行胰液膀胱引流式胰肾联合移植,均采用心脏死亡的供体。HLA配型平均为2.13。均选择胰液膀胱引流式和体循环回流血管吻合方式,免疫抑制剂方案均用他克莫司,霉酚酸酯和泼尼松治疗。观察移植后患者移植物肾功能、血糖、淀粉酶等及并发症。结果与结论：最短随访8.5个月,最长随访105.5个月,平均住院时间为37.7（13～82）d。移植后13例患者胰腺功能恢复,2例于移植后即切除移植胰腺。移植后除1例患者肾脏功能延迟恢复外,其余患者肾脏功能立即恢复。2例患者因慢性排斥反应丢失移植胰腺和移植肾。移植后主要并发症为排斥反应,返流性胰腺炎和血栓形成。提示胰肾联合移植是治疗终末期糖尿病并发肾功能衰竭的一种安全而有效地治疗方法,其远期效果理想,完善的围移植期管理、预防和及时处理并发症、合理应用免疫抑制剂是影响患者和移植物长期存活的重要因素。     

一例胰—十二指肠—肾同期移植术的监护

胰一十二指肠一肾同或移植术是互型糖尿病并发尿毒症的一种治疗手段，以恢复正常的胰肾功能。使肾联合移植的优点是抑制肾排斥反应的同时，预防胰腺排斥反应，从而提高胰腺移植的成功率。【问我院于1994年4月29日成功地为1例糖尿病并发尿毒症病人施行了膀阶引流式胶一十二指肠一肾同或移植术。术后胰肾功能恢复，至1996年5月随访。病人存活良好，生活基本自理。现将有关移植术术后监护报告如下。直病例介绍病人男，47岁。糖尿病病史25年，按1型糖尿病内科治疗。4年前出现下肢水肿，血压升高，双眼白内障，双目仅有光感，因尿毒症，血肌酥值…     

胰液膀胱引流式胰肾联合移植长期存活15例随访

背景:胰肾联合移植是治疗1型糖尿病合并终末期肾病的首选疗法,但由于移植风险高,并发症多,国内开展并不广泛.目的:总结胰液膀胱引流式胰肾联合移植长期存活的临床经验,观察其远期效果并分析影响因素.方法:对15例患者行胰液膀胱引流式胰肾联合移植,均采用心脏死亡的供体.HLA配型平均为2.13.均选择胰液膀胱引流式和体循环回流血管吻合方式,免疫抑制剂方案均用他克莫司,霉酚酸酯和泼尼松治疗.观察移植后患者移植物肾功能、血糖、淀粉酶等及并发症.结果与结论:最短随访8.5个月,最长随访105.5个月,平均住院时间为37.7 (13～82) d.移植后13例患者胰腺功能恢复,2例于移植后即切除移植胰腺.移植后除1例患者肾脏功能延迟恢复外,其余患者肾脏功能立即恢复.2例患者因慢性排斥反应丢失移植胰腺和移植肾.移植后主要并发症为排斥反应,返流性胰腺炎和血栓形成.提示胰肾联合移植是治疗终末期糖尿病并发肾功能衰竭的一种安全而有效地治疗方法,其远期效果理想,完善的围移植期管理、预防和及时处理并发症、合理应用免疫抑制剂是影响患者和移植物长期存活的重要因素.     

胰肾联合移植术患者术后并发症的观察及护理

目的 探讨胰肾联合移植术术后并发症发生情况与护理措施.方法 2009年2月至2010年2月采用胰、肾联合移植不同术式治疗胰岛素依赖型糖尿病伴有肾功能衰竭尿毒症患者7例,回顾性分析了此期间所发生的并发症,并针对性地实施护理措施.结果 胰肾联合移植术术后并发症有感染、急性胰腺炎、急性排斥反应及出血.针对性地实施护理措施,减少了并发症的发生.结论 术后及时发现急性胰腺炎和出血征象,积极给予针对性的护理措施,合理使用免疫抑制剂,预防感染,加强基础护理,使胰肾联合移植成为治疗胰岛素依赖型糖尿病伴有肾功能衰竭尿毒症的常规手术.     

胰肾联合移植后的免疫抑制治疗

背景：胰肾联合移植已经被公认为是糖尿病（包括1型和2型）合并终末期尿毒症的有效治疗手段,由于胰腺为高免疫原性器官,合理的免疫抑制治疗是保证胰腺移植成功的关键。目的：探讨胰肾一期联合移植后免疫抑制药物的合理应用。方法：纳入2005-01/2009-06在中山大学附属第一医院器官移植中心完成胰肾一期联合移植的患者9例,其中男5例,女4例,胰液引流均采用空肠引流方式。术后采用白细胞介素2单克隆抗体诱导的四联免疫抑制方案：白细胞介素2单克隆抗体＋他克莫司＋麦考酚酸＋激素,并逐渐过渡至单用他克莫司维持治疗。回顾性分析以上9例患者围手术期及长期随访情况。结果与结论：胰肾一期联合移植后,除1例早期死亡外,其余8例患者移植后1周内肌酐降至正常水平,移植后停用胰岛素时间为（11.5±3.5）d,空腹血糖恢复至正常时间为（15.4±6.3）d。8例患者随访4～50个月期间,共有4例发生移植肾急性排斥,其中1例在接受床边血液透析过程中并发心脑血管意外后家属放弃治疗,其余3例患者经抗胸腺细胞球蛋白或激素冲击治疗后移植肾功能均逆转恢复,随访过程中未发现移植胰腺排斥。说明胰肾联合移植是治疗糖尿病合并终末期糖尿病肾病的有效方法,术后早期采用白细胞介素2单克隆抗体诱导的四联免疫抑制方案并逐渐过渡至单用他克莫司维持治疗是安全的。     

肝胰肾联合移植1例的观察与护理

肝胰肾联合移植是目前治疗肝硬化失代偿、胰岛素依赖性糖尿病合并慢性肾功能不全（尿毒症期）的有效措施。但由于目前国际、国内开展肝胰肾联合移植的手术例数甚少,经验不足,给治疗和护理带来较大的难题。本文总结了我院成功完成的1例肝胰肾联合移植的术前、术后护理,以及排斥反应的观察和护理体会。     

7例胰肾联合移植术术后并发症的观察与护理

目的探讨胰肾联合移植术后并发症的观察与护理要点。方法回顾性分析7例胰肾联合移植术后并发症的发生情况及处理方法。结果7例患者中，4例急性排斥反应，其中3例使用ATG及MP冲击治疗后肾功能逆转，1例行CRRT治疗并发心脑血管意外家属放弃治疗；发生4例次消化道出血，2例次肺部感染；3例术后1周出现精神症状，经及时治疗护理后痊愈；无一例发生胰肠吻合口漏。结论胰肾联合移植术后并发症发生率高，加强术后出血、感染、胰肠吻合口漏、排斥反应等并发症的观察护理是提高患者及移植物存活的关键。     

胰肾联合移植术的护理配合

胰腺移植是为胰岛素依赖型糖尿病病人提供正常胰腺 ,术后能生理性调节胰岛素的分泌 ,维持正常血糖。胰肾联合移植能同时治疗糖尿病及并发的糖尿病肾功能衰竭 ,这是目前其他治疗措施所不能比拟的。 2 0 0 0年 8月和 2 0 0 1年 4月及 9月我院泌尿外科为 3例糖尿病合并肾功能衰竭病人进行了胰肾联合移植手术 ,均取得了成功。现将手术配合报告如下。1　临床资料　　 3例胰肾联合移植手术中 ,男性 2例 ,年龄均为 5 4岁 ,其中1例糖尿病肾病两年 ,腹膜透析维持 19个月 ,应用胰岛素控制血糖 ;1例糖尿病 11ａ ,尿毒症出现 6个月 ,行血液透析。女性 1…     

胰肾联合移植5例分析

背景:胰肾联合是治疗糖尿病合并终末期肾病的最有效方法.但这些患者由于长期糖尿病史,心血管系统疾病相对较复杂,且手术涉及胃肠道,并应用大剂量的免疫抑制约物,移植前准备和移植后处理是胰肾联合移植成功的重要保障.目的:对胰肾联合移植的免疫抑制用药、凝血药物应用、围手术期以及移植后管理注意事项等进行多方面讨论,为胰肾联合移植提供一些临床经验.方法:回顾性分析2003/2008解放军第三○九医院泌尿外科进行胰肾联合移植5例患者的临床资料,总结免疫抑制剂、抗凝药物的应用及围手术期临床监测重点等治疗经验.结果与结论:5例患者均为男性,平均年龄43岁,均为1型糖尿病合并终末期肾病,移植前胰岛素用量为1.5～2.4U,(kg·d),其中1例合并糖尿病视网膜病变,多次眼底出血;2例合并明显冠状动脉粥样硬化性心脏病,移植前心脏射血分数分别为52%和50%.移植胰腺外分泌液均经肠道引流.3例恢复顺利,肾功和血糖均恢复正常.其中1例于移植后第7天出现排斥反应,激素冲击后肾功能恢复;1例移植后出现移植十二指肠急性排斥反应,肠瘘,最终移植胰腺切除,但移植肾脏保留;2例恢复顺利无并发症发生;1例移植后消化道出血,多器官衰竭死亡.胰肾联合移植是治疗糖尿病合并终末肾病的最有效方式.移植胰腺外分泌经膀胱引流由于并发症较多,已被经肠道引流取代.移植肾功能的恢复足胰肾联合移植成功的关键.移植后早期他克莫司可不必急于口服,可待血肌酐恢复到300 pmol/L.时再考虑应用.凝血药物的应用是移植胰腺功能恢复的重要因素之一,空肠造瘘是围手术期预防肠液向移植胰腺返流的重要治疗措施,且移植后随访期建议应用通便药物,预防便秘发生,减少肠液返流引起的急性胰腺炎的发生.     

Pancreas transplantation for the prevention of diabetic nephropathy

Diabetic nephropathy is the leading cause of kidney failure in the United States. Poor glycemic control, hypertension, and smoking have been implicated as risk factors for the development and progression of diabetic nephropathy in patients with type 1 diabetes mellitus. Improved medical therapy including angiotensin-converting enzyme inhibitors and tight glycemic control with use of intensive insulin therapy have been shown to reduce the progression of diabetic nephropathy substantially based on albumin excretion rates. Despite these improvements in medical management, many patients still experience progression from early diabetic nephropathy to end-stage renal disease. Successful pancreas transplantation leads to normal glycemic control in patients with type 1 diabetes, but historically it has generally been limited to patients with both kidney failure and diabetes. In this review of the current treatment of diabetic nephropathy, we examine the potential role of preemptive pancreas transplantation in patients with diabetic nephropathy.     

Clinical features and health-care costs of diabetic nephropathy

The nephropathy complicating insulin-dependent diabetes mellitus (IDDM) has been well studied, but that complicating non-insulin-dependent diabetes mellitus (NIDDM) is less well defined. In patients with IDDM, the glomerular filtration rate is often increased early in the course of the disease, approaches normal with insulin therapy, but tends to remain slightly elevated throughout the ensuing 10-15 yr of insulin dependency. After the onset of overt azotemia, end-stage renal disease (ESRD) develops in approximately 5 yrs. Proteinuria may be intermittently positive in the earliest stages of diabetes, evolving into intermittent and then persistent microalbuminuria, which in turn blossoms into macroalbuminuria. Because 40-50% of IDDM patients develop proteinuria and two-thirds of this subpopulation develop ESRD, some 20-30% of any given cohort of IDDM patients eventually need dialysis or transplantation. Evidence indicates that diabetic nephropathy is associated with a greater incidence of eye, nerve, heart, and peripheral vascular disease. Nondiabetic renal disease complicating IDDM and NIDDM is associated with a lesser frequency and severity of these extrarenal manifestations. The prevalence of retinopathy increases with advancing nephropathy. Roughly two-thirds of the deaths from IDDM are related to renal failure, and most of the remainder are caused by associated cardiovascular disease. Transplantation from living relatives carries the best prognosis for survival, and little difference is seen between hemodialysis, peritoneal dialysis, and cadaver transplantation. The health-care costs of treating diabetic nephropathy are also reviewed.     

Transplantation of the kidney--optimal treatment of patients suffering from diabetes mellitus type 1 with terminal chronic renal failure

AIM: To assess long-term results of renal transplantation in patients with diabetes mellitus of type 1 (DM-1) with terminal chronic renal failure (tCRF); to detect risk factors of low survival of the patients and development of dysfunction of renal transplant. MATERIAL AND METHODS: A retrospective comparative analysis of 418 recipients of the kidney with non-diabetic nephropathies (NDN) and 113 recipients with DM-1. RESULTS: Survival of DM-1 patients with tCRF after allotransplantation of the kidney was lower than in patients with NDN. Low survival risk factors for DM-1 patients after transplantation of the kidney are: DM-1 duration up to tCRF 25 years and more, minimum 3-year history of dialysis before transplantation, age at transplantation over 45 years, persistence of anemia (hemoglobin < 110 g/l) after operation. Survival of the transplanted kidney in DM-1 and NDN patients was the same. Risk factors of dysfunction of the transplanted kidney are the following: acute crises of rejection and delayed function of the transplant, arterial hypertension > 130/80 mmHg, proteinuria > 300 mg/day. Survival of the transplanted kidney is higher in transplantation from the relative donor, does not depend on the kind and duration of previous dialysis. Causes of a decline in the function of the transplanted kidney (by the data of puncture biopsy of 34 transplants) are the following: acute rejection crises (38%), chronic transplantation nephropathy (24%), toxic nephropathy (18%), recurrent diabetic nephropathy (6%), chronic pyelonephritis (6%). Lethality in DM-1 patients after renal transplantation is 2 times higher than in patients with NDN. Death was due to cardiovascular diseases, gangrene of the lower limbs, infectious complications (in 31%, 15% and 35% cases, respectively). CONCLUSION: Transplantation of the kidney is an optimal treatment in DM-1 patients with tCRF.     

膳食中限制蛋白质摄入与干预糖尿病的相关性

Background: Diabetic nephropathy is one of severe complications of diabetes mellitus (DM). With the increasing of incidence of DM, diabetic nephropathy (DN) has become the most common cause of renal failure in the end stage. More and more patient receive treatment of dialysis and kidney transplantation. The effect of protein intake on pathophysiology of DN has been taken more and more seriously. Studies have shown that restriction of protein intake could delay the progress of renal failure, relieve symptoms of uremia, and provide good prognosis of DN.     

Advanced glycosylated end products and hyperglycemia in the pathogenesis of diabetic complications

Protein alteration resulting from a nonenzymatic reaction between ambient glucose and primary amino groups on proteins to form glycated residues called Amadori products is termed the Maillard reaction. By dehydration and fragmentation reactions, Amadori products are transformed to stable covalent adducts called advanced glycosylation end products (AGEs). In diabetes, accelerated synthesis and tissue deposition of AGEs is proposed as a contributing mechanism in the pathogenesis of clinical complications. Uremia in diabetes is associated with both a high serum level of AGEs and accelerated macro- and microvasculopathy. Diabetic uremic patients accumulate advanced glycosylated end products in "toxic" amounts that are not decreased to normal by hemodialysis or peritoneal dialysis but fall sharply to within the normal range within 8 h of restoration of half-normal glomerular filtration by renal transplantation. It follows that the higher mortality of hemodialysis-treated diabetic patients compared with those given a renal transplant may relate, in part, to persistent AGE toxicity. Pharmacologic prevention of AGE formation is an attractive means of preempting diabetic microvascular complications because it bypasses the necessity of having to attain euglycemia, an often unattainable goal. Pimagidine (aminoguanidine) interferes with nonenzymatic glycosylation and reduces measured AGE levels leading to its investigation as a potential treatment. The mechanism by which pimagidine prevents renal, eye, nerve, and other microvascular complications in animal models of diabetes is under investigation. Separate multicenter clinical trials of pimagidine in type 1 and type 2 diabetes, where proteinuria is attributable to diabetic nephropathy, are in progress. The effect of treatment on the amount of proteinuria, progression of renal insufficiency, and the course of retinopathy will be monitored.     

Risk of chronic renal failure in patients with non-insulin dependent diabetes mellitus with diabetic nephropathy and the stage of permanent proteinuria and arterial hypertension: role of clinical factors

AIM: To reveal prognostic factors which determine the risk of development of chronic renal failure (CRF) in patients with diabetes mellitus (DM) type II associated with diabetic nephropathy (DN) at the stage of continuous proteinuria in combination with arterial hypertension (AH). MATERIAL AND METHODS: A total of 60 AH patients suffering from type II DM with permanent proteinuria were examined. Chronic renal failure was registered in 21 patients. RESULTS: Among CRF patients, more frequent were males, high proteinuria and nephrotic syndrome, IHD, macroangiopathy of the lower limbs, VLDLP. CONCLUSION: Independent predictors of CRF in diabetes mellitus type II with AH and proteinuria were male gender, overweight, faster development of stable proteinuria from the time of diabetes diagnosis.     

Losartan and other angiotensin II antagonists for nephropathy in type 2 diabetes mellitus: a review of the clinical trial evidence

BACKGROUND: End-stage renal disease (ESRD) in patients with type 2 diabetes mellitus (DM) is associated with a bleak prognosis. The life span of patients with DM who have undergone renal transplantation or who are undergoing dialysis is up to 30% shorter than that of individuals in the general population. Preventing or delaying the progression of renal disease from microalbuminuria to nephropathy, and ultimately, to ESRD is thus a crucial goal of DM management. OBJECTIVE: This article reviews the growing worldwide problem of type 2 DM and ESRD, the renoprotective benefits of angiotensin II (AII) antagonists (AIIAs) such as losartan in patients with or without type 1 or 2 DM, potential mechanisms of renoprotection of AIIAs beyond blood pressure (BP) control, and the clinical-practice implications of available megatrials. METHODS: Articles included in this review were identified using a MEDLINE search for English-language studies published between 1990 and 2003 and included the search terms diabetic nephropathy, type 2 diabetes mellitus, microalbuminuria, proteinuria, angiotensin II antagonists, angiotensin-converting enzyme inhibitors, and cardiovascular disease. Articles describing major clinical trials, new data, or new mechanisms pertinent to the management of type 2 DM were selected for review. RESULTS: Currently, AIIAs such as losartan represent the only evidence-based treatment strategy for patients with type 2 DM and proteinuria. The Irbesartan in Patients with Type 2 Diabetes and Microalbuminuria (IRMA-2) study, the Reduction of End Points in Non-Insulin Dependent Diabetes Mellitus with the Angiotensin II Antagonist Losartan (RENAAL) study, and the Irbesartan Type 2 Diabetic Nephropathy Trial (IDNT) indicate that AIIAs postpone the progression of type 2 diabetic renal disease at all stages, ranging from microproteinuria to overt nephropathy and ESRD, RENAAL showed that losartan improves renal outcomes in patients with type 2 DM and nephropathy over and above that attributable to BP control alone. The renoprotective effect of losartan corresponded to an average delay of 2 years in the need for dialysis or kidney transplantation. CONCLUSIONS: AIIAs such as losartan should perhaps be considered mandatory therapy in patients with diabetic nephropathy and should complement existing management strategies, such as reduced dietary protein intake, strict blood glucose control, and standard antihypertensive therapy. Collectively, these measures should improve survival and quality of life and reduce the health care burden of managing patients with diabetic nephropathy.     

Soybeans ameliolate diabetic nephropathy in rats

Diabetic nephropathy is one of the most frequent and serious complications of diabetes mellitus. Soybeans have been shown to reduce urinary albumin excretion and total cholesterol in non-diabetic patients with nephrotic syndrome. However, reports focusing specifically on diabetic nephropathy are scarce and the available results are inconsistent. It was reported that soybean consumption reduced urinary protein excretion in type 1 diabetic patients with diabetic nephropathy, whereas it was found to elicit an increase in urinary protein excretion when soybeans were consumed by type 2 diabetic patients. This study aims to investigate the effects of soybean in diabetic nephropathy, particularly the effects of consuming soybeans on the histopathology of diabetic nephropathy, using aquaporin (AQP) and osteopontin (OPN) expression as diagnostic markers. Male Sprague-Dawley rats were assigned to one of three groups: control, diabetic with red chow diet and diabetic with soybean diet. For histological examination, the expression of OPN and AQP, renal function and hemoglobin A1c were evaluated at the end of the study. Improvements in glomerular and tubulointerstitial lesions were demonstrated in the diabetic rat group given a soybean diet. OPN and AQP expression were suppressed in the kidney specimens of diabetic rats with the soybean diet. In conclusion, soybeans may prevent the weight loss and morphological disruption of the kidney associated with diabetes mellitus. Soybeans also may improve glycemic control. It seems likely that long-term control of blood glucose levels using a soybean diet could prevent the progression of diabetes mellitus, and therefore, nephropathy could be prevented.