二磷酸果糖注射液致急性高磷血症及肾功能衰竭19例文献分析

目的探讨注射用二磷酸果糖（FDP）致高磷血症诱发急性肾功能衰竭的发病机理，为临床合理应用FDP提供借鉴。方法回顾《中国期刊全文数据库》1999-2006年国内医学期刊报道的18例个案和作者所在医院的1例个案，对患者性别、年龄、用药情况及发生不良反应的时间及原因进行统计分析。结果19例患者血磷明显升高，出现了急性肾功能衰竭及多系统损害。结论二磷酸果糖可引发高磷血症导致急性肾功能衰竭及多系统损害，老年患者尤应加以关注。     

阿昔洛韦致急性肾功能衰竭3例分析及文献复习

目的探讨阿昔洛韦致急性肾功能衰竭(ARF)的临床特征。方法报道3例阿昔洛韦诱导的ARF的临床表现,实验室检查及肾组织活检结果,并对相关文献进行复习。结果①3例均为中年患者,平均年龄51.6岁,2例患者在用药24h内起病;②临床表现不典型,仅1例以少尿为主要表现,2例伴有明显的腰痛,3例均无蛋白尿和镜下血尿;平均血肌酐水平385μmol/L;③3例均行肾图检查,均提示C段排泄延缓,1例肾组织活检提示部分肾小管扩张,肾小管内可见晶体样物质,伴肾间质明显水肿。④全部患者均予以利尿、护肾等常规对症处理,肾功能于3~11d内完全缓解。结论阿昔洛韦导致的ARF以肾小管内梗阻为主要病理机制,腰痛是其突出的临床特征,患者多呈良性经过,预后佳,规范用药是预防的重要措施。     

扩容利尿剂致原发性肾病综合征肾小管间质损害分析

在原发性肾病综合征治疗中,常因药物原因引起肾小管间质损害致急性肾功能衰竭.临床上因肾病综合征高度水肿常应用扩容利尿剂,有时因应用不当引起肾小管间质损害造成急性肾功能衰竭.利尿剂引起的肾损害有时非常隐匿,易被临床医师忽略,而不合理用药更易发生肾损害,应引起临床医师注意.     

急性胰腺炎合并肾脏损害研究

目的 :探讨急性胰腺炎与肾脏损害的关系。方法 :对 14 8例急性胰腺炎中出现 4 9例肾脏损害的发病机理、临床表现、预后进行分析。结果 :水肿型急性胰腺炎肾脏损害发生率 5 88% (5 / 85 ) ,重症急性胰腺炎肾脏损害发生率 74 2 4 % (49/ 6 6 )。水肿型胰腺炎肾损害治疗 7～ 10天肾功能完全恢复正常 ,重症胰腺炎所致肾损害 4例发生急性肾衰 ,2例经血液透析治愈 ,2例死亡 ,另有 3例重症胰腺炎死于休克及多器官功能衰竭。结论 :急性胰腺炎合并肾脏损害的机理主要是休克 ,胰酶的激活 ,免疫复合物的损伤 ,内毒素的积蓄及局部因素。肾脏损伤的临床表现轻重不一 ,为氮质血症、肾小管功能障碍、急性肾功能衰竭。肾脏的病变与急性胰腺炎的严重程度有关。     

100例急性肾功能衰竭临床分析

目的探讨分析急性肾功能衰竭患者的临床特点及治疗。方法回顾性分析2008年1月至2010年1月来五大连池市第一人民医院就诊的100例透析治疗的急性肾功能衰竭患者的临床资料。结果 100例中肾前性20例,肾实质性63例,肾后性17例;70例患者进行了血液透析;治愈率79例,未愈率9例,病死率12例。结论肾实质性急性肾功能衰竭占首位,透析可降低急性肾功能衰竭的病死率。     

药物引起急性肾功能衰竭36例临床分析

目的:对36例药物引起急性肾功能衰竭进行分析。方法:对36例药物引起急性肾功能衰竭病人的用药种类、肾损害的临床特点及其治疗转归等方面进行分析。结果:36例药物引起急性肾功能衰竭患者,经停用肾损害药物。并给予护肾、支持、激素、透析等治疗后,患者临床症状消失,尿常规及肾功能恢复正常。结论:药物引起急性肾功能衰竭,经积极治疗后可以恢复正常。     

宫颈癌术后放射治疗期间合并急性肾功能衰竭1例的护理

急性肾功能衰竭（ARF）是指各种病因导致的肾功能急骤减退,以肾小球滤过率明显降低所致的进行性氮质血症,以及肾小管功能障碍所致的水、电解质、酸碱平衡紊乱为临床表现的一组综合征[1]。我科2009年7月出现1例盆腔肿瘤引起的急性尿路梗阻致急性肾功能衰竭,经采取积极有效的救治和护理措施,患者康复出院,现将护理体会报道如下。     

急性胰腺炎并发急性肾功能衰竭

自1956年Lucke描述急性胰腺炎可致“下肾单位肾病”以来,已报告了近30例患者发生此现象。急性胰腺炎发生急性肾功能衰竭者,常由剖腹术、胃肠道出血或休克所致。因循环虚脱而产生急性肾小管或肾皮质坏死,致使出现急性肾功能衰竭。有的患者因麻醉药对肾脏有毒性作用,引起急性肾功能衰竭。     

超声气压弹道碎石术治疗上尿路结石梗阻致急性肾功能衰竭36例疗效观察与护理体会

目的探讨输尿管镜、经皮肾镜超声气压弹道碎石术治疗上尿路结石梗阻致急性肾功能衰竭的治疗与护理体会。方法对36例上尿路结石梗阻致急性肾功能衰竭的患者进行综合分析。结果B超、腹部平片(KUB)、CT等检查明确诊断,采取输尿管镜、经皮肾镜超声气压弹道碎石术解除梗阻,全部患者急性肾功能衰竭症状消失或明显减轻,血尿素氮(BUN)、肌酐(Cr)恢复正常或明显降低。结论对上尿路结石梗阻致急性肾功能衰竭的患者及早解除梗阻,做好术前、术后积极的护理配合,是挽救肾功能的关键。     

本院24例抗生素等药物致肾毒性损害的回顾性分析

目的观察抗生素等药物致肾毒性损害的临床表现及病理改变。方法对2008年10月至2011年10月我院收治的24例临床诊断为药物性肾损害并发肾功能不全的病历资料进行回顾性分析。结果本组导致肾损害的药物主要包括抗生素、非甾体类抗炎药、抗肿瘤药物、免疫抑制剂。本组24例肾损害患者发生急性肾功能衰竭18例,病理诊断显示急性肾小管坏死12例,急性间质性肾炎6例,治疗后15例愈合出院,3例转为慢性肾损害;6例发生慢性肾功能衰竭,病理诊断显示慢性间质性肾炎,死亡1例,余缓解后出院。结论应用肾毒性药物时要注意用药的剂量、疗程、患者的年龄及生理状态,内科并发症也是用药的重要考虑因素,应用肾毒性药物期间要注意监测患者的尿常规及肾功能变化,及早发现并干预病情发展。     

东菱克栓酶联合二磷酸果糖治疗急性脑梗死

目的;观察东菱克栓酶(DF 521)联合二磷酸果糖(FDP)治疗急性脑梗死的疗效与安全性.方法;80例脑梗死患者随机分为治疗组与对照组各40例.治疗组;用DF 521,首剂10 BU,第3天及第5天再分别用5 BU,总剂量20 BU,静脉滴注;FDP 50 mL•d 1,静脉滴注,qd,共用10 d.对照组;用右旋糖酐40注射液500 mL内加丹参注射液20 mL•d 1,静脉滴注,qd,共用14 d.结果;治疗组总有效率92.5%,显效率70.0%,对照组总有效率70.0%,显效率37.5%.结论;DF 521联合FDP治疗急性脑梗死疗效显著,用药过程中未见出血等明显副作用.     

血必净对脓毒症大鼠肾脏细胞凋亡及相关蛋白表达的影响

目的 探讨早期应用血必净对脓毒症导致急性肾损伤后肾小管细胞凋亡的影响,及凋亡相关蛋白Bcl-2和Bax表达的变化。方法 54只SD大鼠,♂,随机分为假手术组、脓毒症组、血必净组,每组18只;各组再分为3个亚组,每组6只。根据实验要求分别以术后12,24,48 h作为时间观察点,在各时间点检测大鼠的血液生化指标,测定肾脏血流、并留取肾脏组织观察病理学变化,测定肾小管损伤评分,采用原位末端标记法测定肾小管凋亡细胞,并计算积分光密度值（IOD）。采用免疫印迹法测定Bcl-2、Bax的变化。结果 血必净组能明显改善肾功能,稳定血流动力学,减轻组织病理学变化,减少肾小管细胞凋亡,肾小管损伤评分和IOD值与脓毒症组相比有显著差异（P<0.01）。同时,血必净组能升高Bcl-2的表达,抑制Bax的表达,保持Bcl-2/Bax的平衡,与脓毒症组相比有显著差异（P<0.01）。结论 早期应用血必净可以减少肾小管细胞在脓毒症进程中的凋亡,改善脓毒症导致急性肾损伤的病理学改变,保持Bcl-2/Bax的平衡,减轻脓毒症导致的肾损伤。     

Renoprotective effect of trolox against ischaemia-reperfusion injury in rats

1. Although alpha-tocopherol has been shown to improve renal function following ischaemia-reperfusion (I/R) injury, its clinical use is not common because alpha-tocopherol requires several days of pretreatment to exhibit anti-oxidative benefits. The advent of trolox, a water-soluble analogue of alpha-tocopherol, has raised the possibility that this compound may function more rapidly during acute oxidative stress than the conventional alpha-tocopherol. 2. The present study was undertaken to determine the effects of the short-term administration of trolox on renal excretory function following I/R in rats. 3. Male Wistar rats were subjected to 45 min unilateral renal artery occlusion followed by 120 min reperfusion. The control I/R group was subjected to I/R and received saline as an intravenous bolus (2 mL/kg) followed by a continuous infusion of 2 mL/kg per h starting 30 min before ischaemia, whereas the three trolox-treated I/R groups were given an i.v. bolus of trolox (2.5 mg/kg) followed by a continuous infusion (12 mg/kg per h) starting at 30 min before ischaemia, 5 min before reperfusion and 5 min after reperfusion, respectively. Renal function, malondialdehyde, glutathione and histopathology were evaluated. 4. Ischaemia-reperfusion produced a significant deterioration of renal function, which was accompanied by an elevated malondialdehyde and depleted glutathione content. Kidneys from control I/R rats demonstrated tubular cell transformation, brush border loss, vacuolation, cast formation and tubular obstruction. These changes were attenuated by trolox treatment, with the best improvement achieved when trolox was delivered 5 min before reperfusion. 5. The results demonstrate the renoprotective effects of the short-term administration of trolox on I/R injury. These findings indicate the ability of trolox to overcome a major drawback of using alpha-tocopherol and suggest that trolox may offer a therapeutic advantage over alpha-tocopherol in acute ischaemic renal failure settings.     

Recent advances and developments in the treatment of acute renal failure

Acute renal failure is commonly encountered in contemporary medical practice. The most severe form of acute renal failure is often referred to as acute tubular necrosis (ATN). The ATN syndrome results in loss of most kidney function for a period of several days to a few weeks. The current mortality rate of ATN is ~ 50% and has not changed significantly in recent decades. Most ATN results from either ischaemic or nephrotoxic damage to the kidney. Subsequently, either apoptosis or necrosis results in death of renal tubular epithelium and loss of most renal function. This review will focus on several patents that exhibit diverse strategies to prevent, attenuate or hasten recovery from ATN.     

内科常用药物相关的急性肾衰竭

药源性急性肾衰竭（DARF）是指药物引起的以急性水、电解质紊乱和酸碱平衡失调及氮质血症为主要特征的一组临床综合征。DARF是一种常见的药源性疾病，约占肾实质性急性肾衰竭的19％～40％。其临床特点是在用药数日或数周内出现少尿或非少尿型ARF，部分患者可同时出现药疹、药物热、贫血、肝功能损害、神经系统损害等表现。DARF最常见的临床病理类型有急性肾小管坏死、急性间质性肾炎。DARF的发病机制主要为药物引起肾血流动力学改变导致肾灌注量减少、对肾小管细胞的毒性作用导致急性肾小管坏死、免疫反应导致急性间质性肾炎、药物结晶沉积导致管腔阻塞或免疫介导的肾小球肾炎等。DARF的相关危险因素包括药物的肾毒性作用、剂量、疗程，以及患者的机体状态如：高龄、血容量不足、糖尿病、既往肾损害或肾功能不全等。DARF的常见致病药物有抗生素、非甾体抗炎药、利尿剂及某些中药等。本文重点介绍内科常用的心血管系统药物、消化系统药物及抗病毒药导致DARF的临床特点及其防治。     

URODILATIN (INN: ULARITIDE) AS A NEW DRUG FOR THE THERAPY OF ACUTE RENAL FAILURE FOLLOWING CARDIAC SURGERY

1. Acute renal failure is a severe complication following major cardiac surgery. 2. The effects of urodilatin were evaluated in a randomized, double-blind trial in patients suffering from incipient acute renal failure following cardiac surgery. 3. In the urodilatin group (n= 7) acute renal failure was reverted, whereas in the placebo group (n= 7) six patients had to be haemofiltered or haemodialysed (P < 0.005). 4. Urodilatin induced a rapid onset of diuresis in contrast to placebo-treated patients, who remained oliguric. 5. In the placebo group four of seven patients died while still on haemodialysis (mortality rate 57.1 %) during a postoperative follow-up period of 60 days, while all patients treated with urodilatin survived. 6. On the basis of these results it would appear that urodilatin is an effective drug for the treatment of incipient oliguric acute renal failure following cardiac surgery and for avoiding haemodialysis/haemoflltration.     

急性坏死性胰腺炎时肾机能障碍机制的探讨

目的：为明确急性坏死性胰腺炎（ａｃｕｔｅｎｅｃｒｏｔｉｃｐａｎｃｒｅａｔｉｔｉｓ．ＡＮＰ）与急性肾功能衰竭（ａｃｕｔｅｒｅｎａｌｆａｉｌｕｒｅ．ＡＲＦ）的关系。方法：在大鼠急性胰腺炎模型上分别取血及胰、肾组织检查，测定血肌酐、内毒素、内皮素及肿瘤坏死因子。结果：提示急性坏死胰腺炎时上述各项指标明显增高，与对照组相比有统计学差异（Ｐ＜０．０５），且与组织坏死严重度相平行。结论：急性胰腺炎时内毒素、肿瘤坏死因子、内皮素的升高与急性肾功能衰竭有密切关系。     

Contrast medium-induced nephropathy: strategies for prevention

Contrast medium-induced nephropathy (CIN) is the third leading cause of acute renal failure in hospitalized patients. The exact mechanism by which contrast media induce renal failure is complex and not completely understood. Alteration in renal hemodynamics and direct toxicity to tubular cells have been proposed. The most important risk factor for development of CIN is preexisting renal insufficiency. Identification of patients with risk factors for development of CIN is essential, as measures for prevention of CIN can be instituted. Administration of fluids such as sodium chloride has been the traditional cornerstone of preventive therapy. Alkalization of tubular fluid with intravenous sodium bicarbonate has dramatically reduced the frequency of CIN in patients with baseline impaired renal function. Based on available evidence, use of sodium bicarbonate constitutes the most reliable and effective option. Prevention of CIN has also been achieved with periprocedural use of N-acetylcysteine, but not as consistently as with sodium bicarbonate. Although many studies evaluated different N-acetylcysteine dosages and routes of administration, the optimal regimen has yet to be determined. Combinations of these preventive therapies are just emerging and require further research.     

Ochratoxin and Kidney Disease in the Human

Abstract

Ochratoxin A (OTA), produced by several species of Aspergillus and Penicillium, is known for its nephrotoxicity in pigs and rats. Human exposure to this toxin, essentially by consumption of contaminated food and drinks derived from cereals, could be potentially nephrotoxic. There is a paradox between the risk of OTA for human renal disease, due to the wide distribution of this mycotoxin throughout the world, and the rarity of reported cases demonstrating its role in chronic renal disease. Possible OTA-induced acute renal failure was recently reported in Italy after a farmer and his wife worked 8 hours in a granary closed for several months. Renal biopsy in the woman who developed nonoliguric acute renal failure revealed lesions of acute tubular necrosis. A strain of Aspergillus ochraceus producing OTA was isolated from the wheat. Chronic nephrotoxicity due to OTA is probably more usual and makes the diagnosis more difficult. Balkan Endemic Nephropathy, a chronic tubulo-interstitial renal disease, could be due to OTA. Epidemiologic studies showed that in areas where high OTA levels are reached in food and in the blood of the population, there is a high incidence of nephropathy and renal tumours. The demonstration of DNA adducts in kidneys of animals exposed to OTA and similar adducts in renal tissue and tumours from individuals in the endemic region of the Balkan countries highlights a new molecular epidemiological approach. Karyomegalic interstitial nephritis, characterized by karyomegaly in proximal and distal tubular epithelial cells, has been reported in nine patients. Karyomegaly could be due to an environmental toxin that interferes with DNA replication. Involvement of the oxidative pathway in genotoxicity of OTA is known and oxidant stress induces DNA damage. Therefore, karyomegaly could be a histological marker of interstitial nephritis due to OTA. In developing countries where the prevalence of end stage renal failure due to nephropathy of uncertain etiology is high. OTA and probably other mycotoxins could be major environmental factors in the occurrence of renal disease.     

Effects of acute renal failure induced by uranyl nitrate on the pharmacokinetics of liquiritigenin and its two glucuronides, M1 and M2, in rats

Objectives Liver disease and acute renal failure (ARF) are closely associated. The pharmacokinetics of liquiritigenin (LQ), a candidate therapy for inflammatory liver disease, and its metabolites M1 and M2 were evaluated in rats with ARF induced by uranyl nitrate (U‐ARF rats). Methods LQ was administered intravenously (20 mg/kg) or orally (50 mg/kg) in U‐ARF and control rats, and uridine diphosphate‐glucuronosyltransferases (UGT) activity and uridine 5′‐diphosphoglucuronic acid (UDPGA) concentrations were determined in the liver and intestine. Key findings After intravenous LQ administration, U‐ARF rats displayed significantly slower LQ renal clearance but no significant changes in the LQ area under the plasma concentration–time curve (AUC) compared with controls. This was because of similar hepatic UGT activity and UDPGA levels between two groups, which resulted in comparable non‐renal clearance, as well as the limited contribution of LQ renal clearance to total LQ clearance. However, the AUC and AUC_M/AUC_LQ ratios of M1 and M2 were significantly increased in U‐ARF rats because of decreased urinary excretion of M1 and M2. Similar results were observed following oral administration because of the comparable LQ intestinal metabolism in both groups and decreased urinary excretion of M1 and M2 in U‐ARF rats. Conclusions U‐ARF rats displayed decreased urinary excretion of LQ glucuronides, resulting in significantly greater AUC and metabolite ratios of M1 and M2 following LQ administration.