随着透析技术的成熟,尿毒症不再是难以克服的顽症,接受透析治疗的病人不仅能继续存活,甚至还可以有很好的生活质量。腹膜透析简称腹透,作为肾脏替代治疗的主要手段之一,它是利用人体的腹膜作为透析膜,用高渗腹透液清除体内毒素和水分,从而延长患者的生命。由于腹透技术在中国起步相对较晚,还不为广大医务人员及患者所认识,尤其是对它的认识上还存有某些误区,阻碍了腹透在我国的应用和发展。误区1:腹透不作为第一选择 上世纪七十年代起,血透成为大多数尿毒症患者赖以生存的治疗方式,仅当患者由于内瘘、活动性出血等原因不能行血透时,才会考虑腹膜透析。因此很多人误认为腹透是患者的第二选择。其实不然,除了小部分患者有腹透或血透禁忌症外,大部分患者可以自己选择透析方式。积极参与治疗方式的选择有利于建立患者对治疗的信心和顺应性,提高生存率和生活质量。 目前认为,尽管残存肾功能已经不足以维持患者生命,但它对患者水分清除、营养维持等控制仍有很大作用,因此如何在透析后保护残存肾功能成为肾科领域中的一大课题。已经很明确,在最初2年的透析中,腹透对残余肾功能的保护更为有利,残余肾功能的毁损减缓一半。因而现已被推荐为尿毒症患者肾脏一体化治疗(即血透、腹透和肾移植)的首选。误区2:腹透不能长期进行 由于对腹透认识上的误区或其他非医疗因素的干预,许多腹透患者是在血透失败、全身状况差等万不得已的情况下才选择腹透的,甚至在情况好转后再转为血透。其实腹透同样可以长期进行,国内著名的中山医科大学附属第一医院701例长期随访的患者中,56%的病人技术生存期已超过5年,40%已经超过10年。据报道,日本的腹透患者平均生存率已达8年。潍坊市目前生存最长的腹透患者已达13年。误区3:腹透影响生活学习 上个世纪腹透发展最初阶段,相关技术还欠成熟,需要患者用消毒液清洗透析管道,操作过程较繁琐,容易因污染出现腹膜炎。但目前国内采用的系统是一次性双袋系统,无需消毒液,并大大简化了操作程序,因而也适用于儿童和老年人。由于腹透是在家中进行,操作过程的简化使患者操作时间缩短,许多患者可以进行家务、短途旅行,甚至参加工作。尤其是自动化腹透机的使用,使患者从白天手工透析中解放出来,改为夜间由机器代替操作,这更接近正常人生活,更方便患者重返工作岗位。误区4:腹透会影响肾移植有人认为,腹透治疗和肾移植同在腹腔,腹透治疗会影响今后选择肾移植。有研究显示,肾移植前进行腹透治疗有多方面的好处:腹透操作独立,与血透相比肝炎感染率低,同时贫血程度轻,避免了输血等肝炎病毒感染机会,有利于肾移植后抗排异药的使用;腹透治疗本身或对残肾的保护使移植后新肾脏功能恢复时间缩短;移植的肾脏放在髂窝,在腹膜外,并不影响腹膜透析进行,因此,在等待移植肾恢复工作或移植肾失败情况下均可进行腹透治疗。做腹膜透析一样可以做肾移植,而且成功率甚至优于血透。误区5:腹透不可以性生活晚期尿毒症患者,可出现各种病症,在进行有效的替代治疗如血液透析、腹膜透析和肾移植后,尽管许多症状可以明显减轻甚至消失,但性功能和性生活问题,仍长期困扰着患者。相当部分的患者或配偶,担心、顾虑性生活将加重病情而放弃过性生活。这是一个很大的误区! 肾衰不等于性衰,慢性肾衰患者以及透析或肾移植者,对于性生活,一不要有顾虑,应该努力尝试;二不要过度,应该节制次数,提高质量;三是配偶要支持和宽容。而且腹膜透析者的性生活要相对好一些。误区6:腹膜透析不能洗澡,生活不便 腹膜透析病人在开始的2周内可以在有保护措施下洗澡,而半年以后甚至可以在无保护措施下洗澡。误区7:腹膜透析容易发生腹膜感染 随着腹膜透析技术的提高和产品的改进,腹膜炎的发生率已经很低。据相关医学文献统计,每个腹膜透析病人平均4年左右才发生一次腹膜炎,在经济和环境卫生好的国家和地区甚至可以做到6年以上才发生一次腹膜炎。而且随着药物和医疗技术的不断发展,腹膜炎已经不是什么可怕的感染了。 误区8:腹膜透析效果不如血液透析事实上不是这样,腹透患者早期(1-3年)的生存率要高于血透,5年生存率和血透相似,腹膜透析患者的生活质量也远远好于血液透析。
一、避免感染:如感冒、咳嗽、嗓子痛、拉肚子等,这都是感染,感染会明显加重病情,因此,要尽力避免,若一旦感冒或感染,以服用中药制剂为好,如复方大青叶合剂、感冒冲剂、双黄连口服液等,抗生素可服用罗红霉素,先锋霉素4号等,若较重,请及时到医院就诊治疗。 二、休息、避免劳累:这一点很重要,因为劳累(包括劳力、劳神和房劳)会降低机体免疫力,加重病情,因此需要休息,但也无必要卧床休息,可从事一般活动及轻体力,以不感疲劳为度。 三、饮食注意:1、低盐饮食:若有水肿或高血压应低盐饮食,每日3克为宜,约一汤匙,但不要求无盐饮食,若无水肿和高血压,可以普通饮食或偏淡一点儿。2、低蛋白饮食:减少豆类、肉类、蛋、奶等摄入,可减轻肾脏负荷及损害,每日每公斤体重0.6克为宜,但操作起来有一定困难,可 以“比平素吃的少一些”为标准进行掌握,但不能禁蛋白饮食。3、低嘌呤饮食:这样可减少尿酸的产生,减轻肾脏损害,应少吃海鲜、动物内脏等,不喝啤酒及白酒。4、高钙饮食:肾病病人往往呈现低钙状态,尤其是用强的松的病人,可多吃点儿脆骨、虾皮,多喝牛奶等。5、若是糖尿病病人:应少吃甜食,饮食总量亦应控制。6、若高血钾:禁吃桔子、香蕉、红枣、土豆、藕、磨菇、海带、紫菜等。7、若低血钾:应多吃上述食物。8、猪腰子,即猪肾,吃这个对肾病并无帮助,所谓“以脏补脏”并无科学道理,再者,动物的肾脏中往往含有水银、铅、铬等重金属,对肾脏有害。 四、禁用、慎用以下药物:1、解热镇痛药:禁用!如去痛片、阿司匹林、安乃近、扑热息痛、速效伤风胶囊、感冒通、康泰克等。2、非甾体抗炎药:禁用!如扶他林、布洛芬,芬必得、消炎痛、炎痛喜康等。3、肾毒性抗生素:(1)、氨基甙抗生素:严禁应用!!!如庆大霉素、链霉素、卡那霉素、丁胺卡那霉素、小诺霉素、西梭霉素等。(2)、磺胺类:禁用!如复方新诺明、磺胺嘧啶等。(3)、喹诺酮类:慎用、少用!如诺氟沙星、氧氟沙星、左氧氟沙星、环丙沙星等。(4)、 其它:万古霉素,慎用。4、血浆代用品:禁用!如低分子右旋糖酐、706代血浆。5、渗透性利尿剂:禁用!如甘露醇、甘油果糖。6、静脉输注的各类氨基酸:禁用!。7、慎用或禁用某些中药:(1)单味药:关木通、雷公藤(生药)、广防己(木防己)、青木香、马兜铃、朱砂莲、厚朴、细辛、寻骨风、天仙藤、青风藤、鱼胆、猪苦胆,雄黄、苍耳子、草乌、益母草、天麻、斑蝥、蜈蚣、望江南子、麝香等。(2)成药:龙胆泻肝丸、妇科分清丸、导赤丸、排石冲剂、八正合剂、甘露消毒丹、金砂五淋丸、桔核丸(上述8种成药含关木通); 舒筋活血丸,玄珠狼疮丸(上述2种成药含广防己);冠心苏合丸、纯阳正气丸、十香返生丸(上述3种成药含青木香);止咳化痰丸、二十五味松石丸(上述2种成药含马兜玲)。其他还有:耳聋丸、朱砂安神丸、跌打丸、大黄清胃丸、小儿金丹片、分清五淋丸、安阳精制膏等。(3)成方:防已黄芪汤、当归四逆加吴茱萸生姜汤。 8、避免接触下列重金属:汞、锂、镉及金制剂。 五、及时复查:肾病,往往症状、体征比较少,不能单凭自我感觉来判断病情的轻、重,好转、恶化或是否痊愈,或是否复发,只有进行相应的检查后进行综合分析,才能进行准确判断,因此定期或不定期复查很有必要,以免在不知不觉中病情逐渐进展,导致严重后果。
西医所说的“肾”与中医所说的“肾”是有很大区别的,而肾炎与“肾虚”更是两码事。西医里的肾,是指人的造尿器官,左右各一个。肾炎则是指两侧肾脏非化脓性免疫介导的炎性病变,病人可以有乏力、腰痛、水肿、高血压、血尿、泡沫尿、尿液中有蛋白、红细胞、管型等,也有相当一部分病人平常并没有什么不适感觉。肾炎可发生于任何年龄阶段的人,但以青年男性多见,常见原因为在劳累,抵抗力低下的基础上,发生感染而引起,部分病人发病原因及诱因不明确。肾炎患者绝大部分呈现慢性过程。而中医里的“肾”,则是人的五脏之一,其功能有藏精、主水液、主骨生髓、主纳气等六七种之多。“肾虚”,是指肾脏精气亏损的病理现象,可由禀赋不足或肾精耗损太过所致,临床表现多见精神倦怠、乏力、眩晕、耳鸣、健忘、腰痛、腰酸、遗精、阳痿、出汗、手足发凉或手足心发热等。因此,肾炎和“肾虚”完全是两码事儿,没什么关系。从西医角度看,肾脏与性方面是没有直接关系的,但是,患肾炎期间,要适当休息,包括性生活的适当节制。肾炎痊愈了,不会影响性生活的。
肾病和糖尿病、高血压、早期肿瘤等疾病一样,很多患者往往没有症状,没有不良感觉,甚至还和健康人一样正常的工作、学习和生活,但实际上肾病已经存在,病变正在活动和进展,甚至已相当严重,这时如果不能及时发现、及时治疗,往往会造成严重的后果。作为肾科医生所见到的这样的例子实在太多了!非常令人心痛!它使很多家庭陷入巨大的痛苦和困境中!现列举3例这样的病人,介绍如下,供您参考,以使您对此有所认识、有所裨益,也参示于亲友,防患于未然。例一、×××,女,中年,个体,面黄,乏力已2年,到某医院检查有贫血,但未找出具体原因,用多种治贫血药,无效,后出现恶心、呕吐,又怀疑患有胃病,遍做上消钡透、胃镜及螺旋CT等均未发现异常,后到一家大医院就诊考虑为血液系统疾病,抽骨髓检查,也正常,再后偶碰到一位肾科大夫才看出是肾病,但一查肌酐已609.32umol/L,达肾功衰竭期,而现已达尿毒症期。食欲不振、恶心、呕吐是尿毒症最常见的表现,当有这些症状时,尤其是顽固不愈者一定要查一查肾脏。例二、×××,男,青年,某局干部,发现高血压5年,无水肿、腰痛等,5年来一直当原发性高血压(即高血压病)治疗,未曾查尿,后出现乏力、恶心,到某医院就诊,疑为肝病,查B超、肝功等未发现异常,后疑肾病,查肾功示肌酐达2600umol/L,已到尿毒症期,当年做了肾移植。现患者一般情况还算可以,但被移植后昂贵的药费压得喘不过气来,更担心的是未来什么时侯会发生排斥?非常后悔在5年的高血压期间未发现是肾脏的问题,而且这期间还用过肾毒药物。例三、×××,男,老年,某医院职工,高血压已8年,一直当原发性高血压(即高血压病)治疗,效果不好,于2年前才发现是肾不好,但也没正规治疗,从3个月前病人出现乏力、恶心、腰痛、耳聋,一查肌酐已达206.3umol/L,双肾也已明显萎缩,血压仍没有完全控制。发现高血压要想到有可能是肾的问题,应该查查尿常规、肾功能及双肾B超,若是肾的问题就应尽早正规系统的治疗。 从以上我们可以了解到,当身体出现不适时一定要重视,要警惕,因为有可能存在发生病变的危险,当出现一些肾病线索症状时就要想到有可能是肾病,要及早请专科医生诊断明白,并要早期、正规、系统的治疗,这样才能取得好的效果。早期发现肾病的7大线索症状是:1、乏力,易疲劳(这是一个很常见,但极易被忽视的肾病早期症状);2、腰酸、腰痛、腿酸; 3、眼皮、双下肢浮肿; 4、尿中有泡沫或尿红;5、高血压;6、恶心、呕吐、纳差、上腹不适;7、贫血。 第1-5个提示肾炎,第5-7个提示肾功能不全。若有上述情况最好到医院查一查,以排除肾病。(尊重患者起见,文中隐去其真实姓名、年龄、单位等)。
Radix and Rhizoma Rhei (RR) has the effect of alleviating hypertrophy of kidney and lowering the hyperfiltration of glomeruli.The authors treated 32 cases of early stage diabetic nephropathy by adding RR to the routine treatment and good effect was obtained.The study is reporte as follows. METHODSClinical Materials Sixty-two in-patients of the authors’ hospital hospitalized from Oct.1992 to Oct.1994 were enrolled and divided randomly into RR group and control group.Among the 30 cases in the control group 9 were male and 21 female,aged 20~75 years,with history of diabetes mellitus (DM) of 12 months to 9.4 years,5.3 years in average,and histort of diabetic nephropathy (DN) of 4.5 months to 9.4years,4.8 years in average,4 cases among them were insulin dependent and 26 cases were non-insulin dependent.In the 32 patients of the RR group,8 were male and 24 female,their age ranging from 21 to 75 years,with DM history of 14 months to 9.5 years,5.6 years in average, DN history of 3.9 ,months to 9.5 years,5.0 years in average,4 were insulin dependent and 28 non-insulin dependent. All the patients fit in with the following diagnostic standard :(1) Having DM history definitely or with fasting blood glucose level>7.8 mmol/L or/and with blood glucose level>11.1 mmol/L for once only is enough (The diagnostic standard of DM stipulated by the World Health Organization,1980).(2) With diffuse enlargement of bilateral kidney by B-ultrasonic scanning,creatinine clearance rate>120 ml/min,or postkinetic urinary microalbumin excretion increase,or persistene micro-albuminuria.(3) With proteinuria examination showing negative result and renal function normal.Treatment Hypoglycemic agent was given to both groups by administering 2.5~10mg of euglucan twice every day,and regular insulin injections were given to 13 cases (6 cases in the control group and 7 in the RR group) subcutaneously 3 times per day (12 u in the morning,8 u at noon and 12 u at evening) before meals.The following drugs were withdrawn: hypolipemic agent,diuretic,kidney protecting drug,angiotensinase inhibitor and β-receptor blocking agent.To the RR group,the RR in powder form was given additionally,5g each time twice a day,orally with warm water.Parameters of Observation The following parameters were observed before and after 3 months of treatment.(1) Size of bilateral kidney estimated by B-ultrasonic scanning (average value of 3 times of examination). (2) Creatinine clearance rate (CCr) by calculating from creatinine levels in blood and urea,with the formula:CCr(ml/min) = 24 h Urea creatinine (mmol/L) ──────────────× 694 Blood creatinine (μmol/L)(3) Urea microalbumin (UMA) excretion and β2-microglobulin (β2-mG) determined with radioimmunoassay.(4) 24 h urea protein determined by sulfosalicylic acid-sodium sulfate turbidimetric analysis.Statistical AnalysisData were dealt by homogeneity test of variance, and comparison of effects between groups was analysed with t-test. Table.Changes in Parameters of the Two Groups (x±s)Group Size of Kidney CCr UMA Ureaβ2-mG Urea Protein ──────── ────── ───── ────── ───── (Length×Width,cm) (ml/min) (μg/min) (mg/L) (g/24h) Control Pre-t. 13.68±1.25×7.51±0.72 152.83±8.35 58.26±43.00 1.67±0.07 0.45±0.13(30) Post-t 13.46±1.25×7.52±0.73 145.00±8.19 54.30±38.20 1.69±0.07 0.42±0.13 RR Pre-t. 13.57±1.26×7.46±0.70 152.91±8.38 58.17±43.40 1.71±0.06 0.44±0.14(32) Post-t. 11.84±1.49×5.64±0.65﹡ 112.85±5.82﹡﹡ 20.35±13.80 ﹡﹡ 1.62±0.06 0.33±0.07﹡﹡Notes:* P﹤0.05,﹡﹡P﹤0.01,compared with pre-treatment and post-treatment of the control group; the numeral in bracket is the number of casesRESULTS As shown in the table,before treatment,the parameters of the two groups were not different significantly (P﹥0.05). After treatment,in the RR group,the CCr got lowered,the enlarged kidney shrunken and the urea protein excretion reduced. Compared with before treatment or with the control group, the differences were significant (P﹤0.05 or 0.01).However,the change of ureaβ2-mG excretion after treatment in the RR group was insignificant (P﹥0.05).DISCUSSION Since XU Xi-yan,et al applied RR,in the 60’s,on the basis of supporting body resistance in treating azotemia with definite effectiveness,other researchers have found that good effect could also be reached by applying RR without inducing diarrhea (Zhejiang Journal of TCM 1982;17(5):212), suggesting that RR might realize its effect through other way than inducing diarrhea.Recent researches showed that RR could lower the hyper-filtration of glomeruli, inhibit markedly the proliferation of mesenteric cells,and be of an antagonistic effect against some cellular factors such as interleukin-6.It is shown,therefore, that RR could influence the pathogenic mechanism of nephropathy in different aspects. RR has been affirmed by the 4 th session of National Conference of Nephropathy as an important medicine for delaying progress of chronic renal failure.Based on the above-mentioned effects of RR, the authors used RR in treatment of early stage DN,and results showed that its curative effect was markedly superior to that of medicines used for the control group.In the RR group, the urea protein significantly decreased,CCr lowered and enlarged kidney shrank in different degrees,while in the control group these changes were not evident. Judging from this,we can say RR acts mainly on the mesenteric tissue of glomeruli, the proliferation of which (mesenteric cells and stroma) plays a very important role in pathogenesis of glomerulosclerosis.RR could inhibit the proliferation of mesenteric tissue, and suppress the effects of auto-,para- and intra-cellular secretion of some cellular factors (particularly the sclerotic factor) on glomeruli, so as to alleviate the glomerulosclerosis, and delay the process of kidney damage. Sinceβ2-mG is filtrated by glomeruli, and absorbed at proximal tubule, its excretion in urea would be increased when there is injury of proximal tubule, and so it is recognized as a sensitive criterion indicating damage of proximal tubules. After treatment, theβ2-mG level of the two groups were similar, without significant difference, suggesting that the influence of RR on proximal tubule of early stage DN patients was truly not much.In the therapeutic course, there were 3 cases in the RR group who manifested mild diarrhea after taking RR .Among them, 1 case had a history of chronic colitis, no special treatment was appoied to them, and the therapy was not affected by the diarrhea.CJIM 1997,3:222-223.
Hydroxyethyl Starch (HES) commonly is widely used as plasma volume expander. They are often used preoperatively and in cases of hypovolemia.But they may have side effects on renal function [Kumle et al. 1999].Dehne et al.[1997] reported that HES infusion to intensive care patients could increase excretion of specific tubular proteins such as alpha1-microglobulin,Tamm-horsfall-protein and brush border enzyme acetyl-beta-glucosaminidase.Animal studies have also shown severe alterations of the proximal tubules after haemodilution with HES[standl et al 1996]. Therefore HES should not be used to treat hypovolemia in Idiopathic nephritic syndrome(INS),though it may be an effective fluid for resuscitation of hypovolemic patients[Palumbo et al 2006].There are few reported cases of HES–induced acute renal failure (ARF) in fluid management of INS patients or acutely ill patients [Adrienne et al .2001, Ding et al. 2003,wang et al. 1996]. We report a 73-year-old woman with mesangioproliferative glomerulonephritis associated reversible ARF with acute tubulointerstitial nephritis(AIN) caused by HES.Case Report A 73-year-old female patient was admitted to hospital because of moderate periorbital and pretibial edema, on October 12, 2007. with no evidence of fatigue ,loin pain, gross hematuria, skin rash or fever. The urine output was 950-1600ml/day. The patient had no history of upper respiratory infection, chronic kidney disease, hypertension, gout ,diabetes or ischemic heart disease. physical examination: Bp 190/100mmHg, T 36.70c, Laboratory findings: WBC 5.5-2.8×103/mm3 ,7% eosinophils,RBC 3.87×106/mm3,hemoglobin 120g/L, Plateletst 226×103/mm3, Na139 mmol/L ,K3.7 mmol/L ,CL 100 mmol/L ,Ca 1.91 mmol/L , P1.31 mmol/L ,ALT 25IU/L,albumin 28.1g/L,CH 8.06 mmol/L,Tg 4.56 mmol/L,HDL 1.76 mmol/L,LDL 4.71mmol/L,blood sugar 4.2mmol/L,BUN 5.3mmol/L,creatinine 115 umol/L, The C3-level was 500g/L and C4-level 130g/L. ASOimmunoglobulins ,ANA, anti-DNA, antiglomerular basement membrane antibodies, ANCA, cryoglobulins, circulating immune complexes, hepatitis B and C viruses ,HIV antibodies were either normal or negative. Urinalysis revealed 4+protein and 1+blood. Proteinuria ranged from 4.37 to 6.0g/daily and renal ultrasound demonstrated mildly enlarged kidneys.ECG findings showed normal sinusal rhythm,chest x-ray was found normal. There was no diabetic retinopathy. The diagnosis of INS was made and treatment was started with Prednisone ,Tripterygium, Heparin, Dipyridamole, Furosemide and other symptomatic supportive treatment. On the 10th day after admission, HES (500ml of 6% HES were infused once daily ) was added to the previous regimen to treat the intractable hypovolemia, because of hypoproteinemia persisted.On the 14th day ademission,she was noted to have a rising BUN and serum creatinine concentration and she suffered from progressive oliguria. The urine output decreased from normal levels to 250-200ml/day which was associated with rapidly deteriorating renal function. In the following 3 days, creatinine rose to 586umol/l and BUN to 29.5mmol/L.HES-induced ARF was suspected and HES was stopped. She was treated for ARF by hemodialysis and diuretic therapy.At this time a renal biopsy was performed showing a mild diffuse mesangioproliferative glomerulonephritis with moderate interstitial edema containing a severe inflammatory cell infiltrate composed of lymphocytes, monocytes,neutrophils and eosinophils as well as variable tubular ectasia.No acute tubular necrosis was observed. In a few glomeruli synechia and mild epithelial cell proliferation were seen. The blood vessels were normal. No sclerotic glomerular changes were observed.Immunofluorescence showed deposits of IgG, IgM and C3 in the mesangium and in the capillary walles. Thus, the histopathological diagnosis was mesangioproliferative GN with tubulointerstitial changes resembling acute tubulointerstitial nephritis. ARF with severe tubulointerstitial changes secondary to HES was diagnosed and the original kidney disease was associated to be mesangioproliferative glomerulonephritis. She was treatment with methylprednisolone 0.5g/day for 3 consecutive days. The treatment was continued with Prednisone orally 60mg/day,combinaed with hemodialysis,diuretics and other symptomatic treatment. There was no worsening of the renal function,and subsequently renal function recovered fully. She was discharged and after 6 months of follow-up had a serum creatinine of 112umol/L ,proteinuria had declined to 0.18g/day and she is now doing well.Discussion ARF in patients with NS is a rare and serious complication that has numerous causes.The most common of them are severe hypovolemia ,interstitial edema ,tubularobstruction,altered glomerular permeability and drugs. Although the relationship between HES and ARF appears established by well-documented cases, only a few HES -associated ARF cases have been reported so far [Adrienne et al. 2001, Ding et al .2003,wang et al. 1996]. HES-indused ARF is more frequently among older people, particularly in patients with preexisting renal failure,glomerulosclerosis or diabetes. The highest risk for HES-induced ARF exists during the first 10 days of treatment or when the HES dose is increased[Ding et al. 2003]. The most common clinical presentation of HES-induced ARF is progressive oliguria .Although some of the cases are mild with some patients even fully recovered after the treatment ,HES-induced ARF may be severe and sometimes fatal. in our patient, the renal function and laboratory values were normal during the 10 days before HES infusion and oliguric renal failure developed immediately after exposure to HES. At this same time, the patient was on no other nephrotoxic drugs and had been hemodynamically stable throughout her hospital stay. Therefore,a causal relationship between HES and ARF was considered. Our patient’s renal function was corrected to normal values while other authors reported that in most cases renal function did not recover fully and that there was a progress to end-stage renal failure. Some patient also died from complications related to persistent severe ARF. Li et al.[2004]found that 8 of 13 patients with ARF secondary to HES experienced a progress to end- stage renal disease. Recently, another paper reported an association between HES-induced ARF and prognosis. Five patients with HES-induced ARF were reported : only in 1 of the patients renal function returned to normal,whereas in 4 patients the renal function did not recover and progressed from acute to chronic renal failure. Moreover, this study has confirmed by renal biopsy that the pathology in patients with ARF due to HES is an osmotic hephropathy [Ding et al .2003].Concerning the prognosis, Severely persistent oliguria, elevated serum creatinine and multiple organ failure are frequentily associated with a poor prognosis[Ding et al. 2003,wang et al .1996] Our patient did neither suffer from acute tubular necrosis nor from osmotic nephropathy, but from acute tubulointerstitial nephritis which is in accordance with previously previously reported cases of ARF-induced HES [Li et al.2004]. In conclusion,this case suggests that a patient poisoned with HES may have the typical features of oliguric ARF. At should be considered, as a very severe reaction. The mechanism of ARF is not fully understood. Some authors have suggested that possible pathophysiological causes for such a development are most likely to be found in an increased permeability of the glomerular basal lamina[ Waldhausen P,et al 1991]. Whereas other studies have shown that the pathological Substrate of ARF due to HES is an osmotic nephrosis [Ding et al. 2003] or osmotic nephrosis-like lesions[suttner et al. 2004],our findings suggest that an immune disease due to a hapten induced by HES may be a possible factor in the pathogenesis of ARF. Therefore, it is important for clinicians to bear in mind the possibility of ARF due to HES and it has been proposed that ,whenever possible, HES should not be used in INS patients to avoid severe complications.ReferencesKumle B, Boldt J, Piper S, Schmidt C, Suttner S, Salopek S 1999 The influence of different intravascular volume replacement regimens on renal function in the elderly. Anesth Analg. 89:1124-1130Dehne MG, Mühling J, Sablotzki A, Papke G, Kuntzsch U, Hempelmann G 1997 Effect of hydroxyethyl starch solution on kidney function in surgical intensive care patients.Anasthesiol Intensivmed Notfallmed Schmerzther. 32:348-354Standl T, Lipfert B, Reeker W, Schulte am Esch J, Lorke DE 1996 Acute effects of complete blood exchange with ultra-purified hemoglobin solution or hydroxyethyl starch on liver and kidney in the animal model. Anasthesiol Intensivmed Notfallmed Schmerzther. 31:354-361Palumbo D, Servillo G, D'Amato L, Volpe ML, Capogrosso G, De Robertis E, Piazza O, Tufano R 2006 The effects of hydroxyethyl starch solution in critically ill patients.Minerva Anestesiol. 72:655-664Adrienne De Labarthe MD, Frédéric Jacobs MD, Franois Blot MD, and Denis Glotz MD2001 Acute renal failure secondary to hydroxyethylstarch administration in a surgical patient. The American Journal of Medicine, 111: 417-418Ding. A.H, Zhang. A P, Wang .YX,Tu .XW 2003 pathologic characteristics in patients with acute renal failure due to Hydroxyethyl starch. Chinese Journal of Nephrol 19: 285Wang. F.A, Wang. JQ 1996 Clinical analysis of 6 patients with acute renal failure caused by Hydroxyethyl starch. Acta Aacademiae Medical Qingdao Universitatis 32:135Li,H.Y, Zhang.H, Cao. W.L, Guo.Q, Wu.C.L 2004 Clinical analysis of 13 patients with acute renal failure caused by Hydroxyethyl starch. Clinical focus 16:39-40Waldhausen P, Kiesewetter H, Leipnitz G, Scielny J, Jung F, Bambauer R, von Blohn G1991 Hydroxyethyl starch-induced transient renal failure in preexisting glomerular damage. Acta Med Austriaca 18 Suppl 1:52-55Suttner S, Boldt J 2004 Anasthesiol Intensivmed Notfallmed Schmerzther. Volume replacement with hydroxyethyl starch: is there an influence on kidney function? 39:71-77.Clin Nephrol, 2009,71:329-332.
银屑病是一种多基因遗传背景下的T细胞异常的免疫性疾病[1],可以合并肾脏损害[2-3],其临床表现和病理类型多种多样[4-23],我院近6年以来收治4例,现报告如下:一.一般资料4例病人均为我院从2000年4月至2007年3月以肾病就诊的住院治疗患者,2例为男性,2例为女性,年龄最大者为58岁,最小者为17岁,平均35.75岁。二.皮肤损害4例患者在肾脏病发病前均在多家医院诊断为银屑病,银屑病病史分别为7年,15年,20年和11年,平均13.25年,住院期间又经我院皮肤科会诊进一步确认诊断,4例均为寻常型,其中3例为稳定期,1例为活动期,病史7年至28年,平均18年,均服过多种中西药物及偏方,均未服过激素、环孢素(ScA)、甲氨蝶呤(MTX)等。三.肾脏病变肾脏发病时间为15天至4年,平均12.5个月,3例表现为肾病综合征(NS),1例表现为无症状性镜下血尿和蛋白尿(AHAP),其中3例经肾活检确诊病理诊断,4例病人均有镜下血尿,无肉眼血尿,24小时尿蛋白定量平均为3.65克/d,1例血压升高,3例血压正常,抗“O”均正常,1例血沉增快,免疫球蛋白、补体、抗核抗体、抗中性粒细胞胞浆抗体等均无异常,具体临床资料见表1。表1 4例银屑病合并肾病患者临床资料 诊断 性别 年龄 银屑病史 肾病病程 尿蛋白 血尿 水肿 血压 Scr Ccr B超 (岁)(年)(月) (g/d)(BLD)(mmHg)(umol/L)(ml/min)例1 NS 男 31 7 48 3.89+++有145/100 96.7 88.51 正常例2 NS 女 32 15 0.5 5.5 +~++ 有 120/78 89.0 75.49 肾饱满例3 NS 女 5820 1 4.02 ++ 有 130/85 57.4 100.76 正常例4 AHAP男 22 11 0.3 1.18 +++无 120/80 103.5 87.78 正常注:AHAP:无症状性镜下血尿和蛋白尿四.肾脏病理 本组病人除例3拒绝进行肾活检外,余例均进行肾穿刺活检行病理检查,2例NS患者中1例为IgA肾病(IgAN),1例为早期膜性肾病(MN),AHAP患者为系膜增生性肾炎(MsPGN),3例患者病理表现详见表2。五.治疗情况 3例肾活检者均在住院后一周内进行。例1至例3病人均给予强的松,低分子肝素,虫草制剂,潘生丁,速尿等处理,其中例2在治疗第16天时尿蛋白转阴,尿潜血减少,余2例NS患者在足量激素治疗8周后尿蛋白也明显减少,例3在治疗第10周时尿蛋白转阴,例1尿蛋白一直未转阴,此3例NS病人在治疗半年时尿潜血一直存在。例4给予强的松40mg,每日1次,雷公藤多甙40mg,每天3次,治疗3周时尿蛋白转阴,尿潜血也减少但一直存在,偶尔转阴。所有病例均未予CsA、骁悉、爱若华等新免疫抑制剂。表2 3例银屑病合并肾病患者病理资料全球硬化 系膜 内皮C 上皮C GMB 嗜复蛋白 新月体小管间质 炎C浸润 IgG IgA IgM C3 C1qFRA1 2/17 中度增生- - - 可见 - 灶状萎缩 轻纤 大量 - + +++ + - -2 无 无 - - 增厚 可见 - - - - - + - + + ± -4 无 中度增生 - - - 可见 - 灶状萎缩 轻纤 可见 - + + + - ± -注:GMB:肾小球基底膜 FRA:纤维蛋白原相关抗原六.讨论 近年来银屑病合并肾损的报道越来越多,临床上也确能时常见到这样的病人,现已认识到银屑病是一种具有多基因遗传背景的T细胞异常的免疫性疾病[1],和肾脏病的发病具有相关性,均是通过免疫机制异常而介导[4],其临床表现可为NS,慢性肾炎综合征,AHAP,慢性肾衰等,其病理类型呈多样性,从文献报道来看,常见3型,最常见者为IgAN[4-9],其次为肾淀粉样变性[10-12],当然,银屑病合并淀粉样肾者85%为关节炎型,考虑与关节炎继发淀粉样变有关[12],再次为MN[13-15],其它尚可见局灶节段性硬化[16],微小病变[17,18],MsPGN[19],膜增生性肾炎[20],局灶增生性肾炎[21],新月体肾炎[22],脂蛋白肾病[23]等,但均为零星报道。 本组4例病人中3例行肾活检,病理诊断明确,治疗也收到较好的效果,4例病人有如下特点:(1).性别差异不明显:一般认为银屑病合并肾损者多见于男性青壮年,女性相对少见,但本组病人男女例数相等。(2).病理类型多样性:3例活检者分别为3种病理类型,虽然例数少,但和文献报道有一致性。病理改变也相对较轻,全球硬化不多见,无新月体、血管病变及明显广泛的小管间质病变等。(3).两病发生相关联:4例病人肾脏病变均发生于银屑病之后,且两者病情波动呈一定相关性,其中例1曾有单独治疗银屑病好转后肾病也好转的病史,另外,从病史、临床表现及肾脏病理结果看未找到其它引起肾病的证据,尤其是药物性肾损,故可以认为两者发病有相关联,存在类似的免疫异常机制[4]。(4).激素、CTX、雷公藤多甙等治疗效果尚可:这可能和本组病人病理改变较轻有关。 治疗银屑病的常用药物如MTX、非甾体抗炎药、CsA等均可引起肾损[24],但本组病人均未服用上述药物,故可排除,部分治疗银屑病的中药如雄黄、石膏、麦饭石等均含砷,具有一定肾毒性,从本组病人病理结果看也未发现中药肾损证据。参 考 文 献1. 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Lipoprotein glomerulopathy associated with psoriasis vulgasis: Report of 2 cases with apolipoprotein E 3/3. AM J Kidney Dis, 2003,42:1-6.24. Heuvels J, Maximus A, Bosmans J L, et al. Renal abnormalities in psoriatic patients: a review. Nephron, 1999,82:1-6.中国中西医结合皮肤性病学杂志, 2008, 7 : 214-216.
[摘要] 一位65岁老年,男性患者,患高血压病15年,近服依那普利后出现急性肾功能衰竭(ARF),活检证实为急性间质性肾炎(AIN),虽经血透、激素及其它对症支持治疗,但终死于严重并发症。经查病人无肾动脉狭窄、肾脏血管炎、心衰、低容量,未合用利尿剂及肾毒性药物(非甾体抗炎药、环孢素A(CsA)、甘露醇等),也没有基础肾病。经文献检索,依那普利致AIN国外仅见一例报道,致急性肾小管坏死(ATN)也仅见一例报道,其它依那普利致ARF之报道均没有病理证实。依那普利致AIN在国内尚未见报道。临床上应用广泛的依那普利能引起如此严重的肾脏副作用,理应引起我们的高度重视。[关键词] 马来酸依那普利;急性肾功能衰竭;急性间质性肾炎ACEI是临床上高血压和慢性肾病的常用治疗药物,但它可以在没有基础肾病、肾动脉狭窄、肾脏血管炎、心衰、低容量、未合用利尿剂及肾毒性药物(非甾体抗炎药、环孢素A、甘露醇等)的情况下发生严重的肾脏方面副作用[1-10]。我们遇到一例高血压病人因服用依那普利后发生急性肾衰(ARF)的患者,经活检证实为急性间质性肾炎(AIN),经激素、血液透析(HD)、利尿、抗感染及其它对症支持处理,虽肾功能有明显好转,但终死于严重并发症。现报告如下,以引起肾内科医师,心内科医师,神经内科医师的高度重视。病例介绍:患者,男,65岁,以上腹部疼痛,恶心,呕吐 5天于2008年1月13日入院。患者入院前5天服依那普利(扬子江药业集团生产)10mg,次日又服2次,每次10mg,血压由平素140/90mmHg降至120/60mmHg,当天晚上,病人出现上腹疼痛不适,并恶心,但未呕吐,第3天发现眼睑面部浮肿,同时出现尿少,此后的2-3天中尿量“很少”,约50-100ml/天,(但具体量不详),上腹疼痛加重,并出现呕吐,村医测血压已升至 160/90 mmHg,同时发现双侧大腿出现点状散在斑丘疹,无瘙痒感,无发热及关节痛。收住我院消化科,在查大生化时发现血肌酐(SCr)达1413umol/L,以ARF转入我科治疗。患者既往有高血压病15年,最高达200/100mmHg,但平素控制在140/90mmHg左右,并患有颈椎病,腰椎管狭窄症。此前无感染、外伤、及其它用药史,无糖尿病、冠心病史及肾病史。服依那普利前未曾查尿。查 体:T:36.5OC,BP:190/105mmHg,轻度贫血貌,双眼睑浮肿,睑结膜轻苍白,唇色白,咽无充血,扁桃体无肿大,双肺呼吸音清,未闻及干湿性罗音,心界不大,心率82次/分,律齐,各瓣膜听诊区未闻及明显病理性杂音。上腹部无明显压痛,腹水征(±),肝脾未触及,双肾区无叩痛,双下肢中度凹陷性浮肿。辅助检查:尿RT:PRO+++,BLD++,WBC 10-15/HP,尿β2-MG 2226(100-300ug/L),尿中嗜酸性粒细胞未能检测。血RT:RBC2.66*1012/L,HB93g/L,WBC4.68* 109/L,嗜酸性粒细胞百分比2.1%(0.5-5%),嗜酸性粒细胞绝对值0.1(0.05-0.5*109/L),PLT 302* 109/L。血生化:SCr1413umol/L,尿素氮(BUN)26.4 mmol/L ,UA483 umol/L, Na134 mmol/L,钙2.06mmol/L ,磷2.04 mmol/L,FBS 5.1 mmol/L, ALB 33.9 /L,ALT37U/L,AST26U/L,ALP217 U/L,血淀粉酶78U/L,尿淀粉酶15U(0-100U/L)。凝血六项均正常;免疫球蛋白:IgG 5.63g/L(8-16), IgA 1.01g/L(0.7-3.3), IgM 0.93g/L(0.5-2.2),C3 1.10g/L(0.8-1.6),C4 0.43g/L(0.1-0.4), CH50 80U/ml(50-100),ANA、ds-DNA、抗SM、多肽抗体谱、HAV-IgM、乙肝五项、HCVAb-IgG、HEVAb-IgG、HIV、ANCA、出血热抗体等均阴性或正常;PTH54.37 ng/L(15-65)。EKG正常;X片示肺部感染,双侧少量胸水;CT示双侧少量胸水,少量心包积液,肺部感染。B超提示:左右肾大小为11.6*6.2*6.4及10.4*6.8*6.5cm3 ,包膜光整,形态饱满,实质回声弥漫性增强,CDFI血流信号减少。初步诊断:1.ARF-AIN;2.高血压肾病?;3.高血压病(2级,中危);4.肺部感染(轻度)。治疗及其结果:入院后先行HD,应用袢利尿剂,抗生素及对症支持处理:速尿、头孢曲松、丹参注射液、奥美拉唑、施维舒、促红素、铁剂、止血敏、邦亭、能量合剂、脂肪乳等。患者入院后第1天尿量“0”ml。发病第1-6天(此天数为发病天数,非住院天数,下同)尿极少,每天约10-50ml,第7至40天尿量渐增多,波动于80-520ml之间。患者发病第15天,(入院第9天)在B超引导下行肾穿刺活检术,用18G穿刺针,穿出3条肾组织,其病理结果(济南军区总医院做)如下:共9个肾小球,全球硬化1个,未硬化肾小球细胞数90个左右,见系膜区轻度增宽,系膜基质轻度增多,系膜细胞 2-5个。毛细血管腔开放,内皮细胞和上皮细未见增生,基膜未见增厚。Masson染色下未见嗜复红蛋白质沉积。小球无粘连,未见新月体。肾小管无明显萎缩,间质水肿,可见炎细胞浸润。部分小管管腔中可见蛋白质管型。间质血管壁未见明显异常。免疫荧光:IgG,IgA,IgM,C3,C1q, FRA 均未见沉积。病理诊断:1.系膜增生性肾小球病变(轻度).2.急性肾小管间质病变。病理结果提示为急性肾间质肾炎,具体见附图。在加强HD及其它处理的情况下给予甲基强的松龙(MP)80 mg/天,静滴治疗,共用8天后,改至40mg,用18天,后渐减至24mg/天,用7天后,渐停掉。患者第34天时出现所插股静脉管处感染,出现菌血症,血培养为大肠埃希菌生长。第41天至第59天尿量增至600-900ml之间。第56天时病人自述全身难受,喘憋明显,表情呆滞,极少言语,坐卧不安,时哭泣,时胡言乱语,时呈极痛苦状,在排除心肺脑等实质病变后,考虑合并有反应性精神病,予以氯丙嗪、黛力新等治疗,但效果不理想。第60天至61天,此2天时间里尿量超过1000ml/天,达1140-1020ml,但此时患者极度抑郁,也呈现出明显衰竭状态。共计HD 21次,间断应用利尿剂,用MP 33天(80mg*8天,40mg*18天,24mg*7天),抗生素一直应用,其中泰能用5天,未出现霉菌感染,但感染也未能控制,终因全身衰竭明显,于第63天死亡。讨 论:ACEI在高血压的治疗中发挥着重要作用[11-12],而且对延缓慢性肾脏病的进展有肯定性作用[13] ,但我们也知道此类药物可引起一些少见但严重的肾脏副作用[1-10],其中包括引起MN大量蛋白尿,低醛固酮血症性高血钾,可逆性或不可逆性急性肾衰[1-10,14-15]。又知ACEI也可发生过敏反应[5,12,15-16]。有报道卡托普利可引起过敏性间质性肾炎,出现发热,斑丘疹,嗜酸性粒细胞增高和Coomb’s阳性溶血性贫血[15-16]。而依那普利则可引起皮疹和血管N性水肿 [12]及急性间质性肾炎[4],但依那普利致严重肾损害,经病理证实为AIN、急性肾小管坏死(ATN)者,在国内尚未见报道,在一组36例药物性AIN中也没有依那普利引起者[17],国内著名AIN研究学者在谈到药物性AIN时,也未提及依那普利的肾毒性问题[18-20]。我们这例病人从整个病史,临床表现,其中包括出现皮疹,B超像(双肾增大、饱满),病理结果等来看,符合AIN改变, 虽有轻度系膜细胞及系膜基质的增生,但病人无嗜复红蛋白沉积,免疫荧光全部阴性,因此,可排除系膜增生性肾小球肾炎。65岁老年人,在9个肾小球中出现一个硬化的小球,而又无相对更多的节段性或全球硬化,无小球粘连,无间质纤维化,无小管萎缩,无血管透明样改变等,出现一个硬化的小球可视为正常退行性改变,因此也可排除慢性肾衰(CRF)或/和高血压肾病引起的CRF。病人服药后急性发病,突然少尿,肾脏饱满增大,ARF诊断明确,病理未提示新月体性肾炎、ATN及血管炎改变。故三者均可排除。那么就只有一种情况可解释整个病情,就是AIN,虽然病理上没有见到非常典型的AIN的表现:间质明显水肿,大量炎细胞的浸润和不同程度的肾小管上皮细胞肿胀,变性等,但我们仍考虑为AIN诊断,间质无明显水肿其可能的原因之一就是病人在肾活检前4小时进行了一次HD,脱水达4kg,从而导致肾间质水肿减轻;谌氏在谈到药物性,感染性,特发性AIN这3种急性AIN的鉴别诊断时认为,虽然很不可靠,但其诊断主要依靠病史及肾外表现(如有无药物过敏表现)[19],再结合病人有用药史,皮疹,无感染表现,可排除感染性和特发性AIN,故可诊断为药物性AIN。依那普利致AIN的机理为:1.血流动力学改变:研究显示ACEI能刺激前列腺素分泌,在低容量时和应用利尿剂时能进一步降低肾小球滤过率(GFR)[2,11-12]。但病人平素血压控制在140/90mmHg左右,用药后为120/60mmHg,应该不会引起严重的血流动力学改变及如此严重的长时间的少尿期。虽开始以胃肠症状为主,但呕吐量很少,因体液丢失而致肾前性ARF的可能性不存在,既使存在也是极次要的,因此血流动力学明显改变而致ARF不能解释其ARF的原因。2.AIN:可引起典型的AIN[4]。此例病人虽没有“发热,皮疹,关节痛”,三联症, 嗜酸粒细胞也不高,但毕竟药物性AIN具有上述典型“三联症”表现的也只有15%[21]。 国内学者也谈到在14例药物性AIN患者中,无一例具备发热,皮疹,嗜酸粒细胞升高者[20]。而且病理已证实其主要改变为间质病变。另外,轻度系膜增生在此并没有什么特别的意义。也有报道药物性AIN可有系膜增生表现[22]。3.ATN:国外有学者报到依那普利可致ATN,但不排除合用之CsA因素的影响[23],本例已排除此种情况。因此,我们认为该患者是依那普利过敏引起的AIN-ARF。关于药物性AIN其治疗主要是对症支持治疗,可以用激素,有HD指征时应HD[17].其肾功能大都可以恢复[24]。依那普利应用十分广泛,所致ARF理应引起我们的高度重视。国外的一组913例死亡病人分析中,有75例曾因用依那普利后出现BUN或SCr较用药前升高达50%及以上水平,其中因严重肾功损害而死亡者竟有10例,其危险因素有:老年患者、大剂量应用、有潜在肾病、用储钾利尿剂、合用非甾体抗炎药等[25]。我们这例病人虽经积极治疗,从尿量看已走出少尿期,肾功能有所好转。但因发生严重的反应性精神病,不进饮食,又合并插管处感染引起败血症,终至严重的全身衰竭状态而死亡,未直接死于ARF,而是死于ARF的严重并发症,殊为遗憾。就其死因笔者认为与下列因素有关:1.ARF严重且长时间未能恢复:这是基础死因,也是产生并发症的重要基础,病人发病前6天基本无尿,经治疗2个月时尿量才超过1000ml/天,此时已有多种严重并发症产生,而且,透前病人的SCr也在600umol/L-700umol/L之间这样一个较高的水平。2.反应性精神病:病人性格内向,病情长时间得不到缓解,肉体和心灵的双重痛苦,使病人顾虑重重,花费又大等等,导致出现反应性精神病,到后期病人极度抑郁,不言语,不进任何饮食,综观整个病情,笔者认位这是导致病人死亡的第一直接因素。3.严重感染:股静脉插管处感染,应用抗生素未能控制,又带管透析5次后才拔管,处理欠及时,血培养为大肠埃希菌生长,虽应用三代头孢类抗生素及泰能等,但终未能完全控制感染,也是病人死亡的一个重要因素。4.药物刺激:病人非过敏体质,素也无胃疾,但发病后用多种药物如止血敏,邦亭等出现明显胃肠反应,考虑和SCr较高也有一定关系。5.全身衰竭:这是上述四种因素共同作用的结果,最后致呼吸循环衰竭而死亡。参 考 文 献[1] Donker AJM. 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12月5日,潍坊市中医院成功医治一名重症肾衰竭病人。患者小武遭遇肾脏“罢工”半个月,致使一直处于“无尿”状态而痛苦异常。医生冒险查明原因,对症施治用大剂量药物将其“激活”,患者小武的肾脏重新开工,身体逐步恢复正常。 小武家在临沂市沂水县,今年27岁,长年在青岛即墨打工。 今年9月份,他因一场车祸创击头部,出现脑出血,经治疗痊愈。出院之后,小武又出现发热、恶心呕吐、腹痛等症状,随后出现腰痛、腿肿、尿量少,最后发展到停止排出小便,发热、腹痛更加明显,并出现明显腹胀。焦急的家人把小武送入当地医院,但是由于小武病症复杂,病情急迫,医生给予迅速转院的通知。 随后,小武又被辗转送入潍坊市中医院。该院肾病科赵洪军医师为小武接诊检查之后,发现他血液的肌酐水平达到了900多,明确了小武患的是重症急性肾衰竭,此时肾脏基本不工作了,不能排毒和排水,到此时小武的肾脏“罢工”时间已超过一周,在临床上这种情况往往结果难以预料。 面对小武焦急的家人,赵洪军医师制定了首先给予血液透析疗法缓解急症,然后进行肾穿刺进一步明确病因,再给予对症治疗的方案。但是这个治疗方案在实施当中,让医生颇感压力,小武车祸造成过脑出血病史,而透析治疗需要的肝素会诱发再次脑出血,非常危险,若不用肝素,血液易凝固,阻塞透析管路,达不到透析效果。另一方面肾穿刺是在肾脏处于严重的发炎状态下,凝血不好,很容易产生手术后尿血、肾包膜下血肿及腰痛等并发症,在临床上属于高危检查,所以医生对小武的治疗如履薄冰,小心翼翼。 经过逐步探查和增减用量,为小武找到了最合适的肝素用量,让他首先顺利通过了血液透析这一关,整体症状开始缓解。但是小武肾脏仍处于“罢工”状态,24小时排尿量不足20毫升,处于典型的临床无尿状态。在这种状态下一周时间之后,赵洪军医师感觉时机较好了,为小武进行肾穿刺,令人欣慰的是,穿刺手术非常成功,病因得到明确—小武所患是急性间质性肾炎。发炎的肾脏把肾小管挤压变形,导致肾小管处于“关闭抑郁”的状态,所以完全排不出尿液。 根据这一明确的诊断结果,医生采取了将其“激活”的治疗方案,采用大剂量的激素冲击治疗,结果显示这一方案切合病症,在应用激素冲击治疗的次日,当天的尿量即超过了100ml,从临床标准上,开始使病人走出了无尿期,肾病的专业的俗语说“急性肾衰竭,尿液贵如油”,确实,看到了尿,就看到了希望,说明遭破坏的肾脏正在修复中,经过一周之后的观察,小武排尿量逐日增加,恢复到每日500毫升以上,再经过一段时间治疗就能康复出院了。(赵长林)(转载于http://www.wfszyy.com/yyreview.asp?id=1987)
自2002年慢性肾脏病临床实践指南提出慢性肾脏病(chronic kidney disease,CKD)概念、分期及评估方法以来,CKD已广泛接受和应用。随之,对CKD的流行病学也进行了大量工作。美国和澳大利亚等国报道成人CKD发病率超过10%左右,而我国虽然目前仍无严格流行病学方法的调查,但从已发表的数据看,其发病率与上述两国相似,成人中CKD发病率为10%左右。终末期肾病占CKD总数的1%。由于CKD患者数量巨大,ESRD人数也明显上升。庞大的患者数以及终身治疗的需要,给医疗系统和社会带来了沉重的负担。美国的数据显示,在2001年有超过40万的ESRD患者,治疗费用超过230亿美元;预计到2010年患者数上升为65万,总治疗费用也必将随之上升。 ESRD的替代治疗包括腹膜透析(腹透)、血液透析(血透)和肾移植。由于肾移植受到肾源等限制,目前透析仍是ESRD患者最主要的治疗手段。自20世纪70年代末以来腹透已经有了很大的发展,尤其在亚洲发展良好。上海透析登记系统的数据显示,2006年腹透患者数为1999年的近3倍;透析患者中腹透比例也从1999年的16%增长到2006年的20%;治疗率约为51.5/百万人。越南在2004年底时全国仅一家腹透中心,患者数也十分有限,但到了2007年底全国腹透患者数已达到700余例。印度、泰国及我国台湾的腹透发展情况也相似,尤其是泰国制定了“PD First(腹透优先)”的政策,预示了腹透广泛应用的前景。腹膜透析生存率改善 随着治疗技术不断发展和改进,腹透患者的生活质量不断提高、预后不断改善、生存率不断提高。Heaf等对丹麦透析患者登记系统的4921例患者的数据分析结果显示,腹透患者与血透患者预后相当,尤其在刚进入透析的前两年,腹透患者有明显的生存优势。Mehrotra等回顾分析了USRDS的数据,发现1996-1997年腹透患者1年的病死率为17.2%,到2002-2003年则下降到14.0%,而同期血透的病死率维持在22%~23%。美国USRDS最新的2007年度报告显示,近20年来腹透患者的生存率不断提升,血透患者的生存率则没有显著变化。腹透患者开始透析后90d、第1、2、3年的生存率已超过血透患者,而5年和10年的生存率与血透非常接近,并有超越的趋势。有意思的是,Rumpsfeld等对澳大利亚和新西兰透析患者登记系统3702例新腹透患者的单因素和多因素Cox比例分析结果显示,亚裔人腹透病死率分别比白种人低36%和32%,其差异均有统计学意义。这种差异的原因仍不清楚,是否与生活习惯及体质量有关,仍需更多的资料加以证实。 PD患者满意度调查显示,其对治疗的满意度和向他人推荐该治疗的意愿也较高。Barendse等在英国对140例连续性非卧床腹膜透析(CAPD)患者进行满意度调查,结果显示总体满意度、治疗中不适感和向他人推荐该治疗的意愿的评分均优于血透。Juergensen等对腹透和血透患者进行的生活质量评估业得到相似的结果,腹透患者的总体影响、家庭生活、独立等方面的生活质量评分均优于血透患者。残余肾功能是透析患者病死率的重要预测因子,保护残余肾功能对改善生存率起着至关重要的作用。大量的队列研究和随机对照研究显示腹透患者中残余肾功能的保护对患者生存率有显著影响,残存肾GFR每提高5-10L周-1. (1.73m2)-1可降低11%-47%的病死率。除了改善生存率外,残余肾功能对于透析患者还有众多的临床益处,包括提高透析充分性、保留肾脏内分泌功能、加强中分子物质(如β2微球蛋白等)清除,以及改善容量负荷、血压、微炎性反应状态、高磷血症和营养状态等诸多方面。残余肾功能与患者的生活质量也有显著关系,NECOSAD研究中,使用了SF-36和KD-QOL量表评估了患者的生活质量,多元线性模型显示,随着残肾GFR的增加,SF-36和KD-QOL各领域的评分也显著上升。证据表明腹透较血透能更好地保护残肾功能,血透患者残肾功能的下降速率比腹透患者快24%-80%。Pecoits-Filho等对文献进行回顾分析结果显示,残肾功能降低可引起体液超负荷,加重慢性全身性炎性反应,从而提高了腹透患者病死率和并发症发生率。 腹透技术的提高也是患者生存率提高的重要因素。Mehrotra等报道,从1996年到2003年,持续性腹透患者的比例从62.8%上升到67.2%,转到血透的患者从12.7%下降到11.6%;腹透的导管事件(移除导管、更换腹透导管、更换为血透导管、更换为血管移植物)的发生率低于血透患者的导管事件(移除导管、更换导管、更换为血管移植物),而同期患者的病死率也不断下降。此外,腹透置管技术的发展也提高了技术生存率。Carbtree等采用新型腹腔镜技术(包括腹直肌鞘隧道、选择性预防性网膜固定术和选择性预防性粘连松解术),在200例患者中成功率为99.5%,仅1例患者发生导管机械性梗阻,而2年的导管存活率也接近100%.腹膜透析相关感染率下降 腹膜炎是腹透的主要并发症之一,也是导致腹透技术失败的主要原因之一。随着腹透技术不断改进,尤其是双联双袋的广泛使用,腹膜炎发生率在近年来有了明显的下降。日本平均腹膜炎发生率约为1例/53.3患者月,少数为1例/74患者月。越南的腹膜炎发生率从1997年的1例/20患者月下降到近期的1例/30-60患者月。Brown等报道,过去25年间澳大利亚腹膜炎发生率从6.5/患者年下降到0.35例/患者年。Perez-Fontan等回顾性分析了18年间693个感染性腹膜炎事件,腹透患者腹膜炎发生率呈逐年下降趋势,18年里下降超过了50%,而且期间腹膜炎引起的死亡占所有腹透相关死亡的比例低于5%。我国也与其他国家一样,腹透感染率已显著下降,腹膜炎发生率约为1例/40-50患者月,少数单位已达到1例/60患者月。 USRDS2007年的数据显示,感染引起的住院率在血透和腹透患者中有明显的不同,近15年来腹透患者透析相关的感染(腹膜炎)住院率呈显著下降的趋势,而血透患者透析相关的感染(血管通路)的住院率显著上升,并已超过腹透;腹透因肺炎引起的住院率始终低于血透,而与肾移植相似;腹透因菌血症或败血症引起的住院率也低于血透,但略高于肾移植。 多个研究表明,腹透的丙肝发生率低于血透。Akpolat等对透析前丙肝抗体检测阴性的患者经透析治疗1年后丙肝病毒感染的情况进行了观察,发现201例血透患者中有17%出现丙肝抗体阳性,而在286例腹透患者中只有近6%出现。香港2006年的资料显示,CAPD患者丙肝抗体阳性发生率为1.8%,而血透患者为16.4%。Johnson等对亚太10个国家和地区的患者登记系统的共201 590例患者(血透173 788例,腹透27 802例)进行分析,发现丙肝病毒抗体阳性的发生率在腹透和血透患者中分别为0.7%和18.1%,治疗期间腹透患者新发丙肝病毒抗体阳性率低于血透患者(危害比0.3,95%可信区间0.13-0.75),并认为不同的透析模式可以显著影响丙肝病毒的感染。未来展望 腹透作为肾替代治疗的方式用于临床已历经了30余年,目前传统腹透液在患者超滤、营养代谢,尤其是糖代谢的纠正和心血管并发症防治等方面还有一些问题需要解决,新型腹透液的问世能有助于进一步提高疗效和改善患者预后。艾考糊精腹透液以大分子的艾考糊精作为渗透剂,不易被腹膜吸收,能有效维持胶体渗透压,在腹透患者中能较好地改善超滤、改善左心功能、增加中小分子毒素清除、改善技术生存率。在无尿ESRD患者中,艾考糊精腹透液联合APD治疗2年的生存率约78%。与葡萄糖腹透液比较,艾考糊精腹透液能降低胰岛素抵抗和碳水化合物的吸收,有助于改善糖代谢。在中国进行的双盲、随机对照注册临床试验中,艾考糊精腹透液能显著增加夜间长程留腹超滤量,在腹膜平衡试验高转运、高平均转运甚至低平均转运的患者中尤为显著,同时也能增加小分子毒素的清除、降低血钠和血氯水平。这些结果与以往国外报道的研究结果基本一致。 为了进一步阐明腹膜透析在肾替代治疗中的作用,优化治疗方案,相关的多中心随机对照研究也在开展,如IMPENDIA研究观察不同腹透液组合对糖尿病CAPD患者代谢的影响。此外,腹透与血透在生存率方面的差异也存在较多争论,有幸的是国内也即将开展一项随机、对照、多中心的大型研究,为临床决策提供更多的偱证依据。我们对这些研究的结果拭目以待。(摘自中华肾脏病杂志,2009年第3期;作者,北京协和医院 副院长 肾内科主任 李学旺;专致谢意)。