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排序方式: 共有1175条查询结果,搜索用时 15 毫秒
1.
Pharmacokinetics and pharmacodynamics of benazepril hydrochloride in patients with major proteinuria
Ch. Schweizer G. Kaiser W. Dieterle J. Mann 《European journal of clinical pharmacology》1993,44(5):463-466
Summary We have investigated whether the pharmacokinetics and pharmacodynamics of the ACE inhibitor benazepril hydrochloride are altered with proteinuria by studying 8 patients with major proteinuria of different causes who were given a single dose of 10 mg p.o.The maximum plasma concentration of benazepril was found between 0.5 and 2 h after dosing (median 1 h). Its elimination was almost complete within 6 h. Peak plasma levels of benazeprilat, the active metabolite of benazepril, were observed between 1 and 6 h (median 2.5 h). The elimination of benazeprilat from plasma was biphasic, with mean initial and terminal half-lives of 3.0 and 17.3 h, respectively. On average, the pharmacokinetic parameters of benazepril and benazeprilat in the patients did not differ from those in a historical control group of healthy volunteers, but intersubject variability in the AUC and half-lives of benazeprilat was greater in the patients.Plasma ACE was completely inhibited from 1.5 to 6 h after dosing, and at 48 h the mean inhibition was still 42 %. Plasma renin showed substantial intersubject variation. Mean supine blood pressure (systolic/diastolic) was reduced from baseline by a maximum of 18/13 mm Hg at 6 h. Proteinuria was diminished after benazepril in 7 patients.In conclusion, the results of this study suggest that proteinuria in the nephrotic range does not require a change in benazepril dosage. 相似文献
2.
J.-M. Halimi M. Buchler A. Al-Najjar I. Laouad Valérie Chatelet J.-F. Marlière H. Nivet Y. Lebranchu 《American journal of transplantation》2007,7(3):618-625
BACKGROUND: Microalbuminuria and macroalbuminuria constitute risk factors for ESRD and death in non-transplanted populations. Whether microalbuminuria (especially in non-proteinuric patients) and macroalbuminuria constitute risk factors for graft loss and death is presently unknown in renal transplantation. METHODS: We retrospectively assessed the association between urinary albumin excretion (UAE) and ESRD and death in renal transplantation. RESULTS: UAE was measured in 616 (397 proteinuric; 219 non-proteinuric patients) renal transplant recipients. They were grafted for 62 months (range: 6-192). During the 40 months (3.7-99) thereafter, 31 patients underwent dialysis and 32 died. Microalbuminuria (vs. normoalbuminuria) and macroalbuminuria (vs. microalbuminuria) were powerful risk factors for graft loss [OR: 14.25 (2.88-52.3) and 16.41 (7.46-36.0), respectively, both p < 0.0001], even after adjustments on renal function and diabetes. Among the 219 non-proteinuric patients, microalbuminuria (vs. normoalbuminuria) was a significant risk factor for graft loss [OR: 23.09 (1.93-276.4), p = 0.0132]. Both microalbuminuria (vs. normoalbuminuria) [OR: 5.55 (2.43-12.66), p < 0.0001] and macroalbuminuria (vs. microalbuminuria) [OR: 4.12 (1.65-10.29), p = 0.0024] were predictive of death. CONCLUSIONS: Microalbuminuria and macroalbuminuria are powerful independent predictors of ESRD and death. Microalbuminuria is a risk factor for graft loss even in non-proteinuric patients. UAE provides additional information on renal and patient prognosis as compared to proteinuria and renal function. 相似文献
3.
目的: 几乎没有研究报道妊娠高血压综合征 (妊高征 ) 患者尿蛋白对新生儿出生体重的影响, 该研究欲探讨妊高征患者不同水平尿蛋白对新生儿出生体重的影响关系。方法: 1997年 1月 ~2004年 6月期间, 住院分娩患中、重度妊高征产妇 136例, 对新生儿出生体重与各种因素进行回归分析及t检验分析。结果: 单变量回归分析尿蛋白、孕龄分别与新生儿出生体重有高度显著性关系 (P<0. 01); 尿蛋白和孕龄一起进入多元回归分析, 校正影响因素, 尿蛋白和孕龄仍然是影响新生儿出生体重显著性因素 (P<0 .01); 与妊高征尿蛋白 ( +) 比较, 尿蛋白 无显著性影响新生儿出生体重 (P>0. 05), 尿蛋白 有显著性影响新生儿出生体重 (P<0. 01)。结论: 新生儿出生体重与妊高征患者尿蛋白丢失有关, 尿蛋白 丢失将严重影响新生儿出生体重。 相似文献
4.
Focal segmental glomerulosclerosis 总被引:3,自引:0,他引:3
Over the last 2 decades, we have learnt that focal segmental glomerulosclerosis (FSGS) is a ubiquitous phenomenon underlying the progressive deterioration of many different types of renal diseases in both pediatric and adult populations. FSGS may also be the primary renal lesion, whether in new disease entities such as glycogen storage disease and human immunodeficiency virus infection, or in idiopathic FSGS. Although the mechanism which triggers the development of primary FSGS still remains unknown, laboratory and clinical studies have identified several key pathophysiological events leading to end-stage renal disease. While therapeutic modalities have not changed remarkably, a recent study, although uncontrolled, demonstrated an impressive efficacy of intravenous steroid pulse therapy in inducing remission. Nevertheless, it remains largely unknown whether such a forced remission decreases the overall risk of developing chronic renal failure. Studies have revealed an important pathophysiological role of angiotensin and the therapeutic efficacy of angiotensin converting enzyme inhibitors in progressive loss of renal function in diseases where glomerulosclerosis is secondary; however, it remains to be verified whether these results hold true in primary FSGS. As a result of the improvement in allograft survival rate, the benefit of renal transplant outweighs the risk of recurrence of FSGS, hence transplantation continues to be a vital therapy for FSGS patients who have reached renal failure. Thus, FSGS is not one disease, but rather a range of lesions seen in many settings. The type of lesions and the patient's unique genetic factors contribute to prognosis, and also may dictate choice of optimum therapy. 相似文献
5.
去甲斑蝥素对蛋白负荷肾病大鼠干预的研究 总被引:3,自引:0,他引:3
目的 观察去甲斑蝥素对蛋白负荷肾病大鼠蛋白尿及肾脏病理的影响。 方法 摘除SD大鼠右肾,腹腔注射牛血清白蛋白,建立蛋白负荷肾病模型后分成模型组和去甲斑蝥素组;对照组仅注射生理盐水。检测各时间点各组大鼠尿蛋白定量(24 h)。第5周末处死大鼠,检测血常规及生化指标;肾组织行光镜、电镜及免疫荧光染色作病理学检查。 结果 与对照组比较,模型组肾重/体重、各时间点尿蛋白定量(24 h)、肾小球硬化指数、小管间质病理损伤积分均显著升高(P均 < 0.01), 血清白蛋白(Alb)显著降低(P < 0.01)。电镜结果显示模型组小鼠肾小球系膜区有明显电子致密物沉积,足突融合;免疫荧光显示IgG和C3沉积于系膜区(3+~4+)。去甲斑蝥素干预后,肾病大鼠除Alb升高(P < 0.01)外,上述其余指标均显著降低(P < 0.05或0.01);系膜区有散在电子致密物沉积,足突灶状融合;IgG和C3免疫荧光染色强度减弱。各组间Scr、BUN、ALT及血常规差异均无统计学意义。 结论 去甲斑蝥素能显著降低蛋白负荷肾病大鼠尿蛋白,减轻其肾小管间质病理损伤,且无肝肾毒性及骨髓抑制等严重不良反应。 相似文献
6.
目的 研究pcDU6载体质粒介导的转化生长因子β1(TGF-β1)短发夹RNA(shRNA)对人血清白蛋白(HSA)致人肾近曲小管上皮细胞(HK2细胞)增殖,TGF-β1、结缔组织生长因子(CTGF)和纤连蛋白(FN)表达的影响,并探讨有关机制。方法 构建TGF-β1shRNA的pcDU6载体质粒,体外培养HK2细胞株。采用脂质体转染将表达TGF-β1shRNA的pcDU6质粒载体(pcDU6-A1-A2和peDU6-B1-B2)分别导人实验组细胞。用HSA(5g/L)刺激HK2细胞12h或24h。四甲基偶氮唑盐(MTF)比色法测定细胞增殖水平。RT-PCR半定量分析HK2细胞中TGF-β1、CTGF和FNmRNA的表达水平;双抗夹心酶联免疫吸附法检测HK2细胞培养液中TGF-β1及FN蛋白质水平。结果 HK2细胞在HSA刺激下,其TGF-β1、CTGF及FNmRNA的表达明显上调,培养液中TGF-β1和FN的蛋白质含量亦明显升高(P〈0.05)。与pcDU6空载体组比较,pcDU6载体质粒介导的TGF-β1shRNA干扰组TGF-β1、CTGF及FNmRNA的表达明显下调(P〈0.05)。TGF-β1shRNA转染HK2细胞后12h或24h,细胞培养液中TGF-β1和FN蛋白质含量明显下降,HK2细胞增殖被部分抑制(P〈0.05)。在细胞增殖、TGF-β1、CTGF及FN基因表达方面,TGF-β1shRNA干扰组组间比较,以及pcDU6空载体转染组与HSA刺激组比较,差异均无统计学意义。结论 peDU6载体质粒介导的TGF-β1shRNA能够明显抑制HSA刺激下HK2细胞增殖、TGF-β1、CTGF和FN基因的表达。HSA刺激HK2细胞增殖及CTGF和FN基因的过表达可能通过TGF-β1介导。 相似文献
7.
Alvestrand A.; Gutierrez A.; Bucht H.; Bergstrom J. 《Nephrology, dialysis, transplantation》1988,3(5):624-631
The effect of blood pressure reduction on the progression rateof chronic renal failure (CRF) was studied in 28 patients withCRF of diverse aetiology entering a prospective study (observationtime 724 months, mean 16 months). Endogenous creatinineclearance was 1266 ml/mm (mean 30±3 ml/mm). Weaimed to keep the blood pressure below 160/90 mmlHg. Dietaryprotein was not restricted. The progression rate of CRF wasassessed from the regression coefficients of the regressionsof creatinine clearance and the inverse of s-creatinine, respectively,on time. Progression rate and the means of all recordings ofmean arterial blood pressure (MAP) and urinary protein excretion,respectively, in each patient during the prospective phase werecompared with retro spective data from the proceeding period(observation time 425 months, mean 19 months). The patientsreceived various combinations of antihypertensive drugs includingdiuretics, beta-blockers and vasodilatory drugs. In 19 patientsMAP decreased from 109±2 to 102±2 mmHg (groupI), whereas MAP increased from 105±2 to l08±2mmHgin nine patients (group II). In group I proteinuria was significantlylower (P<0.05) and the progression of CRF was approximately50% slower (P.<0.01) in the prospective phase than in theretrospective phase; no changes were observed in group II. Calculatedfor all patients, significant correlations were observed betweenthe change in MAP and the change in progression rate and proteinexcretion, respectively. These results indicate that loweringof blood pressure results in decreased proteinuria and retardationof the progression of CRF irrespective of the aetiology. 相似文献
8.
Eight patients with Alport's syndrome and massive proteinuria (129±60.57 mg/m2 per hour) were treated with cyclosporin A (CyA) for 8 months. The average dose of CyA administered to all patients was 4.21±0.26 mg/kg per day and blood CyA levels of 63.4±4.1 ng/ml were attained. In five patients, proteinuria abated during the 3rd week of treatment. In the remaining three, all of whom had low creatinine clearance (82.0, 46.0 and 43.2 ml/min per 1.73 m2 respectively), proteinuria persisted but at levels lower than before treatment: 32.5±15.9 mg/m2 per hour versus 183.3±29.7 mg/m2 per hour. No permanent decrease in creatinine clearance was observed in any of these patients throughout treatment. In those patients in whom proteinuria abated, it reappeared 2 weeks after discontinuation of CyA treatment. We observed no significant increases in angiotensin II plasma levels in our patients during CyA administration. Although we have shown that CyA will reduce massive proteinuria in patients with Alport's syndrome, we cannot yet recommend its use as a therapeutic measure. 相似文献
9.
复方肾华治疗大鼠改良慢性血清病肾炎的实验研究 总被引:2,自引:0,他引:2
目的 观察复方肾华胶囊对改良大鼠慢性血清病肾炎模型的治疗作用。方法 采取传统大鼠慢性血清病肾炎模型制作方法加上切除大鼠一侧肾脏、隔日饮饲牛血清白蛋白 (BSA)酸化水、腹腔注射大肠杆菌内毒素 (LPS)等措施 ,制作肾炎模型 ,与西药蒙诺作对照 ,观察中药肾华对肾炎大鼠尿蛋白、血生化、凝血指标、肾功能、病理、免疫荧光以及增殖细胞核抗原 (PCNA)表达的作用。结果 肾华胶囊能够显著减轻肾炎大鼠肾脏重量及肾重指数、降低肾炎大鼠尿蛋白、升高血清蛋白、降低胆固醇、甘油三酯、改善肾功能、纠正凝血功能紊乱、减轻肾脏病理改变、减轻免疫荧光变化、减弱PCNA的表达。结论 中药肾华胶囊对大鼠慢性血清病肾炎模型有较好的治疗作用 相似文献
10.
Emine Sözeri Dietrich Feist Hans Ruder Karl Schärer 《Pediatric nephrology (Berlin, Germany)》1997,11(3):307-311
Renal lesions have repeatedly been described in Wilson’s disease (WD). We investigated the excretion of total protein, albumin,
low (LMW) and high molecular weight (HMW) proteins, N-acetyl-β-D-glucosaminidase (NAG), and calcium, as well as creatinine clearance, in 24-h urine samples of 41 patients with WD aged 6 – 37
(mean 17) years who had been treated for a period of 0 – 15 (mean 4.5) years with D-penicillamine (900 mg/day). The amount of all protein excreted was significantly increased compared with controls, 39% of
patients presenting with total proteinuria more than two standard deviations from the mean of controls. The changes in protein
excretion depended on the duration of treatment. LMW proteinuria was elevated almost exclusively in the first 2 years after
the start of treatment, indicating early tubular damage. This is supported by an initially high excretion of β2-microglobulin, NAG, and calcium. Increased excretion of HMW proteins, including albumin, persisted over longer periods, which
suggests glomerular injury in some patients, possibly related to the use of D-penicillamine. Creatinine clearance remained roughly within normal limits. We propose that renal function should regularly
be checked in patients with WD.
Received October 26, 1995; received in revised form August 27, 1996; accepted September 20, 1996 相似文献