N-Allylsecoboldine as a novel agent prevents acute renal failure during endotoxemia

Blockades of cytokine and oxygen radicals release are considered to be beneficial in reducing multiple organ injury and increasing the survival rate in sepsis/septic shock. Thus, we examined the protective efficacy of N-allylsecoboldine, a secoaporphine derivative with antioxidant and alpha1-adrenoceptor blocking activities, in rats treated with endotoxin (E. coli lipopolysaccharide, LPS). Pretreatment of LPS-treated rats with N-allylsecoboldine significantly attenuated the late-phase hypotension, hypoglycemia and incremental plasma tumor necrosis factor (TNF)-alpha. Overproduction of plasma nitrate in endotoxemia was not changed but the continuous decrease of urinary nitrate appeared to be partially ameliorated by N-allylsecoboldine. However, N-allylsecoboldine inhibited the inducible nitric oxide synthase (iNOS) protein expression in the renal cortex of endotoxemic rats. N-allylsecoboldine also improved the endotoxemia-induced organ injury as demonstrated from the conspicuous recovery of marker enzymes in the LPS-treated rats. Endotoxemia was associated with renal dysfunctions as indicated by decreases in renal blood flow, urinary potassium excretion, and renal nitrate clearance. However, pretreatment with N-allylsecoboldine showed significant alleviation of these renal dysfunctions. In addition, a lower dose of N-allylsecoboldine ameliorated the mortality of LPS-treated mice. This study demonstrates N-allylsecoboldine's ability to avail against acute renal failure and increase survival rate during endotoxemia. These beneficial effects may be attributed to the inhibition of iNOS expression, TNF-alpha production, and free radical scavenging activities. However, the role of alpha1-adrenoceptor antagonism for N-allylsecoboldine in sepsis remains unclear.     

临床药师参与别嘌醇致重症药疹并急性肾衰竭患者的药学实践

临床药师全程参与1例别嘌醇致重症药疹并急性肾衰竭患者的药物治疗,对其不良反应进行了关联性评价,协同医师制定了糖皮质激素的治疗方案,及时调整了抗菌药物,分析了患者血糖升高的原因及对策,对患者进行了严密的药学监护、用药教育及出院后随访。临床药师建议被医师采纳,患者皮疹逐渐消退,感染得到控制,肾功能好转。     

Fatal dyspnea in a patient with renal failure

A 67-year-old woman with hypertension, diabetes, hypothyroidism and chronic renal failure reported to the hospital for her regularly scheduled hemodialysis, complaining of shortness of breath. Despite fluid removal during her hemodialysis, she remained tachypneic and developed stridor. She was admitted to the hospital for a work-up of a known mediastinal mass, thought to be a goiter. However, she deteriorated over the next several hours and expired. A post-mortem examination confirmed fatal pulmonary emboli. This case illustrates the fact that, while most patients with chronic renal failure are considered to be at low risk for pulmonary emboli, it is often not diagnosed when present. In this paper, we will review the epidemiological data supporting this notion, examine proposed pathophysiological mechanisms, and review the diagnostic approach that should be considered in the setting of chronic renal failure.     

Diuretics induced uremia and nonrecovery of renal function in a patient with acute renal failure caused by sepsis

Sepsis is a clinical syndrome related to severe infection and is characterized by systemic inflammation and injury to multiple organs and functional systems. Sepsis is one of the main causes of acute renal failure (ARF). Diuretics are frequently administered during ARF. However, there is scant evidence that diuretics provide any benefit to the patients with ARF. This case report highlights the occurrence of uremia and nonrecovery of renal function after administration of diuretics in a patient with ARF caused by sepsis. It is suggested that physicians should be cautious in prescribing diuretics to patients with ARF due to septicemia. Diuretics cause uremia and may lead to false diagnosis of chronic renal failure and nonrecovery of renal function. The patient may unnecessarily require prolonged dialysis.     

一例慢性心力衰竭合并肾功能不全患者的药学监护

目的探讨临床药师在心力衰竭合并多种疾病患者合理用药中的作用。方法临床药师通过参与1例心力衰竭伴多种疾病患者的药物治疗,从多角度进行监测,分析治疗方案,提出用药调整和补充,并对治疗全过程用药进行干预及优化。结果通过药学监护措施,避免了潜在的药物治疗风险,解决了药物治疗存在的问题。结论药学监护提高了临床药物治疗水平,减少了不良反应的发生率,对保障药物在临床使用过程中安全、有效具有重要意义。     

1例急性心衰患者的药学监护

1例72岁男性患者,以间断心慌、胸闷、气喘20余年,再发加重1 d入院。住院期间,临床药师对患者进行药学监护,主要包括:纠正长期应用呋塞米后的电解质紊乱、硝普钠的用药剂量及可能出现的不良反应监测、多巴胺的有效剂量和不良反应监测、华法林的抗凝强度以及肝肾功能等指标监测,并根据监护结果提出药物剂量调整的使用建议,同时对患者进行用药教育,提高用药依从性,保障用药安全、有效。     

1例慢性肾功能衰竭伴上消化道出血患者的药学监护

1例52岁男性患者,以慢性肾功能衰竭入院。入院后查血生化、血象等指标,监测血压,结果显示患者血压、贫血控制不佳,水电解质和酸碱平衡紊乱,结合实验室检查结果给予降压、抗肾性贫血、纠正水电解质和酸碱平衡紊乱等治疗。入院第6天,患者出现严重上消化道出血并发症,给予抑酸、生长抑素治疗。在临床治疗过程中,临床药师针对该例肾病患者的具体情况,选用适宜的降压药物、抗肾性贫血药物、利尿药物,计算用药剂量,尤其是对合并严重消化道出血并发症时,针对抑酸药物、生长抑素指导用药方法,同时实施治疗药物监测。出院后1个月随访,患者血压、血红蛋白、水电解质和酸碱度等指标恢复正常。     

Clearance of phenylethylmalonamide during haemodialysis of a patient with renal failure

Information is presented for the serum concentrations during haemodialysis of primidone, phenobarbitone, and phenylethylmalonamide (PEMA) in a patient with renal failure receiving chronic primidone therapy. The concentrations of drug and metabolites fell during haemodialysis, but PEMA concentrations were above normal at all times. The average renal clearance of PEMA during 6 h of dialysis was found to be 84.7 +/- 4.6 ml min-1.     

碘普罗胺致急性肾衰竭

1例65岁男性2型糖尿病患者,因反应迟钝伴口齿不清入院。头颅磁共振成像示脑梗死(急性期),给予肠溶阿司匹林(0.1g,1次/d)、依达拉奉(30mg,1次/d)及甲钴胺等药物治疗。因胸部、腹部CT增强扫描,连续2d各使用造影剂碘普罗胺100ml(含碘30g),第3天出现双下肢水肿,尿量400ml/24h,随后无尿,静脉给予呋塞米未见好转。复查血肌酐475μmol/L,尿素氮24.5mmol/L。诊断为急性肾衰竭,考虑与碘普罗胺有关。连续血液透析治疗5d后,患者尿量增加,血肌酐降至284μmol/L。17d后血肌酐231μmol/L,尿素氮14.4mmol/L。患者双下肢水肿明显好转,出院。     

布洛芬致急性肾功能衰竭

1例40岁男性患者因右下肢疼痛给予布洛芬50 mg,3次/d.约2个月患者出现心悸、恶心、呕吐,尿量减少(300 ml/d)遂入院.尿常规示蛋白(++),肾功能示BUN 51.7 mmol/L,SCr 1490.4 μmol/L.给予降血压、血液净化等治疗.1个月后肾功能逐渐正常.     

Suprofen-induced acute renal failure

A case report of acute flank pain with reversible renal failure in a young adult after taking three doses of suprofen is presented. Blood urea nitrogen and serum creatinine values returned to normal from significantly elevated levels on admission.     

Agranulocytosis possibly caused by ranitidine in a patient with renal failure

A 70-year-old Japanese woman with renal dysfunction under hemodialysis presented with vomiting and chill with fever. Over the previous 24 weeks she had been taking 75 mg of ranitidine after hemodialysis. Other medications taken were prednisolone, furosemide, alpha-calcidol, amlodipine and calcium carbonate. Before starting ranitidine, she had been treated with famotidine for about 2 years without complication. Hematological inspection on admission revealed agranulocytosis with WBC of 400/mm3. Ranitidine was discontinued and granulocyte colony-stimulating factor (G-CSF) was started. On Day 3, laboratory data showed slight improvement of cytopenia with WBC of 1,000/mm3. On Day 6, her hemogram showed marked improvement with WBC of 11,700/mm3 and G-CSF was discontinued. She was discharged on Day 10. Several cases describing ranitidine-induced cytopenia are associated with the use of ranitidine at a dose of 150 mg/day or higher, and adverse reactions were found within 2-35 days after beginning ranitidine treatment. In the case described here, however, the adverse reaction occurred after a longer treatment period with ranitidine at a lower dose. In conclusion, ranitidine should be administered with great caution to patients with severe renal dysfunction.     

对1例重症肺炎伴肾功能衰竭患者的药学监护

1例87a男性患者,因重症肺炎伴呼吸衰竭、休克、肾功能衰竭入ICU,先后予以莫西沙星、头孢哌酮舒巴坦联合万古霉素和卡泊芬净抗感染,多巴胺升压、氢化可的松抗休克以及肠外营养等治疗。该患者有糖尿病史,在肠外营养支持过程中,对患者血糖情况进行监测;根据患者肝肾功能情况,及时调整抗菌药物剂量,并对莫西沙星致神经系统不良反应进行监测。治疗期间,临床药师在药物剂量调整,营养状况评估,潜在的药物不良反应,生命体征监测特别是肝肾功能情况等方面提供了全面及时的药学服务。     

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。     

1例抗生素致肾衰竭患者脑病的药学监护

目的:探讨1例肾衰竭患者脑病发作原因及针对该类患者的抗感染药物使用原则。方法:对1例先后使用3种抗生素出现脑病的肾衰竭患者进行药学监护,同时检索、查阅相关文献,探讨脑病发生的原因。结果:患者脑病很可能由厄他培南、头孢他啶导致;对于肾衰竭患者,抗感染药物的选择要根据药敏结果、肌酐清除率、药效学及药动学参数;存在脑病高危因素的患者须在已调整的剂量基础上进行减量。结论:当肾衰竭患者发生感染时,医务人员使用厄他培南应格外谨慎,必要时可选择广谱抗菌药物如哌拉西林/他唑巴坦或氟喹诺酮等进行替代治疗。     

治疗急性失代偿性心力衰竭新药奈西立肽

B型利钠肽由于其在诊断、预后及治疗心力衰竭的特殊价值而备受关注.奈西立肽已成为治疗急性失代偿性心力衰竭的一线药物,它能迅速降低急性失代偿性心力衰竭患者肺毛细血管楔压和周围血管压力,提高心脏每搏输出量、心脏指数,并产生利钠利尿及阻滞肾素-血管紧张素-醛固酮系统的作用.其扩张血管作用呈剂量依赖性,且不引起反应性心动过速,能显著改善呼吸困难等临床症状,与多巴酚丁胺相比疗效相似,但较少引起心律失常;较硝酸甘油更安全有效.其主要不良反应是剂量依赖性的低血压、头痛和腹痛.