8例溶血性尿毒症综合征临床分析

目的探讨溶血性尿毒症综合征（HUS）的临床特点和治疗方法。方法回顾性分析自1997年12月至2007年12月收治的8例HUS患者的临床特点及治疗方法。结果成人7例,儿童1例。诱因为产后3例,呼吸道感染2例,肠道感染1例,呼吸道合并肠道感染1例,无明显诱因1例。8例均表现为溶血性贫血、血小板减少和急性肾衰竭。病情属重型5例,轻型3例。肾损害表现为少尿1例,无尿2例,肉眼血尿3例,高血压8例,水肿6例。8例均采用综合治疗：抗感染、降压等一般治疗;血液透析、改善肾循环、血液灌流、血浆置换、新鲜冰冻血浆输注以及肾上腺皮质激素等。2例治愈,4例好转,2例病情恶化放弃治疗。治疗后血液系统及生化指标均有改善,血红蛋白（Hb）、血小板（PLT）、血肌酐（SCr）、总胆红素（TBIL）、血乳酸脱氢酶（LDH）与治疗前比较,差异有统计学意义（P〈0．05）。结论HUS较罕见,属临床急症,早期诊断、及时正确治疗有助于改善短期预后。     

溶血性尿毒症综合征39例临床分析

溶血性尿毒症综合征 (ＨｅｍｏｌｙｔｉｃＵｒｅｍｉｃＳｙｎｄｒｏｍｅ ,ＨＵＳ)是以伴有红细胞形态异常的急性微血管性溶血性贫血、血小板减少和急性肾衰竭为特征的临床综合征。病情危重 ,死亡率高 ,但如能及早诊治 ,预后大有改观〔1〕,本文回顾性地分析了近 10年来笔者所治ＨＵＳ患者的临床资料和山莨菪碱联合抗凝治疗的疗效 ,对ＨＵＳ的病因、诊断与治疗措施作粗浅的探讨。资料与方法1　临床资料1.1　入选病例的诊断标准　根据溶血性贫血 ,末梢血有破碎红细胞 >2 % ,血小板减少 ,急性肾衰竭 ,Ｃｏｍｂ·ｓ试验阴性以确诊〔1〕。1.2　一…     

溶血性尿毒症综合征的研究进展

溶血性尿毒症综合征是一少见面凶险疾病。是小儿急性肾衰的重要病因，近年本病的研究有较大突破，使病死率明显下降，本文综述近年来在其病因，发病机理以及诊断和治疗方面的研究进展。     

溶血性尿毒症综合征的研究进展

溶血性尿毒症综合征是一少见而凶险疾病 ,是小儿急性肾衰的重要病因 ,近年本病的研究有较大突破 ,使病死率明显下降 ,本文综述近年来在其病因、发病机理以及诊断和治疗方面的研究进展     

溶血性尿毒症综合征的血浆置换治疗

目的；观察血浆置地溶血性尿毒症综合征的治疗效果，方法：对５例明显诊断的溶血性尿毒症综合征病人进行单滤式膜式血浆置换治疗，每次置换冰冻新鲜血浆２５００ｍｌ，平均每倒置换５．２（３－９）次，结果５例病人在血浆置换术后迅速好转，血小板水平显著上升，肌酐水平显著下降。总胆     

氯酸钾致溶血性尿毒症综合征2例报告

溶血性尿毒症综合征是一个临床经过比较凶险、预后较差的疾病〔1〕,它的临床特点是微血管性溶血性贫血、急性肾衰竭和血小板减少三联综合征〔2〕其病因是多方面的〔3〕,现报道 2例 (母和其子 )服用氯酸钾所致的急性溶血性尿毒症综合征。1　病例　　例 1 :患者男性 ,3 4岁 ,因腹痛腹泻 5ｄ ,发热、黄疸、无尿 4ｄ ,于 1 999年 7月 2 9日入院。患者入院前 5ｄ其母误将氯酸钾约 1 0 0 ｇ拌入淀粉中做成凉粉服用。服后出现腹痛、腹泻 ,腹泻为水样便 ,次日出现发热 ,皮肤、巩膜黄染 ,恶心、呕吐 ,呕吐物为咖啡色样胃内容物 ,黑便 ,尿呈酱油色 ,尿…     

溶血性尿毒症综合征的研究进展

溶血性尿毒症综合征（ＨＵＳ）是一种微血管病变性的临床综合征，主要发生于儿童，也可见于年长儿及成人。多种外源性和内源性因素可引发ＨＵＳ，主要的靶器官是肾脏，血栓性微血管病变是其典型的损伤，血管内皮损伤是主要的促进因素。该病发生率虽不高，但死亡率较高，预后差。目前对该病的发病机制尚不明确，而且缺乏有效的治疗手段，有待进一步的研究。     

腹泻相关的溶血性尿毒症综合征的远期预后

目的:由于对腹泻相关的溶血性尿毒症综合征(HUS)患者的远期预后仍有一些不同的看法,为此收集有关的文献进行分析,探讨腹泻相关的HUS的远期预后以及影响预后的各种原因.     

反复发作成人溶血性尿毒症综合征一例

患者：男，30岁。因乏力、恶心、腹痛、解酱油色小便1d入院。患者分别于4年前及1年前出现上述同样症状在外院住院治疗，两次均诊断为急性肾衰竭(ARF)，经血液透析(血透)治疗后，好转出院。     

溶血性尿毒症综合征诊治进展

溶血性尿毒症综合征(hemolytic uremic syndrome,HUS),于1955年首先由Gasser报道.它是一种以微血管性溶血性贫血、血小板减少和急性肾衰竭为临床特点的综合征[1].本文就近年来HUS的病因、诊断及治疗研究进展作一综述.     

溶血尿毒综合征的诊治进展

溶血尿毒综合征(HUS)属于血栓性微血管性疾病。以微血管性溶血性贫血(可找到红细胞碎片)、血小板减少、肾功能损伤为特点。微血栓主要分布于肾脏。感染、多种毒素、抗内皮细胞抗体、药物等因素使内皮损伤是发病的关键。近年来随着对HUS的病因和发病机制有了新的认识,输注血浆和血浆置换是目前治疗HUS最有效的方法,已大大提高了HUS患者的生存率。     

恶性疟合并溶血尿毒综合征的诊疗探讨

目的探讨恶性疟引起的溶血尿毒综合征（HUS）的诊断及治疗要点。 方法对本院2008至2014年13例恶性疟引起的溶血尿毒综合征患者的临床特点、辅助检查及治疗情况进行回顾性分析。 结果入组患者中男性12例,女性1例,年龄22～60岁,均符合恶性疟疾合并溶血尿毒综合征的诊断。其中10例合并脑型疟,1例合并消化道出血,2例出现呼吸循环衰竭。经抗疟原虫治疗、激素治疗、补液对症治疗以及呼吸机、血液透析滤过等,入组的13例患者中1例死亡,1例自动出院,11例治愈出院,其中5例因急性肾功能衰竭行血液透析滤过治疗肾功能恢复,随访11例治愈患者均未出现慢性肾功能损害,2例病例出现再燃。 结论疟疾的早期诊断及治疗,对控制溶血及阻止脏器损害具有重要作用;大剂量长疗程使用蒿甲醚可增强抗疟原虫效果,早期应用激素可有效阻止溶血,减轻肾脏损害,对严重溶血、急性肾功能衰竭病例应及时采取血液透析滤过治疗,以降低病死率。     

Racial incidence of hemolytic uremic syndrome

Hemolytic uremic syndrome (HUS) is the most common cause of acute renal failure in children and is caused by infection with verotoxin-productingEscherichai coli. There is no consensus on the relative incidence of HUS in blacks and whites. An equal racial incidence has been reported by two centers with small black populations. A series from Washington D. C. reported a low incidence in blacks. The population of Alabama is 32% black and 66% white. The Children's Hospital of Alabama admission rate has a similar racial distribution (35% black, 65% white). A record review from 1980–1992 identified 45 patients with HUS; 43 (96%) were white and only 2 (4%) were black. Based on census data for Alabama in 1980 and 1990, this gives an average annual incidence of HUS of 0.45 per 100,000 in whites and of 0.043 per 100,000 in blacks (P<0.001, Fischer's exact test). Similar results were found in the group of patients with HUS and a history of diarrhea; whites 0.39 and blacks 0.02 (P<0.001). However, in those with no history of diarrhea there was no significant racial difference: whites 0.05 and blacks 0.02. There were too few blacks to compare clinical course and outcome. We conclude that typical diarrhea-associated HUS is a relatively rare disease in blacks compared with whites. The reasons are unclear.     

De novo hemolytic uremic syndrome following renal transplantation

We report a case of complete recovery of renal function in a patient with de novo hemolytic uremic syndrome (HUS) following renal transplantation. This 3-year-old girl had none of the factors known to contribute to the development of HUS in transplant recipients. This case illustrates the usefulness of renal biopsy in the accurate diagnosis and management of dysfunction in the allograft following renal transplantation.     

Cardiomyopathy: a late complication of hemolytic uremic syndrome

This report describes a child who presented with classic hemolytic uremic syndrome (HUS) and 4 months later developed a life-threatening but reversible cardiomyopathy with global cardiac dysfunction and a left ventricular ejection fraction of 14%. There was no evidence of electrolyte abnormalities, anemia, hypertension, severe fluid overload, or viral infection. Endomyocardial biopsies were consistent with a dilated cardiomyopathy. This paper highlights the importance of considering the diagnosis of associated cardiomyopathy when presenting with late-onset edema following HUS. Received February 12, 1996; received in revised form and accepted August 22, 1996     

Post-dysenteric hemolytic uremic syndrome in Bulawayo, Zimbabwe

An outbreak of dysentery in Zimbabwe was associated with a high mortality, especially in children who developed hemolytic uremic syndrome (HUS). To examine the causes of high mortality from HUS and to suggest measures that could reduce the case fatality rate, clinical and laboratory features of 91 children with dysentery were reviewed. Of these, 14 developed HUS; their findings were compared with age-matched controls with dysentery only. Persistent alteration of consciousness after rehydration, pallor, and oliguria were early clinical indicators of HUS. Leukocytosis and leukemoid reaction, microhematuria, and non-resolving hyponatremia distinguished children with HUS from those with dysentery. While Shigella dysenteriae type I was responsible for the dysentery outbreak in the community, most stool cultures of children with HUS were negative. Mortality from HUS was high. Late recognition of HUS and a lack of peritoneal dialysis could have contributed to the fatal outcome in some cases. Early recognition of HUS through close observation of children with dysentery and appropriate laboratory investigations with referral to a hospital, where peritoneal dialysis is available, should improve the outcome. Received: 24 August 2000 / Revised: 30 July 2001 / Accepted: 31 July 2001     

Childhood hemolytic uremic syndrome is associated with adolescent-onset diabetes mellitus

Extra-renal manifestations of the hemolytic uremic syndrome in children are well described. Pancreatic involvement may manifest as transient hyperglycemia and permanent diabetes mellitus. Two previous case reports demonstrate short periods of “remission” between initial hyperglycemia and the development of permanent diabetes mellitus. We report an unusual case of a two-year-old Caucasian boy whose HUS-associated hyperglycemia resolved shortly after the acute phase of his illness only to recur as permanent diabetes mellitus at puberty. To our knowledge no other case is reported that demonstrates such a long interval between initial presentation and the development of permanent diabetes mellitus.     

A clinicopathological study of 24 children with hemolytic uremic syndrome

This study reports the pattern of renal injury in 24 North American children with hemolytic uremic syndrome (HUS), and the extent of extrarenal involvement in 9 of these children examined at autopsy. Fifteen of the 24 children were studied during the first 16 days of hospital-ization; their renal specimens demonstrated glomerular thrombotic microangiopathy (TMA) in 8 children, cortical necrosis in 1, and varying degrees of glomerular TMA and cortical necrosis in 6 children. Nine of the children were studied after 16 or more days of hospitalization; these patients had prominent renal arterial lesions. Of 9 children examined at autopsy, extrarenal microthrombi were identified in 8. In 4 children who died during the acute phase of the disease, hemorrhagic colonic necrosis (3 children) and pancreatic islet cell necrosis (2 children) were the principal extrarenal lesions encountered. Rare microthrombi were present in the brains of the 3 children who manifested seizures. Southwest Pediatric Nephrology Study Group (SPNSG Central Office, Baylor University Medical Center, Dallas, Tex. USA). Director: Ronald J. Hogg; Associate Directors: Fred G. Silva, F. Bruder Stapleton; Statistician: Joan S. Reisch; Administrative Assistant: Kaye Green. Participating Centers: Baylor College of Medicine, Houston, Tex., Phillip L. Berry, L. Leighton Hill, David Powell, Edith Hawkins; Baylor University Medical Center, Dallas, Tex., Ronald J. Hogg, Kaye Green; Tulane University Medical Center, New Orleans, La., Frank Boineau, John E. Lewy, Patrick Walker; University of Arkansas, Little Rock, Ark., Watson Arnold, Eileen Ellis, M. Melinda Sanders; University of Colorado Health Science Center, Denver, Colo., Gary M. Lum, William Hammond; University of Oklahoma Medical Center, Oklahoma City, Okla., James Wenzl, Geoffrey Altshuler, Sarah Johnson; University of Tennessee, Memphis, Tenn., F. Bruder Stapleton, Shane Roy, III, Robert J. Wyatt, Charles McKay, William Murphy; University of Texas Southwestern Medical Center, Tex., Billy S. Arant, Jr, Michel Baum, Fred G. Silva, Arthur Weinberg, Craig Argyle, Joseph Rutledge, Ed Eigenbrodt; University of Texas Medical School, Houston, Tex., Susan B. Conley, Jacques Lemire, Ron Portman, Ann Ince, Regina Verani; University of Texas Health Science Center at San Antonio, Tex., Michael foulds, Sudesh Makker, Kanwal Kher, Melanie Sweet, Victor Saldivar, Fermin Tio; University of Texas Medical Branch, Galveston, Tex., Ben H. Brouhard, Alok Kalia, Luther B. Travis, Lisa Hollander, Tito Cavallo, Srinivasan Rajaraman; University of Utah Medical Center, Salt Lake City, Utah, Eileen Brewer, Richard Siegler, Elizabeth Hammond, Theodore Pysher