培哚普利对充血性心力衰竭患者血浆细胞间粘附因子-1的影响

目的 :探讨培哚普利对充血性心力衰竭 (CHF)患者血浆细胞间粘附因子 1(sICAM 1)水平的影响及心脏保护机制。 方法 :用酶联免疫方法检测 42例服用培哚普利的CHF患者、42例常规治疗CHF患者治疗前后及 30例健康者血浆中sICAM 1水平。 结果 :① 84例CHF患者血浆中sICAM 1为 ( 5 87.6± 15 2 .1) μg/L ,较健康者 ( 16 7.4± 34.6 ) μg/L显著增高 ( P<0 .0 0 1) ,且随着心功能损害程度加重而升高 ,各组间比较差异有显著性意义 (P <0 .0 5 )。②CHF培哚普利治疗组与常规治疗组治疗前后血浆中sICAM 1浓度〔分别为 ( 5 91.8± 15 5 .2 )、( 332 .1± 115 .8) μg/L ;( 5 80 .0± 134.4)、( 4 2 3.1± 118.1) μg/L〕水平差异有非常显著性意义 (P <0 .0 1) ,且培哚普利治疗组较常规治疗组治疗后血浆中sICAM 1降低更为明显 (P <0 .0 1)。 结论 :培哚普利具有抑制CHF患者sICAM 1水平的作用 ,从而减缓心室重塑的进程 ,保护和改善心功能。     

X综合征患者肱动脉流量介导性舒张功能异常及培哚普利的干预作用

目的观察X综合征患者肱动脉流量介导性舒张(FMD)功能变化及培哚普利的干预作用.方法采用随机、对照、单盲方法将22例X综合征患者分为两组培哚普利+硝酸异山梨酯组(A组,11例),予培哚普利每天2～4 mg,晚顿服,硝酸异山梨酯每次10～20 mg,2次/日,口服.硝酸异山梨酯组(B组,11例),仅予硝酸异山梨酯每次10～20 mg,2次/日,口服.疗程均为6周.疗程前后分别进行肱动脉血管超声检测及活动平板试验.正常对照组20例,不予任何治疗.结果①X综合征患者肱动脉FMD活性较正常对照组明显减弱[(4.7±2.8)%比(13.5±3.1)%,P<0.001].②A组培哚普利干预后肱动脉FMD活性显著增强,与B组比较有非常显著性差异[(9.6±1.7)%比(4.9±2.1)%,P<0.001].③A组疗程结束前1周内典型心绞痛平均发作次数较B组明显减少(2.6±1.4次比4.0±1.6次,P<0.01).A组疗程后与疗程前比较运动诱发的ST段缺血型下移之和(∑ST)明显减少(5.2±1.7 mm比7.9±2.3 mm,P<0.01),运动持续时间显著延长(8.2±2.3 min比6.6±1.6min,P<0.01),而B组疗程前后无显著差异.∑ST减少及运动持续时间延长与肱动脉FMD活性增强具有明显相关性(γ=-0.68,γ=0.62,P均<0.001).结论X综合征患者存在明显的血管内皮依赖性舒张功能障碍.培哚普利通过增强FMD活性,改盖心肌缺血,对该病具有治疗作用.     

氨氯地平和培哚普利联合治疗对高血压病患者肾功能的影响

探讨氨氯地平，培哚普利单独治疗和联合治疗对高血压病患者肾功能的影响。方法 ６６例高血压病患者随机分为三组：氨氯地平组；培哚普利组；氨氯地平和培哚普利联合治疗组。疗程２４周，治疗前后观察肾功能指标变化。结果 １．氨氯地平，培哚普利及联合治疗组高血压病患者治疗后均能显著降低血压及尿蛋白排泄量「２４小时尿白蛋白：１０２±３６．４．１０４．７±４２．７和１０１．４±０．０６５，０．２４±０．６２及０．２３     

替米沙坦对老年高血压伴糖尿病患者左室肥厚的治疗作用

目的探讨替米沙坦对老年高血压伴有糖尿病患者空腹血糖、血清胰岛素、胰岛素抵抗指数及左室肥厚的影响。方法选择老年高血压伴有糖尿病左室肥厚患者120例,随机分为替米沙坦(口服80～160mg/d)组或培哚普利(口服4～8mg/d)组,每组60例,均治疗8个月。治疗前、后检测空腹血糖、血清胰岛素、胰岛素抵抗指数及超声心动图,对比分析治疗前、后上述指标的差异。结果与治疗前比较,替米沙坦组和培哚普利组治疗后收缩压和舒张压明显下降(159/101至142/89mmHg;161/103至145/90mmHg,均为P<0.01);(2)替米沙坦治疗后,空腹血糖、血清胰岛素及胰岛素抵抗指数明显降低〔(8.2±0.9)至(7.3±0.7)mmol/L,(12.8±0.9)至(7.5±0.6)pmol/L及(4.7±0.4)至(4.1±0.3),均为P<0.05〕,左室后壁与室间隔厚度显著下降〔(1.27±0.28)至(1.09±0.21)cm,(1.28±0.31)至(1.09±0.27)cm,均P<0.05〕,左室重量及左室重量指数下降更显著〔(264±98)至(205±62)g,(165±60)至(128±34)g/m2,均为P<0.01〕;培哚普利组治疗后空腹血糖、血清胰岛素、胰岛素抵抗指数无明显的变化,左室后壁与室间隔厚度亦无明显的变化,左室重量及左室重量指数下降显著〔(260±94)至(225±72)g;(163±58)至(139±37)g/m2,均为P<0.05〕。结论替米沙坦在提高胰岛素的敏感性、     

苯那普利与伊贝沙坦联合用药对高血压患者尿蛋白,血肌酐清除率,血肌酐的影响

目的观察苯那普利、伊贝沙坦及两药联用对原发性高血压患者微量白蛋白尿的影响.方法采用随机、单盲、病例对照设计,82例原发性高血压伴微量白蛋白尿的患者,随机接受苯那普利10 mg/d(n＝25)、伊贝沙坦300 mg/d(n＝28)或苯那普利5 mg/d联用伊贝沙坦150 mg/d(联用组n＝29)治疗18周,比较治疗前后及同期各组间的收缩压(SBP)、舒张压(DBP)、尿白蛋白排泄率(UAER)、肌酐清除率(CCr)、血清肌酐(SCr).为达到血压<140/90 mm Hg的控制目标,可以加用吲达帕胺和/或倍他乐克.结果 (1)SBP、DBP同期各组无显著差别,治疗前后比较各组均下降显著(P<0.001);(2)UAER治疗后各组均显著下降(苯那普利组下降18.8%,伊贝沙坦组下降18.5%,联用组下降46.8%,P<0.001),两单药组分别与联用组比较差别显著(苯那普利组P＝0.022,伊贝沙坦组P＝0.025),联用组较单药组下降幅度总体增加28.2%.(3)联合用药组治疗后血肌酐上升(85.9±16.1 vs 94.6±14.5)μmol/L,肌酐清除率下降(85.3±5.8 vs 78.3±4.1)mL/min.结论对原发性高血压伴微量白蛋白尿的患者,苯那普利、伊贝沙坦减少微量白蛋白尿的作用相当,两药联用则作用明显加强.联合用药组血肌酐浓度上升,肌酐清除率下降,可能提示肾小球内压下降,其长期预后意义有待观察.     

美托洛尔和培哚普利对心肌梗死患者自主神经失衡和预后的影响

目的观察心肌梗死(AMI)患者应用美托洛尔、培哚普利后的自主神经失衡的变化及其与预后的关系.方法选择病情、年龄等相匹配的AMI患者随机分为美托洛尔组(n=66)、培哚普利组(n=71)及对照组(n=69).测定三组患者用药前及用药后4周及随访期的24h心率变异性(HRV)、左室射血分数(LVEF)、室性心律失常(室早>1O/h),对比其随访结果.结果(1)服药组的HRV观察指标高于对照组[美托洛尔组正常窦性心搏间期的标准差(SDNN)为(138.5±32.6)ms,相邻心搏间期>50ms的百分数(PNN50)为9.5±1.53,高频功率(HF)为(139.9±33.4)ms2;培哚普利组SDNN(117.3±22.9)ms,PNN509.2±1.6,HF(140.6±20.5)ms2;对照组SDNN(87.4±28.6)ms,PNN506.0±3.5,HF(100.3±21.4)ms2,P<0.05];(2)随访期间服药组的室性心律失常发生率明显低于对照组,美托洛尔组为35.4%,培哚普利组为43.5%,对照组为66.1%,P<O.05;(3)服药组患者的HRV恢复比对照组较早、较快;(4)服药组的EF值正常率高于对照组,美托洛尔组EF为96%,培哚普利组EF为90%,对照组EF为64%,P<0.05;(5)对照组的病死率明显高于服药组,分别为美托洛尔组病死率为10%,培哚普利组为22%,对照组为36%,P<0.05.结论美托洛尔和培哚普利能够使AMI及恢复期心肌梗死患者的HRV升高,改善失衡的自主神经功能及降低的心功能,减少室性心律失常发生率,降低病死率.     

培哚普利对急性冠状动脉综合征患者白介素-6和肿瘤坏死因子-α水平的影响

目的　观察急性冠状动脉综合征患者使用培哚普利治疗后白介素 - 6( IL- 6)和肿瘤坏死因子 ( TNF- α)水平的变化。方法　选择 10 0例诊断为不稳定型心绞痛 ( 73例 )和急性心肌梗死 ( 2 7例 )的病人分为两组 ,A组 ( 5 0例 )接受培哚普利治疗 2周 ,B组 ( 5 0例 )未接受培哚普利治疗。入院时和治疗 2周后分别检测 IL- 6和 TNF- α浓度。结果　入院时 A组 IL- 6和 TNF- α水平与 B组相比无显著性差异 ( 60 8.4± 112 .3 pg/ ml vs5 83 .1± 10 6.4pg/ m l,46.0±10 .4pg/ ml vs 44 .1± 8.8pg/ ml,P>0 .0 5 ) ,治疗两周后两组 IL - 6和 TNF-α水平均有降低 ,而 A组病人两周后 IL -6和 TNF- α水平与 B组相比有显著降低 ( 2 40 .5± 5 0 .4pg/ ml vs414.3± 98.6pg/ m l,16.2± 3 .5 pg/ m l vs3 2 .7± 6.2 pg/ ml,P<0 .0 5 )。结论　急性冠状动脉综合征患者应用培哚普利治疗后 IL - 6和 TNF-α水平降低 ,提示培哚普利可能有直接抗炎作用     

苯那普利对糖尿病肾病UALB、TGF-β1、CⅣ和LAM影响

目的 评价苯那普利对糖尿病肾病(DN)的临床疗效,并探讨相应作用机制.方法 采用随机对照研究,观察苯那普利治疗前后DN患者24 h平均尿微量白蛋白排泄量以及尿转化生长因子β1(TGF-β1)、层黏连蛋白(LAM)和Ⅳ型胶原(CⅣ)的变化.结果 苯那普利治疗6月后,患者24 h尿微量白蛋白平均排泄量为(0.044±0.034) g,尿TGF-β1为(1.48±0.59) μg/L,LAM为(22.74±23.26 )μg/L量,CⅣ浓度为(13.47±10.94) μg/L量,均较治疗前有显著降低(P＜0.05),而对照组则较基线值明显升高(P＜0.05).结论 苯那普利可以有效降低血压、抑制肾脏TGF-β1、LAM及CⅣ的表达、显著减少DN患者尿蛋白的排出,从而发挥其肾脏保护作用.     

培哚普利治疗老年早期糖尿病肾病的疗效观察

为探讨培哚普利对血压正常的老年早期糖尿病肾病患者 2 4h微量白蛋白尿的影响 ,选择住院老年糖尿病患者中 ,血压为 10 0～ 14 0 6 0～ 90mmHg ,2 4h尿白蛋白排泄率为 2 0～ 2 0 0 μg mim的早期糖尿病肾病患者 5 0例 ,随机分为实验组 30例和对照组 2 0例。两组血糖均控制在空腹≤ 7.0mmol L、餐后 2h≤ 10 .0mmol L后 ,检测血压、微量白蛋白尿、肾功能和血清钾离子水平 ,给予实验组培哚普利 2～ 4mg 天 ,对照组给予安慰剂 ;治疗后第 12周和 2 4周分别复检上述指标。结果发现 ,较治疗前比较 ,治疗后第 12周和 2 4周微量白蛋白尿实验组分别下降 4 9.6 % (P<0 .0 5 )和 4 1.4 % (P <0 .0 5 ) ,对照组分别增加 7.8%和 2 .5 % ,两组间同期比较差异有显著性 (P <0 .0 5 ) ;治疗后两组患者的血压、肾功能和血清钾离子水平均无显著变化 ;实验组因咳嗽停药者占 6 .7% (2 30 )。结果提示 ,培哚普利对血压正常的老年早期糖尿病肾病患者有显著减少微量白蛋白尿和保护肾脏的作用     

培哚普利治疗糖尿病肾病30例临床分析

目的探讨培哚普利对糖尿病并发肾病患者的疗效。方法对30例糖尿病肾病住院患者口服培哚普利治疗,治疗前后观察患者24h尿总蛋白定量、8h尿白蛋白定量、血糖、血尿素氮、肌酐,定期复查血清钾,随时复查血压。结果治疗后尿总蛋白较治疗前明显下降,具有统计学意义（P〈0.01）。结论培哚普利能有效减少糖尿病并发肾病患者尿总蛋白量的排出。     

Long term reduction of microalbuminuria after 1 year of angiotensin converting enzyme inhibition by perindopril in hypertensive insulin-treated diabetic patients

We studied the effects of perindopril, an angiotensin converting enzyme (ACE) inhibitor administered during 12 months, on creatinine clearance, albuminuria and glycaemic control in diabetic subjects with mild to moderate hypertension. After 1 month placebo, 40 insulin-treated patients were divided into 3 groups based upon their urinary albumin excretion rate (AER). Group I had a normoalbuminuria (AER less than 15 mg/24 h), group II had a microalbuminuria (AER : 15-150 mg/24 h) and group III had a macroproteinuria (AER greater than 150 mg/24 h and Albustix (+)). They were given perindopril, 4 to 8 mg orally once daily, and received a stable diet. Diastolic blood pressure was normalized within the first 3 months in 80% of the patients. From these, 28 (14.7 and 7 from groups I, II and III respectively) were followed during a total active treatment period of 12 months. They were matched for age, duration of diabetes and hypertension, systolic and diastolic blood pressures, daily insulin dose, postprandial plasma C-peptide and quality of glycaemic control. Mean supine diastolic blood pressure was decreased by 15 and 18% at 1 and 12 months respectively. Heart rate was not significantly modified. At 3 months, plasma ACE activity was nearly totally inhibited while plasma renin activity was markedly increased. In patients of group II, microalbuminuria was reduced from 66 +/- 13 (mean +/- SEM after placebo) to 39 +/- 6 mg/24 h after 1 month perindopril and this effect was maintained at 12 months. In group I, albuminuria remained within the normal range. In group III, macroproteinuria was not consistently modified by perindopril.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased secretion of TGF-beta1 by peripheral blood mononuclear cells from patients with Type 1 diabetes mellitus with diabetic nephropathy.

AIMS: To study transforming growth factor (TGF)-beta1 secretion by peripheral blood mononuclear cells (PBMC) from Type 1 diabetic patients with and without nephropathy. METHODS: Thirty normoalbuminuric Type 1 diabetic patients (urinary albumin excretion rate (AER) < 20 microg/min), 12 microalbuminuric (AER 20-200 microg/min), 10 nephropathic (AER > 200 microg/min), and 13 non-diabetic individuals were recruited. TGF-beta1 secretion by PBMC was measured by enzyme immunoassay (EIA) after 48 h culture with and without phytohaemagglutinin (PHA) (5 microg/ml). RESULTS: After 48 h culture, the highest TGF-beta1 levels secreted by unstimulated PBMC were found in patients with nephropathy (median 6.2 (range 0.9-20.0) ng/ml) when compared to patients with normal albumin excretion (4.1 (0.2-11.3) ng/ml), microalbuminuria (1.8 (0.2-6.4) ng/ml) and healthy controls (1.0 (0.2-7.0) ng/ml); P = 0.02 for the three diabetic groups and P = 0.006 for all groups. At 48 h, the PHA-stimulated TGF-beta1 levels were 12.4 (2.9-30.0) ng/ml in nephropathic, 7.3 (0.5-21.2) ng/ml in normoalbuminuric, and 5.5 (0.5-27.6) ng/ml in microalbuminuric patients (P = 0.05). A correlation was observed between TGF-beta1 and diastolic blood pressure in the subgroup of patients with incipient and overt nephropathy (r = 0.45, P = 0.04). CONCLUSIONS: Type 1 diabetic patients with overt nephropathy show increased TGF-beta1 secretion by PBMC. Diastolic blood pressure levels correlated with TGF-beta1 secretion in diabetic patients with nephropathy. Increased TGF-beta1 secretion by PBMC may be associated with renal and vascular disease in Type 1 diabetes mellitus.     

Pioglitazone reduces urinary podocyte excretion in type 2 diabetes patients with microalbuminuria

In various renal diseases, including diabetic nephropathy, detection of podocytes in the urine indicates severe injury to podocytes in the glomeruli. Pioglitazone is a newly developed antidiabetic agent that attenuates insulin resistance. The aim of the present study was to determine whether pioglitazone affects urinary albumin excretion (UAE) or the number of urinary podocytes or both in type 2 diabetes patients with microalbuminuria. Twenty-eight patients with normotensive type 2 diabetes and microalbuminuria (18 men and 10 women; mean age, 52.5 years) and 30 age-matched normotensive controls (20 men and 10 women; mean age, 51.5 years) were included in the study. Urinary podocytes were detected by immunofluorescence with a monoclonal antibody against podocalyxin. Patients were randomly assigned to 2 groups: a pioglitazone-treatment group (30 mg/day, n = 14) and a placebo group (n = 14). Treatment was continued for 6 months. Podocytes were absent in the urine of healthy controls, but detected in 17 of 28 diabetic patients (60.7%). UAE was reduced from 96.7 +/- 50.5 microg/min to 39.7 +/- 22.9 microg/min (P <.01) in the pioglitazone-treatment group, and the number of urinary podocytes was reduced from 0.9 +/- 1.0 cells/mL to 0.1 +/- 0.2 cells/mL (P <.001). Neither UAE nor the number of urinary podocytes was affected in the placebo group. These data indicate that pioglitazone is effective for reducing UAE and podocyte injury in early-stage diabetic nephropathy.     

Proteolysis of insulin-like growth factor-binding protein-3 is increased in urine from patients with diabetic nephropathy

The insulin-like growth factor (IGF) system has been implicated in the development of experimental diabetic nephropathy. IGF-binding protein-3 (IGFBP-3) modulates IGF actions, and proteolysis decreases its binding affinity for IGFs. The aim of this study was to explore the possibility that proteolysis of IGFBP-3 may be altered in diabetic nephropathy and may therefore modify the intrarenal effects of IGFs. IGFBP-3 proteolysis in urine from diabetic patients with normo- [albumin excretion rate (AER), <20 microg/min], micro- (AER, 20-200 microg/min), and macroalbuminuria (AER, >200 microg/min) was studied in 34 patients with noninsulin-dependent diabetes mellitus (NIDDM), 14 patients with insulin-dependent diabetes mellitus, and 9 controls. Urine samples were analyzed by Western ligand blotting and IGFBP-3 immunoblotting. Protease activity was quantitated using [125I]IGFBP-3 as a substrate. WLB showed three main bands (40-46, 35, and 26 kDa) in control urine and a fainter 18-kDa band. All but the 35-kDa band were immunoreactive with the IGFBP-3 antiserum. The same pattern of IGFBPs was seen in urine from normoalbuminuric diabetic patients. However, the urine of diabetic patients with micro- and macroalbuminuria contained little or no intact 40- to 46-kDa IGFBP-3. In patients with noninsulin-dependent diabetes mellitus, urinary IGFBP-3 protease activity in micro- (n = 13) and macroalbuminuric patients (n = 12; mean +/- SD[SCAP], 75 +/- 25% and 84 +/- 24%) was significantly higher than that in normoalbuminuric patients (29 +/- 9%; P = 0.0001). Similar results were observed in patients with insulin-dependent diabetes mellitus. Proteolytic activity in diabetic urine was due to a serine protease. In conclusion, diabetic nephropathy was associated with IGFBP-3 proteolysis in urine. As similar changes were not observed in patients' sera, this is likely to reflect changes in the kidney or urinary tract, resulting in increased local IGF bioavailability, and therefore may contribute to the structural changes of diabetic nephropathy.     

Influence of glycemic control and hypertension on urinary microprotein excretion in non-insulin-dependent diabetes mellitus

In order to evaluate the influence of glycemic control and hypertension on the development of diabetic nephropathy, we measured urinary excretion of albumin (AER) and other microproteins in non-insulin-dependent diabetes mellitus (NIDDM), and reexamined the 103 patients who had had AER < 300 μg/min at the initial study 12–18 months later. AER in the patients with HbA₁c ≧ 7.5% increased significantly in both the normoalbuminuric (AER < 30 μg/min) and microalbuminuric (30–300 μg/min) groups, whereas no significant change in AER was observed in the patients with HbA₁c < 7.5%. In the microalbuminuric group, AER in both hypertensive and normotensive patients increased significantly. In this group, the change in AER correlated positively with the change in α₁-microglobulin (α 1M). These results indicate that glycemic control has a greater influence on the development of nephropathy in its early stage than hypertension and that α 1M is as a good predictor of nephropathy as albumin.     

Renoprotective effects of low-dose valsartan in type 2 diabetic patients with diabetic nephropathy

It is unknown whether the angiotensin receptor antagonist valsartan exerts a renoprotective effect on patients with type 2 diabetes and diabetic nephropathy independent of its hypotensive effects. Forty patients with type 2 diabetes participated in this study. All patients received valsartan 40 mg, a dose with no clinical effect on blood pressure levels. Blood pressure, urinary albumin excretion (UAE), and creatinine clearance were determined at baseline and at the end of the 6-month treatment period. Antihypertensive and/or antidiabetic drugs, including insulin, were permitted throughout the study. After 6 months of valsartan therapy, mean UAE decreased from 86.8 +/- 196 to 46.9 +/- 97 microg/min (n = 37). In addition, a significant decrease was observed in the UAE of the subgroup of patients displaying diabetic nephropathy (UAE > 20 microg/min, n = 14), from 219.4 +/- 275 to 102.7 +/- 141 microg/min, (P < 0.01). Changes in UAE for valsartan correlated significantly with UAE at baseline (r = -0.935, P < 0.0001). Serum creatinine levels and creatinine clearance remained stable before and after treatment with valsartan. No significant differences were observed between pre- and post-treatment body mass index, glycosylated hemoglobin, or systolic and diastolic blood pressure. In type 2 diabetic patients with diabetic nephropathy, 6 months of treatment with low dose valsartan, an angiotensin-II receptor antagonist, thus reduced UAE with no reduction in systemic blood pressure. The drug may be safely administered in this subset of type 2 diabetic patients. The long-term benefits in terms of risk reduction must still be evaluated in further trials.     

Long-term renoprotection by perindopril or nifedipine in non-hypertensive patients with Type 2 diabetes and microalbuminuria.

AIMS: To assess the efficacy of an angiotensin converting enzyme (ACE) inhibitor (perindopril), a dihydropyridine calcium channel blocker (sustained release nifedipine) and placebo in preventing the progression of albuminuria and decline in glomerular filtration rate (GFR) in patients with Type 2 diabetes and microalbuminaria. METHODS: A prospective, randomized, open, blinded end point study of 77 patients allocated to three treatment groups (23 perindopril, 27 nifedipine, 27 placebo). Drug doses were adjusted to achieve a decrease in diastolic blood pressure (DBP) of 5 mmHg in the first 3 months and additional therapy was given if hypertension developed (supine DBP > 90 mmHg and/or systolic blood pressure (SBP) > 140 mmHg if < or = 40 years; supine DBP > 90 mmHg and/or SBP > 160 mmHg if > 40 years). Median follow-up was 66 months, with 37 patients being followed for at least 6 years. RESULTS: Blood pressure remained within the non-hypertensive range in 83% of perindopril-, 95% of nifedipine- and 30% of placebo-treated patients (P < 0.01). In the first 12 months albumin excretion rate (AER) decreased by 47% only in the perindopril group (P = 0.04). From 12 to 72 months, AER gradients increased by 27% per year only in the placebo group (P < 0.01). After 6 years, macroalbuminuria had developed in 7/15 placebo compared with 2/11 in perindopril and 1/11 nifedipine-treated patients (P = 0.05). GFR did not change in the first 12 months, but thereafter the median GFR gradient (ml/min/1.73 m(2) per year) was -2.4 (P < 0.01) for perindopril-, -1.3 (P = 0.26) for nifedipine- and -4.2 (P = 0.01) for placebo-treated patients. The rate of decline in GFR for the study group as a whole from 12 months to the end of follow-up correlated negatively with mean arterial pressure (MAP) (r = -0.38, P < 0.01). During a 3-month treatment pause in 29 patients AER tended to increase only in the perindopril group (P < 0.07). CONCLUSIONS: Long-term control of blood pressure with perindopril or nifedipine stabilizes AER and attenuates GFR decline in proportion to MAP in non-hypertensive patients with Type 2 diabetes and microalbuminuria.     

前列腺素E1治疗糖尿病肾病Ⅲ期临床疗效观察

目的观察前列腺素E1(PGE1)治疗糖尿病肾病Ⅲ期(DN-Ⅲ)的临床疗效。方法 35例糖尿病肾病(DN)患者予PGE1治疗2周,并观察24 h尿蛋白、24 h尿微量白蛋白、空腹血糖、餐后2 h血糖、血肌酐、血压的变化及不良反应等。结果 PGE1治疗2周后,24 h尿蛋白、24 h尿微量白蛋白较前均明显下降(P0.01),其余检测指标虽较前降低,但差异无统计学意义(P0.05)。患者治疗后无肝功能异常改变,治疗期间无皮疹、血管炎等不良反应发生。结论 PGE1可减轻DN-Ⅲ患者尿蛋白的排泄,延缓DN的发展和恶化。     

Is Hypertension a Major Independent Risk Factor for Retinopathy in Type 1 Diabetes?

Hypertension is an established risk factor for retinopathy. Whether it is an independent risk factor or acts only by association with nephropathy is not known. Therefore, we studied 273 Type 1 diabetic patients. They were divided into four groups. Group 1 (n = 55) were normotensive and normoalbuminuric, group 2 (n = 51) had hypertension but were normoalbuminuric, group 3 (n = 33) had nephropathy but were normotensive, and group 4 (n = 134) had nephropathy and hypertension. Hypertensive patients with normoalbuminuria (blood pressure 146 +/- 19 (+/-SD)/87 +/- 12 mmHg) had the same prevalence of retinopathy as normoalbuminuric normotensive patients (123 +/- 12/75 +/- 5 mmHg). Hypertensive nephropathic patients (blood pressure 147 +/- 18/87 +/- 8 mmHg) had more retinopathy than hypertensive normoalbuminuric patients despite similar blood pressure (normal retina/advanced retinopathy: 3%/73% vs 46%/17%, p less than 0.001). Nephropathic normotensive patients had worse retinal changes than hypertensive normoalbuminuric patients (19%/49%, p less than 0.001) but fewer than the nephropathic hypertensive patients p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prior long term glycaemic control and insulin therapy in insulin-dependent diabetic adolescents with microalbuminuria

Adolescence seems to be a period of increased risk for the initiation of diabetic renal disease in insulin-dependent diabetic children. Poor glycaemic control is a risk factor for diabetic nephropathy. We have therefore evaluated prior long-term glycaemic control in 23 diabetic adolescents with microalbuminuria (albumin excretion rate (AER) 20-200 micrograms/min, median 39.0 micrograms/min) and in 23 matched diabetic controls with AER less than 20 micrograms/min (median 9.3 micrograms/min). Glycaemic control was assessed by mean HbA1 and clinic blood glucose levels over a period ranging from 12 to 84 months (median 48 months). Mean HbA1 was 13.6 +/- 2.0% in the microalbuminuric subjects, compared to 11.5 +/- 2.2% in the controls (P less than 0.002); mean blood glucose levels were 13.5 +/- 3.0 and 11.4 +/- 3.0 mmol/l, respectively (P less than 0.02). There appeared to be a 'threshold effect' (mean HbA1 greater than 12.0%), above which the development of microalbuminuria was more likely. More patients with microalbuminuria than controls had been treated with a single rather than twice-daily insulin injections (P less than 0.001), and glycaemic control was significantly worse in patients treated with one injection. We conclude that poor long term glycaemic control is a risk factor for microalbuminuria, and that improving control during childhood is likely to reduce the prevalence of later microalbuminuria. Two insulin injections, of combined intermediate and short-acting preparations, are more likely to provide better control than a single daily insulin dose.