非离子型造影剂对肾功能正常和肾功能不全患者肾功能的影响

目前 ,非离子型造影剂已经取代离子型造影剂成为心血管介入诊疗和放射介入诊疗技术的主要显影剂 ,有关造影剂的肾毒性研究资料主要来自早期的离子型造影剂〔1〕。非离子型造影剂的应用虽大大降低了各种造影剂副作用的发生率 ,但非离子型造影剂对中国人肾功能 ,尤其是已有功能不全患者的肾功能的影响鲜见报道〔2〕。本研究旨在探讨非离子型造影剂对肾功能正常和肾功能不全患者肾功能的影响。1对象与方法1 .1象研究对象为接受冠状动脉 (冠脉 )介入诊疗手术的住院患者 ,共 43例 ,其中男 31例 ,平均年龄 64( 38～ 78)岁。单纯接受冠脉造影者 1 5…     

肝硬化合并急性肾功能衰竭

急性肾功能衰竭是晚期肝硬化病人严重的并发症,依据发病原因及机制不同分为肾前性、肾性和阻塞性或肾后性肾衰。主要发病机制是有效血容量降低和肾脏低灌注,此外,还有严重感染、NSAID药物及血管造影剂的应用等。补充血容量可逆转肾前性肾衰。但对于I型HRS,特利加乐素、米多君等内脏血管收缩剂联合白蛋白扩容可能有效。肝硬化合并急性肾小管坏死引起的肾性肾衰须采取肾脏替代治疗（CRRT）并停止接触肾毒性药物。     

重视造影剂所致急性肾功能衰竭的预防

现代影像诊断和介入治疗中造影剂的应用日益增多 ,造影剂所致急性肾损害 (又称造影剂肾病 ,ＣＮ)的发生率也明显增加。据统计 ,ＣＮ已成为当前医院内发生的急性肾功能衰竭 (肾衰竭 )的第三位常见原因。ＣＮ是指静脉注射造影剂后发生的无其他原因可解释的急性肾功能减退 ,通常以血清肌酐比造影前升高≥ 2 5 %或 5 0 %作为诊断标准。典型的ＣＮ发生于造影后 2 4～ 4 8ｈ ,多表现为非少尿型急性肾衰竭。目前对造影剂所致急性肾衰竭尚无特效治疗方法。虽然多数病人肾功能可在 7～ 10ｄ左右恢复 ,但仍有 30 %的病人遗留不同程度的肾功能不全。Ｃ…     

用乙酰半胱氨酸预防中度肾功能不全患者行选择性冠脉血管造影术后的肾功能急剧恶化

抗氧化剂乙酰半胱氨酸可用于预防有肾功能损害的患者行计算机体层摄影(CT)扫描时的急性造影剂肾毒性,然而,将它用于冠脉血管造影术的作用仍未明了。作者研究评估有中度肾功能不全的患者行选择性冠脉血管造影术时口服乙酰半胱氨酸预防肾功能急剧恶化的作用。     

非类固醇抗炎药物及肾功能衰竭

非类固醇抗炎药物(NSAID)有抑制环氧合酶作用,减少前列腺素及血栓素的产生。已有报道 NSAID具显著肾毒性,包括急性肾功能衰竭(肾衰)导致肾脏低灌注、急性肾小管坏死及间质性肾炎;尚有报告许多 NSAID 药物在动物中易引起肾乳头坏死,但在     

速尿对造影剂肾病的潜在毒性作用

造影剂可引起急性肾功能衰竭(ARF),既往推荐对高危患者使用静脉补液及输注甘露醇(mannitol)和速尿(furosemide),以预防造影剂肾病的发生,但尚无前瞻性研究的报道。动物实验提示肾髓质缺氧在造影剂肾病中的重要性,同时提出速尿配合补液能缓解髓质缺氧。作者试图确定,速尿合并静脉补液对原有肾功能不全的患者是否有预防造影剂肾病的作用。     

一次性口服心痛定对糖尿病患者造影剂肾病的预防（附68例临床分析）

一次性口服心痛定对糖尿病患者造影剂肾病的预防（附６８例临床分析）朱少铭，陈明，罗超，梅小寒，陈学珍随着诊断技术的不断发展和造影剂的不断改造，造影技术的应用日益广泛，由此导致的肾毒性问题越来越多的出现于临床，在药物中毒所致的急性肾功能衰竭病因中，造影剂...     

急性肾功能衰竭实验室检查的筛选及评价

急性肾功能衰竭综合征(简称ARFS)病因繁多,广义而言,凡血肌酐急骤地升高,超过2mg/d1时,均可称为ARFS;狭义的ARFS是指急性肾小管坏死(简称ATN)。ARFS大致可分为肾前性氮质血症,肾性和肾后性氮质血症,其病因、病程经过及预后各异。若能在早期正确进行有关实验室检查,对于适时处理、缩短病程、改善预后有着重要意义。1.尿量:1970年前,少尿为诊断ARFS的必备症状和条件,但此后不断报道非少     

急性肾功能衰竭

急性肾功能衰竭系指肾小球滤过率骤然(通常为一过性)降低,可伴有或不伴有少尿。梗阻、肾脏灌注减少、各种肾小球肾炎、脉管炎或毒素等可促使这种情况的发生。本文主要讨论由“急性肾小管坏死”引起的急性实质性肾功能衰竭。但在组织学或功能检查时未必能证实有急性肾小管坏死。急性肾功能衰竭分为肾前性、肾性和肾后性。肾后性肾功能衰竭可归咎于梗阻。无尿且腹部平片肾脏正常或增大通常提示梗阻。急性肾小球肾炎、肾皮质坏死或两侧肾动脉血栓栓塞亦可引起无尿。在急性肾小管坏死的最初12～24小时可出现无尿。无尿和多尿交替出现     

造影剂导致的急性肾功能损伤对老年病人肾功能的影响

正随着影像诊断和血管介入技术的迅速发展,造影剂的使用日益广泛,由造影剂导致的急性肾功能损伤(contrast-induced acute kidney injury,CIAKI)也成为一个常见的、不可忽视的问题。CIAKI是医院获得性急性肾功能损伤(AKI)的第三位原因,仅次于血流灌注不足和药物毒性导致的肾损伤[1]。老年病人由于肾脏随着年龄增加逐渐萎缩和基础疾病增多,发生CIAKI的风险较中青年病人更高[2]。     

Effects of dilevalol on renal function

Renal function was measured in a total of 35 volunteers and patients who were given dilevalol, the R,R optical isomer of labetalol. Young normotensive volunteers (n = 6) and elderly normotensive volunteers (n = 12) received single 400- and 200-mg doses of dilevalol, respectively. Renal function was determined in these subjects on the same day before and after dosing. In addition, patients with mild to moderate essential hypertension (n = 11) and hypertensive patients with renal insufficiency (n = 6) were treated with placebo to establish baseline blood pressure and then were given dilevalol, 400 to 1,600 mg/day, for 2 to 6 weeks until blood pressure was controlled. Renal function was determined at the end of the baseline period and again at the end of dilevalol treatment. A subgroup of elderly hypertensives from the 2 protocols used to study hypertensive patients was treated as a separate study group. The only effect on parameters of renal function seen in any of the study groups was a statistically significant 15% decrease in glomerular filtration rate after single-dose treatment in the elderly normotensive group. Effective renal plasma flow, filtration fraction, renal blood flow and renal vascular resistance were unchanged before and after treatment in all groups. Mean arterial pressure was reduced significantly in all groups except in the elderly normotensive volunteers. Dilevalol appears to be a well-tolerated, effective therapeutic agent that is neutral regarding its effect on renal function and potentially useful in a variety of patient populations.     

Effects of statins on renal function

This report reviews data on the development of proteinuria in patients with chronic kidney disease who are treated with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) for dyslipidemia. Although subgroup analyses of statin trials have shown cardiovascular benefits in subjects with chronic kidney disease, concern about statin-induced proteinuria remains high. Experimental studies have suggested that the proteinuria seen with statin treatment results from the inhibition of receptor-mediated endocytosis, the likely mechanism of protein uptake in proximal tubular cells. Transient proteinuria may signify little more than the effective inhibition of cholesterol synthesis at this site. The blockade of protein trafficking in tubular cells is thought to reduce inflammation, slow fibrosis, and diminish proteinuria in the long term. Post hoc analyses of large clinical trials in subjects without overt renal disease have generally supported this notion, showing that statins most benefit patients with the greatest baseline renal deficits. Statins have also been shown to preserve glomerular filtration rate and reduce proteinuria in subjects with nondiabetic renal disease. In conclusion, in the absence of prospective, randomized trials in renally impaired patients, the collective evidence indicates that statin therapy may slow the decrease in renal function that generally attends atherosclerotic disease. The incidence of proteinuria with potent statins is only 1% to 2% when these drugs are given in recommended doses. Several large trials are currently under way to examine the safety and efficacy of statins in renally compromised patients at high risk for cardiovascular disease.     

The influence of catheter-based renal sympathetic denervation on renal function and renal arteries

ObjectiveCurrently investigated non-pharmacological minimally invasive method for the treatment of resistant hypertension is percutaneous denervation of renal sympathetic nerve fibres by radiofrequency catheter-based ablation. We assessed its influence on renal function and renal arteries.MethodsThe first 38 patients treated with catheter-based renal denervation at our centre between September 2011 and December 2012 were included in the study. Changes in renal function and changes in renal artery morphology at 12 months after the procedure have been analyzed.ResultsMean age was 57.6 ± 11 years, the majority (63.9%) were men. Average estimated glomerular filtration rates (eGF) were 1.25 ml/s/1,73 m² before denervation and 1.30 ml/s⁻¹/1.73 m⁻² 12 months after intervention. Changes in eGF did not reach statistical significance. New haemodynamically non-significant renal artery stenosis (40%) has occurred in only one case after procedure.ConclusionIn agreement with the results of several studies, our findings suggest that renal denervation (RDN) appears to be a safe therapeutic approach.     

Effects of renal medullary and intravenous norepinephrine on renal antihypertensive function

Increasing renal arterial pressure activates at least 3 antihypertensive mechanisms: reduced renin release, pressure natriuresis, and release of a putative renal medullary depressor hormone. To examine the role of renal medullary perfusion in these mechanisms, we tested the effects of the infusion of norepinephrine, either infusion into the renal medullary interstitium or intravenous infusion, on responses to increased renal arterial pressure in pentobarbital-anesthetized rabbits. We used an extracorporeal circuit, which allows renal arterial pressure to be set to any level above or below systemic arterial pressure. With renal arterial pressure initially set at 65 mm Hg, intravenous and medullary interstitial norepinephrine (300 ng. kg(-1). min(-1)) similarly increased mean arterial pressure (by 12% to 17% of baseline) and reduced total renal blood flow (by 16% to 17%) and cortical perfusion (by 13% to 19%), but only medullary norepinephrine reduced medullary perfusion (by 28%). When renal arterial pressure was increased to approximately 160 mm Hg, in steps of approximately 65 mm Hg, urine output and sodium excretion increased exponentially, and plasma renin activity and mean arterial pressure fell. Medullary interstitial but not intravenous norepinephrine attenuated the increased diuresis and natriuresis and the depressor response to increased renal arterial pressure. This suggests that norepinephrine can act within the renal medulla to inhibit these renal antihypertensive mechanisms, perhaps by reducing medullary perfusion. These observations support the concept that medullary perfusion plays a critical role in the long-term control of arterial pressure by its influence on pressure diuresis/natriuresis mechanisms and also by affecting the release of the putative renal medullary depressor hormone.     

Hyperuricemia and renal function

Increased serum urate concentration is commonly seen in clinical practice. It does not represent a specific disease, nor is it an indication for therapy. Hyperuricemia can be the consequence of increased uric acid production and/or decreased renal capacity to excrete uric acid. In essential hypertension, it has been described in up to one third of patients and is directly related to an increase in renal vascular resistance and inversely correlated with renal plasma flow. In other words, abnormal renal hemodynamics, commonly seen in the initial stages of the disease, account for the increased serum urate concentration. This can be maintained if a decrease in glomerular filtration rate takes place. The increase in uric acid has been shown to be a potent predictor of the development of cardiovascular events and death. In addition, uric acid, particularly when elevated, could represent an independent risk factor. On the other hand, an altered renal function predicts in an independent manner a higher cardiovascular risk. For this reason, the predictive capacity of uric acid could be partly dependent on the fact that hyperuricemia runs in parallel with a deranged renal function.