水化治疗预防不同肾功能水平病人造影剂相关肾损伤的临床观察

[目的]探讨水化治疗预防不同肾小球滤过率（GFR）病人行冠状动脉介入术后造影剂相关肾损伤的效果,以便指导临床工作。[方法]将血肌酐正常的冠状动脉介入术后139例病人,根据GFR不同分为正常组和异常组,两组病人术后行常规水化治疗。比较两组术前、术后血肌酐、肾小球滤过率、血尿素氮、血清β2-微球蛋白、尿微量白蛋白、24 h出入量情况。[结果]两组术后均未发生造影剂肾病,术后6 h、12 h尿量差异有统计学意义（P〈0.05）;两组血尿素氮、β2-微球蛋白水平比较差异有统计学意义（P〈0.05）;术后第2天尿微量白蛋白与术前差值比较,差异有统计学意义（P〈0.05）。[结论]血肌酐正常的病人中有一部分潜在或已存在肾功能异常,术前应常规计算肾小球滤过率,临床可通过加强水化治疗预防不同肾小球滤过率的冠状动脉介入术后病人造影剂相关肾损伤。     

术后不同饮水方法对减轻冠状动脉介入术后造影剂相关性肾损伤的效果及护理

目的 探讨术后不同饮水方法 对减轻冠状动脉介入术后造影剂相关肾损伤的效果.方法 选择接受冠状动脉介入术患者94例,将研究对象分为自由饮水组(47例)和短期强化饮水组(47例),自由饮水组24h总饮水量不少于2000ml,但对单位时间饮水量无要求;短期强化饮水组要求其术后第1、2、3小时内每小时饮水400-500ml,24h总饮水量不少于2000ml.比较两组术前、术后血肌酐、尿素氮、血清β2-微球蛋白、尿微量白蛋白、24h出入量及有无尿潴留、胃部不适等情况.结果 短期强化饮水组与自由饮水组术后3h、13-24h入量、术后3h、6h、12h尿量、术后第l天尿微白蛋白和术后第1天尿微白蛋白差值比较有差异(P<0.05).结论 术后3h内强化饮水可减少冠状动脉介入术后患者造影剂相关肾损伤.     

不同口服水化护理对冠状动脉慢性完全闭塞病人造影剂肾病的影响

[目的]观察不同的口服水化时间对冠状动脉慢性完全闭塞病人预防造影剂肾病的影响。[方法]选择符合入选标准的60例病人分为A组和B组,A组病人于术前6h及术后8h内进行口服水化,B组病人于术前6h及术后24h内进行口服水化,术后口服水化总量均为约3 000mL;观察术前术后血清肌酐、尿素氮、胱抑素C及尿蛋白肌酐比值等肾功能指标变化。[结果]两组术前血清肌酐及尿素氮、胱抑素C及尿蛋白肌酐比值差异无统计学意义,术后血清肌酐、胱抑素C、血尿素氮、尿蛋白肌酐比值变化比较差异均无统计学意义(P0.05);B组术后口服入量及尿量大于A组。[结论]在饮水量相同的情况下,术后24h内有计划地进行口服水化比在8h内口服水化更有效。     

强化静脉水化疗法对造影剂肾病的保护作用

目的 探讨强化静脉水化疗法对冠脉造影或介入治疗并发造影剂肾病的作用.方法 选取行冠脉造影或植入冠脉内支架的患者122例,随机分为常规静脉水化组(60例)和强化静脉水化组(62例).常规静脉水化组分别于使用造影剂前、后6h给予0.9％ NaC1溶液1.0～1.5 ml/(kg·h)的静脉水化,共12 h;强化静脉水化组于术前12 h静脉滴注0.9％氯化钠液,术后持续6h,在常规静脉水化疗法的基础上增加500～1000 ml的静脉补液.观察两组患者使用造影剂前及使用造影剂24、72 h后的血清肌酐(CRE)和肾小球滤过率(GFR)水平.结果 使用造影剂前两组CRE、GFR差异无统计学意义;在使用造影剂72 h后强化静脉水化组CRE低于常规静脉水化组(P＜0.05),GFR高于常规静脉水化组(P＜0.05).结论 强化静脉水化疗法能降低造影剂所致的肾功能损害及减少造影剂肾病的发生.     

肾损伤因子-1与慢性肾脏病

正慢性肾脏病是指各种原因引起的慢性肾脏结构和功能障碍(肾脏损伤病史3个月),包括肾小球滤过率(glomerular filtration rate,GFR)正常或不正常的病理损伤、血液或尿液成分异常及影像学检查异常,或不明原因的GFR下降[GFR60 mL/(min·1.73 m2)]超过3个月[1]。肾功能评估方法包括血尿素氮、肌酐及评估肾小球滤过率(estimated glomerular filtration rate,eGFR)的检测,但这些指标通常在肾损伤48~72 h后改变[2],敏感性、特异性欠佳。近年多项研究表明,肾损伤因     

水化联合前列地尔预防介入术后造影剂肾病的效果观察

目的 探讨水化联合前列地尔对介入术后肾功能的保护以及造影剂肾病（CIN）的预防效果。方法 726例经皮冠状动脉介入治疗（PCI）或冠状动脉造影（CAG）检查的冠心病（CHD）患者分为对照组（360例）和观察组（366例）。对照组患者在术前、术后通过静脉输注0.9%NaCl溶液进行水化,观察组术前采取与对照组一致的方法水化,术后在水化的基础上30 min内加用前列地尔注射液。收集并比较两组患者的临床资料、手术前后48 h内的实验室检查数据、估算肾小球滤过率（eGFR）以及CIN发生率。结果 两组患者术后48 h的尿素氮（BUN）、血清肌酐（Scr）水平均较术前有一定升高,eGFR较术前显著降低,差异有统计学意义（P<0.05）。进一步分析发现,观察组术后48 h的BUN、Scr、eGFR降低幅度及CIN发生率均明显小于对照组,差异有统计学意义（P<0.05）。结论 水化联合前列地尔注射液可降低CIN的发生率,且对造影剂使用后的肾功能有一定保护作用。     

急诊PCI术后口服水化治疗预防造影剂肾病的水化用量选择与临床效果研究

目的观察急诊经皮冠状动脉介入治疗(PCI)术后口服水化治疗预防造影剂肾病的水化用量选择及临床应用效果。方法选取2015年7月～2018年4月我院接收的急性心肌梗死行急诊PCI患者150例为研究对象,随机分为观察组和对照组,各75例。对照组实施术后6h常规口服水化剂量(1ml/kg/h)。观察组实施术后6h强化口服水化剂量(3ml/kg/h)。于术前、术后24h、48h、72h观察血肌酐与尿素氮变化情况,临床治疗效果及造影剂肾病发生率。结果两组术前血肌酐值与尿素氮值比较差异无统计学意义(P0.05)。两组术后血肌酐值与尿素氮值比较差异有统计学意义(P0.05)。两组术后造影剂肾病发生率比较差异有统计学意义(P0.05)。两组治疗效果比较差异有统计学意义(P0.05)。结论对急诊PCI术后患者实施口服水化治疗方式,能够安全有效实现对血肌酐和尿素氮的控制。而实施强化口服水化剂量(3ml/kg/h)在降低患者造影剂肾病发生率方面更优于常规口服水化剂量(1ml/kg/h),对于提高临床治疗效果具有重要的作用,应用价值突出。     

短期强化饮水预防冠状动脉介入术后造影剂相关肾损伤的效果观察

[目的]探讨短期强化饮水对预防冠状动脉介入术后造影剂相关肾损伤的临床效果。[方法]将2012年4月—2013年3月行冠状动脉介入术的82例病人设为对照组,采用增加饮水量疗法;2013年4月—2014年4月行冠状动脉介入术的98例病人设为观察组,采用短期强化饮水疗法,运用受试者工作特征曲线(ROC)及曲线下面积对血清β2-微量蛋白和血清肌酐诊断的敏感性及特异性进行评价,比较不同时段的出入量以及血清β2-微量蛋白与血清肌酐水平。[结果]血清β2-微量蛋白ROC曲线下面积为0.914(0.852~0.940),血清肌酐ROC曲线下面积为0.835(0.686~0.839),两种检测曲线下面积均优于参考线0.5,差异具有统计学意义(P=0.00);两组病人术后3h入量、术后6h出入量以及24h总出入量比较差异具有统计学意义(P0.01);术后3d以及术后7d观察组病人血清β2-微量蛋白含量与血清肌酐水平均优于对照组,差异具有统计学意义(P0.05)。[结论]短期强化饮水有助于预防冠状动脉介入术后造影剂肾病。     

老年人冠状动脉介入术后造影剂对肾功能的影响

目的了解造影剂对老年人冠状动脉介入诊疗术后肾功能的影响。方法选择经皮冠状动脉介入治疗的老年患者40例,年龄(70.5±8.2)岁,全部选用低渗非离子造影剂,接受水化治疗(静脉水化)。测定造影前、造影后第1天、第3天、第7天肾功能指标。结果尿α1微球蛋白术后第1天、第3天分别为(14.74±14.58)mg/L和(13.86±18.09)mg/L,与造影前(6.71±5.11)mg/L比较,显著增高(P<0.05),第7天恢复到术前水平;血清尿素氮、肌酐、尿微量白蛋白、尿转铁蛋白、尿IgG与术前比较差异无统计学意义;按造影剂肾病诊断标准,仅1例诊断造影剂肾病(2.5%)。结论选用肾毒性小的造影剂、水化能显著降低造影剂肾病的发生,即使出现肾功能损害,1周后可恢复正常。     

N-乙酰半胱氨酸对老年糖尿病患者造影剂肾病的预防作用

目的观察N-乙酰半胱氨酸(N-acetylcysteine,NAC)对肾功能正常或轻度肾功能不全的老年糖尿病患者造影剂肾病的预防作用。方法拟采用低渗造影剂进行增强CT检查70例年龄>60岁、糖尿病史1a以上的正常或轻度肾功能不全患者,随机分为NAC组与对照组各35例,NAC组造影前1d及造影后连续2d口服NAC,600mg/次;2组均给予水化治疗;比较造影前和造影后24,48h2组血肌酐、尿素氮和血胱抑素C水平及造影剂肾病发生率。结果 NAC组无造影剂肾病发生,对照组发生造影剂肾病2例,2组比较差异无统计学意义(P>0.05);增强CT检查后48h,NAC组血肌酐、尿素氮和血胱抑素C水平低于对照组,估测肾小球滤过率水平高于对照组(P<0.05)。结论 NAC联合水化治疗对肾功能接近正常的老年糖尿病患者造影剂肾病有一定预防作用。     

Ruptured renal angiomyolipoma presenting as renal colic

The case of a patient with acute onset of flank pain and hematuria is presented. Initial therapy was directed toward relief of pain believed to be caused by renal colic. It was not until the patient developed atypical features that the true diagnosis, ruptured renal angiomyolipoma, was discovered. The case and discussion emphasize the need to carefully consider a complete differential diagnosis when evaluating patients with flank pain and hematuria who have atypical clinical features or an atypical course.     

Functional renal imaging: nonvascular renal disease

Functional renal imaging—a fast-growing field of MR-imaging—applies different sequence types to gather information about the kidneys other than morphology and angiography. This update article presents the current status of different functional imaging approaches and presents current and potential clinical applications. Apart from conventional in-phase and opposed-phase imaging, which already yields information about the tiusse composition, BOLD (blood-oxygenation level dependent) sequences, DWI (diffusion-weighted imaging) sequences, perfusion measurements, and dedicated contrast agents are used.     

Cortical renal leiomyoma with extension to renal pelvis

We describe a case of renal leiomyoma in a 21-year-old woman who presented with flank pain and hematuria. Urographic and computed tomographic (CT) studies revealed a large right renal mass with polypoid outgrowth protruding into the renal pelvis. Cortical renal leiomyoma with this radiographic manifestation is extremely rare.     

Epidemiology of renal recovery after acute renal failure

PURPOSE OF REVIEW: Recovery of renal function after acute renal failure is an important clinical determinant of patient morbidity. Herein, the epidemiology of renal recovery after acute renal failure will be described, along with potential predictive factors and interventions. RECENT FINDINGS: Renal recovery has been variably defined, most often as recovery to independence from renal replacement therapy. A recent consensus definition for acute renal failure has been published and included provisions for defining renal recovery. Renal recovery to renal replacement therapy independence occurs in the majority by hospital discharge and peaks by 90 days. All of older age, female sex, co-morbid illnesses, especially chronic kidney disease, and late initiation of renal replacement therapy or conventional intermittent renal replacement therapy have been coupled with non-recovery. Analysis of the literature suggests several interventions may influence recovery. SUMMARY: The prognosis is generally good for recovery after acute renal failure. Most patients will be independent of renal replacement therapy by 90 days. Additional research is necessary, however, to understand recovery rates not only to independence from renal replacement therapy, but also to complete and partial recovery. Future studies need to consider the health economic implications for survival and non-recovery. Finally, questions on the role of various interventions require characterization in randomized controlled trials to determine how they may influence renal prognosis.     

急性肾功能损伤与衰竭生物标志物

急性肾功能损伤（ARI）与急性肾功能衰竭（ARF）是加强医疗病房（ICU）的常见疾病．ICU中80％的ARF由急性肾小管损伤所致，而非肾小球或间质性病变引起。其死亡率较高，寻找敏感性和特异性较好的ARI或ARF生物标志物，对早期诊断、治疗和改善预后有着重要意义。本文介绍和评估了ARI或 ARF生物标志物的研究现状。并展望了其未来的前景。[第一段]     

Biomarkers of acute renal injury and renal failure

Acute renal failure (ARF) is a frequent problem in the intensive care unit and is associated with a high mortality. Early recognition could help clinical management, but current indices lack sufficient predictive value for ARF. Therefore, there might be a need for biomarkers in detecting renal tubular injury and/or dysfunction at an early stage before a decline in glomerular filtration rate is noted by an increased serum creatinine. A MEDLINE/PubMed search was performed, including all articles about biomarkers for ARF. All publication types, human and animal studies, or subsets were searched in English language. An extraction of relevant articles was made for the purpose of this narrative review. These biomarkers include tubular enzymes (alpha- and pi-glutathione S-transferase, N-acetyl-glucosaminidase, alkaline phosphatase, gamma-glutamyl transpeptidase, Ala-(Leu-Gly)-aminopeptidase, and fructose-1,6-biphosphatase), low-molecular weight urinary proteins (alpha1- and beta2-microglobulin, retinol-binding protein, adenosine deaminase-binding protein, and cystatin C), Na+/H+ exchanger, neutrophil gelatinase-associated lipocalin, cysteine-rich protein 61, kidney injury molecule 1, urinary interleukins/adhesion molecules, and markers of glomerular filtration such as proatrial natriuretic peptide (1-98) and cystatin C. These biomarkers, detected in urine or serum shortly after tubular injury, have been suggested to contribute to prediction of ARF and need for renal replacement therapy. However, excretion of these biomarkers may also increase after reversible and mild dysfunction and may not necessarily be associated with persistent or irreversible damage. Large prospective studies in human are needed to demonstrate an improved outcome of biomarker-driven management of the patient at risk for ARF.     

Cardiac enzymes, renal failure and renal transplantation

Diagnostic accuracy of the currently available serum markers of cardiac injury, such as myoglobin, creatine kinase and its myocardial isoform, are altered in patients with renal failure. It is shown that cardiac troponins have decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy. Data regarding serum levels of these cardiac biomarkers, especially those of the cardiac troponins, in patients with a transplanted kidney are limited. Current data show that levels of cardiac troponin I are unaltered in patients who have undergone renal transplantation, while levels of cardiac troponin T may be elevated.We believe that cardiac troponin I should be the biomarker of choice for diagnosis of myocardial injury in these patients. However, further trials are required for conclusive results.     

Preservation of renal function in chronic renal failure.

Mechanisms of progression of chronic renal failure (CRF) have been well documented in the rat but may not be relevant in man. Factors which may modify clinical CRF include underlying disease, diet, hypertension, intercurrent events, and adverse or beneficial effects of drug therapy. It has been argued that progression in many forms of renal disease is inexorable below a certain level of renal function. In other diseases, eg primary malignant hypertension, analgesic nephropathy, function frequently improves in both the short and long term with appropriate management. Thus knowledge of the nature of the underlying disease is essential in assessing progression. The value of diet in preserving renal function has been debated, particularly the relative roles of protein and phosphate control. In our own unit, a prospective randomized study showed a benefit of protein restriction. Development of accelerated hypertension is an important cause of progression of renal disease and clinical and experimental evidence supports the view that non-accelerated hypertension is also a factor in progression, amenable to treatment. Various intercurrent events may accelerate progression and function may be lost permanently following sepsis, urinary tract obstruction, renal arterial or venous obstruction, hypotension and in some cases pregnancy. Numerous drugs can have deleterious effects on the kidney. The possibility that converting enzyme inhibitors might preserve renal function is attracting attention but in view of their side effects their place in therapy should be determined by prospective controlled studies in which the above factors are carefully considered.