甘露醇致急性肾衰竭临床分析

甘露醇广泛应用于治疗脑水肿、青光眼和防治急性肾衰竭(ARF),静脉滴注后由于血浆渗透压升高,可使组织脱水,颅内压降低,经肾小球滤过,几乎不被肾小管再吸收,在肾小管保持足够的水分以维持其渗透压,然后以原形经尿排泄。近年陆续见到大剂量应用甘露醇引起急性肾功能损伤的报道,并逐渐引起临床关注。现结合文献,对本院12例由甘露醇引起的急性肾衰竭进行临床分析。     

红霉素引起急性肾衰竭2例

红霉素(Erythromycin)为大环内酯类抗生素,系抑菌剂,主要对革兰阳性菌有较强的抗菌作用,对部分革兰阴性菌也有抑制作用,对某些螺旋体、支原体、衣原体及螺旋杆菌也有效,与青霉素无交叉过敏反应,可用于青霉素过敏的病人.一般剂量时不良反应少见,故在临床上使用广泛.作者近年在使用红霉素过程中,遇到2例急性肾衰竭病人,现报道如下.     

万古霉素引起急性肾衰竭

1例36岁男性白血病患者,因肺部感染给予万古霉素1g加入0.9%氯化钠注射液100mL,1次/12h静脉滴注;莫西沙星0.4g,1次/12h静脉滴注。给药3d后实验室检查示SCr549μmol/L,BUN11.17mmol/L,血K＋3.76mmol/L。停用万古霉素,改用利奈唑胺,继续使用莫西沙星。患者情况恶化,出现恶心、下肢水肿、腹胀,尿量1000mL/d,SCr848μmol/L,BUN19.8mmol/L。遂行血液滤过,3次后患者症状消失,肾功能各项指标均恢复正常。     

抗菌药物不合理使用导致的药物不良反应发生的相关性分析

目的探讨抗菌药物不合理使用与药物不良反应发生的相关性。方法回顾性分析该院收治的200例药物不良反应病例报告,采用Person相关性分析抗菌药物不合理使用方式与各类不良反应表现的相关性。结果抗菌药物不合理使用导致的药物不良反应患者100例（50.00%）,共112例次,使用喹诺酮类药物引起不良反应最常见,构成比为42.86%（48例次）,其次为β-内酰胺类抗生素,构成比为32.14%（36例次）;皮肤及软组织是不良反应发生的主要部位,构成比为（57.00%）,其次为消化系统,构成比为（27.00%）;经Person相关性分析后,给药时间过长、滴速过快、药液浓度过高、剂量过大等因素,均与不良反应显著相关（P〈0.05）。结论抗菌药物的不合理使用仍是该院引起药物不良反应的主要原因,应进一步提高抗菌药物使用的合理性,有利于降低不良反应的发生率。     

抗菌药物所致的心律失常

抗菌药物的发展很快,使传染病的死亡率骤然下降,由过去的60%～90%下降到1%以内[1].但随着抗菌药物的广泛应用,不仅使耐药菌株不断增多,且由其引发的不良反应也日趋增多.以往认为抗菌药物多引发过敏反应,近年发现其所致心律失常亦非罕见.现将近年来国内部分文献中有关抗菌药物引起心律失常的报道归纳如下:     

抗感染药物导致的急性肾损伤

近年来抗感染药物所致急性肾损伤（AKI）有增多趋势。国内资料显示,在药物所致AKI中抗菌药占39.0%～54.0%。引起AKI的抗感染药主要有氨基糖苷类、β-内酰胺类、多肽类和喹诺酮类等。AKI一般发生于患者用药后数日或数周,临床表现为少尿或非少尿型急性肾功能不全,其病理表现为急性肾小管坏死和急性间质性肾炎。发病机制与患者机体免疫反应和药物的直接肾毒性有关。高龄、肾功能不全以及合用其他药物等是AKI的高危因素。一旦发生AKI应立即停药,并给予泼尼松或肾透析治疗。临床医生应重视高危人群的合理用药,避免大剂量或长期用药,加强对患者肾功能监测,以降低AKI的发生率,改善预后。     

抗菌药物不良反应的回顾性分析

对本院2008~2014年的589份抗菌药物不良反应病例的患者年龄、性别、用药天数、剂量、过敏史、合并用药等因素进行回顾性分析,以加强用药监测。     

抗菌药物引起的生殖系统不良反应

目的：对抗菌药物引起生殖系统不良反应的相关报道进行综述。方法：收集近10年来相关献资料，进行分析总结。结果：抗菌药物引起的生殖系统不良反应在临床上较为常见，涉及药物品种较多，而且以男性患多见，发病机理不明。结论：抗菌药物引起的生殖系统不良反应为一种较为严重的药源性疾病，临床一旦发现应及时停药处理，以减轻患痛苦。     

论抗菌药物的不良反应

抗菌药物应用范围颇广,可涉及到各临床科室。提高医院疗效,患者满意度的重要因素,就是合理应用抗菌药物,可在一定程度上减缓细菌耐用性的发生,降低不良反应发生率。所以,医师应从两个方面考虑如何选择抗菌药物:①药物抗菌效果:据药物动力学指标以及抗菌药物对感染菌的活性。②不良反应:由于抗菌药物频繁更新,致使临床医师无法做到很快地全面了解药物特点,不能合理用药,导致不良反应发生率日益增多。所以,临床医师应提高对抗菌药物不良反应的认知度。     

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。     

大剂量甲氨蝶呤化疗相关急性肾衰竭

1例14岁女性患儿因淋巴瘤Ⅳ期入院进行第16次化疗。入院时实验室检查示WBC 5.58×109/L,Hb 88 g/L,PLT143×109/L,SCr 42μmol/L,ALT 38 U/L,心、肝、肾功能大致正常。化疗方案：MTX总量4 g,其中1/3总剂量0.5 h内静脉给予,剩余剂量在随后的23.5 h内静脉给予。同时给予地塞米松5 mg＋阿糖胞苷40 mg＋MTX 12.5 mg鞘内注射,并静脉给予长春新碱1.8 mg。化疗第2天,患儿出现发热、呕吐、腹泻、下肢水肿。第3天实验室检查示WBC 2.49×109/L,PLT 24×109/L,Hb 58.0 g/L;K＋2.74 mmol/L,SCr 179μmol/l,CK 1 089 U/L。化疗后24、42 h患儿MTX血药浓度分别为168.0和65.0μmol/L。血液净化治疗期间,MTX血药浓度分别为36.5μmol/L（66 h）、29.4μmol/L（73 h）2、2.1μmol/L（77 h）和16.0μmol/L（90 h）。化疗第5天患儿尿量降至460 mL,随后无尿,并出现全身抽搐,静脉给予地西泮5 mg后抽搐缓解,但仍有躁动。     

Acute renal failure associated with intravenous immunoglobulins

Intravenous immunoglobulins (i.v.IG) are increasingly used in various clinical situations for which they have been considered to be safe and effective. However, since 1987, some cases of renal toxicity have been reported. Forty-nine cases of acute renal failure have been notified to the French Regional Pharmacovigilance Centers between 1992 and mid 1998. In this series, marked serum creatinine increases (mean 387%+/-181%) appeared within 8 h to 8 days after initiation of i.v.IG therapy. Oliguria was observed in 80% of the cases. Haemodialysis was required for 34% of the patients. The renal failure persisted for a mean duration of 10 days after discontinuation of the i.v.IG treatment. Although risk factors have not been definitely established, preexisting renal impairment and old age seem to predispose to i.v.IG-associated acute renal failure as well as diabetes mellitus or the use of diuretics. The mechanism of renal injury remains speculative but a hyperoncotic overloading may be contributory. Finally, close monitoring of renal function is required in patients with preexisting renal failure, with older age and with diabetes mellitus.     

阿莫西林过量致急性肾衰竭

1例44岁拟行子宫肌瘤切除术患者,为预防感染于术前5d开始给予阿莫西林6.0g溶于0.9%氯化钠注射液500mL中静脉滴注,1次/d。术后约15min患者出现血尿,SCr为140.99μmol/L。考虑急性肾衰竭与阿莫西林剂量过大有关。停用阿莫西林,改为头孢噻肟和美洛西林-舒巴坦,同时给予呋塞米、泮托拉唑。术后14d患者肾功能恢复正常。     

膦甲酸钠相关急性肾衰竭

1例75岁女性患者,因带状疱疹给予膦甲酸钠3 g、1次/d静脉滴注,合并应用甲钴胺、维生素B1和新癀片、阿昔洛韦软膏。第4天,患者四肢及面部出现水肿,伴恶心、食欲不振、皮肤瘙痒。第10天,除阿昔洛韦软膏外,上述药物均停用。第12天实验室检查:血清肌酐142μmol/L,尿素氮8.6 mmol/L;尿比重1.010。考虑为急性肾衰竭、急性间质性肾炎。限制液体入量,给予低盐、低脂、优质蛋白饮食。5 d后患者水肿消退,瘙痒消失。实验室复查:血清肌酐86μmol/L,尿素氮7.4 mmol/L,磷0.9 mmol/L。     

Acute renal failure associated with inhaled tobramycin.

PURPOSE: A case of nephrotoxicity possibly caused by tobramycin inhalation solution is presented. SUMMARY: A 62-year-old Caucasian woman was admitted for treatment of decreased urine output and sepsis secondary to Pseudomonas aeruginosa. Her past medical history was significant for multiple diseases, including chronic renal insufficiency (baseline serum creatinine concentration [SCr] 2 mg/dL). One month postadmission, the patient was diagnosed with health care-associated pneumonia. The patient was initiated on piperacillin-tazobactam and tobramycin 2 mg/kg i.v. She was changed to imipenem-cilastatin with continuation of i.v. tobramycin. A month after discontinuation of her antibiotic regimen, the patient was diagnosed with P. aeruginosa pneumonia. The patient received imipenem-cilastatin, vancomycin, and inhaled tobramycin 300 mg twice daily. At that time, her SCr was 2 mg/dL. Inhaled tobramycin was continued for four weeks, and the patient's SCr steadily rose to a peak of 4.5 mg/dL. During week 1 of treatment, multidrug-resistant P. aeruginosa and methicillin-resistant Staphylococcus aureus were diagnosed. The patient continued to receive i.v. imipenem-cilastatin, vancomycin, and inhaled tobramycin with an SCr of 1.9 mg/dL. However, at the end of week 2, the patient's SCr began to slowly rise (2.3 mg/dL). At week 3, imipenem-cilastatin was discontinued; inhaled tobramycin was continued. The patient's SCr continued to rise (3.2 mg/dL). At week 4, her SCr rose to 4.5 mg/dL, resulting in initiation of hemodialysis and discontinuation of inhaled tobramycin. The patient's SCr never returned to baseline, and renal function was never regained. CONCLUSION: Acute renal failure requiring dialysis occurred in a high-risk patient receiving an extended course of treatment with inhaled tobramycin.     

Acute renal failure associated with an accidental overdose of colchicine

CASE SUMMARY: A 47-year-old man with a history of polyarticular gout was admitted to the nephrology service because of severe renal insufficiency (creatinine 6.25 mg/dl). Three days before admission he had a pain crisis in his knees and ankles and self-administered 20 x 1 mg granules of colchicine p.o. over a period of 4 - 5 hours together with six suppositories each containing 100 mg of indomethacin. The patient began vomiting within 24 hours, experienced diarrhea which persisted for three days and then came to the hospital. The patient reported oliguria during the preceding 24 hours. In hospital, attempts to correct water and electrolyte balance were initiated. The patient became stabilized hemo-dynamically, the diarrhea disappeared within 24 hours, diuresis resumed and the renal function progressively improved. Leukopenia and thrombopenia were diagnosed, the transaminases increased: AST = 79 U/l, ALT = 132 U/l on the eighth day after taking the colchicine. The serology for hepatitis A, B, C and HIV viruses was negative; the serology for CMV and VEB revealed a previous infection. After being discharged from hospital 11 days after admission, the patient presented with the following parameters: hematocrit 39%, leukocytes 5,920/microl (3 470 neutrophils), prothrombin time 13 seconds, urea 44 mg/dl, creatinine 1.29 mg/dl, AST 16 U/l and ALT 35 U/l. DISCUSSION: The patient mistakenly ingested 20 mg ofcolchicine p.o. (0.22 mg/kg). The intoxication was associated with gastroenterocolitis, dehydration and renal failure during the first three days after ingestion. The patient also developed leukopenia, thrombopenia and mild hepatocellular injury. Renal failure due to colchicine intoxication is due to various factors such as depletion of volume/hypotension, rhabdomyolysis and multiorgan failure. In this case, the hypovolemia was probably the fundamental cause of the acute renal insufficiency as demonstrated by the quick recovery after administering fluids. It is possible that indomethacin may have enhanced the toxic effect of colchicine on the kidneys and bone marrow. Some colchicine intoxications, as in this case, are caused by an error in interpreting the dose for treating an acute attack of gout. A way to prevent these errors would be to use a low-dose treatment protocol.