2型糖尿病患者血浆chemerin水平与其冠脉病变程度的相关性分析

目的:探讨2型糖尿病患者血浆趋化素(chemerin)水平与冠脉病变程度的关系。方法:选取2011年1月~2012年2月我院收治的2型糖尿病(T2DM)患者92例,均行冠状动脉造影检查。按冠状动脉造影结果分为单纯2型糖尿病无冠状动脉病变组26例(DM0);合并单支冠状动脉病变组32例(DM1);合并双支以上病变组34例(DM2)。另选取正常健康行冠脉造影检查者25例作为正常对照组(NC)。采用酶联免疫吸附法检测各组入选者血浆chemerin水平,并分析其与冠脉病变程度的相关性。结果:T2DM及T2DM合并冠状动脉病变患者血浆chemerin水平与NC组对比均明显升高,并且与冠状动脉病变严重程度呈正相关(P0.05)。各组血浆Chemerin水平与BMI、HOMA-IR、TC、和APOB各指标间呈显著正相关(r分别为0.781、0.723、0.415、0.694,P均0.01)。结论:2型糖尿病患者冠状动脉病变的发生发展可能与血浆chemerin升高有关。     

血清CTRP4、CTRP5、CTRP6与2型糖尿病合并冠心病患者冠状动脉病变的关系研究

摘要 目的：探讨血清补体1q/肿瘤坏死因子相关蛋白（CTRP）4、CTRP5、CTRP6与2型糖尿病（T2DM）合并冠心病（CHD）患者冠状动脉病变的关系。方法：选取2021年3月～2021年7月我院收治的100例T2DM合并CHD患者为合并组,根据SYNTAX评分分为中重度病变组44例和轻度病变组56例,选取同期收治的100例单纯T2DM患者为T2DM组,另选取同期体检健康志愿者80名为对照组。采用酶联免疫吸附法检测血清CTRP4、CTRP5、CTRP6水平。采用Spearman相关性分析T2DM合并CHD患者SYNTAX评分与血清CTRP4、CTRP5、CTRP6水平的相关性,多因素Logistic回归分析T2DM合并CHD患者冠状动脉中重度病变的影响因素。结果：对照组、T2DM组、合并组血清CTRP4、CTRP5水平依次升高,CTRP6水平依次降低（P＜0.05）。Spearman相关性分析显示,T2DM合并CHD患者SYNTAX评分与血清CTRP4、CTRP5水平呈正相关（rs=0.820、0.833,P均＜0.001）,与CTRP6水平呈负相关（rs=-0.838,P＜0.001）。多因素Logistic回归分析显示,T2DM病程延长和糖化血红白蛋白（HbA1c）、CTRP4、CTRP5升高为T2DM合并CHD患者冠状动脉中重度病变的独立危险因素,CTRP6升高为独立保护因素（P＜0.05）。结论：血清CTRP4、CTRP5水平升高和CTRP6水平降低与T2DM合并CHD患者冠状动脉病变加重独立相关,可能成为T2DM合并CHD患者冠状动脉病变评估指标。     

血尿酸水平与冠状动脉病变程度的关系探讨

目的:探讨血尿酸(SUA)水平与冠状动脉病变程度的关系。方法:将268例疑似冠心病(CHD)患者,经冠状动脉造影分为冠心病组198例和非冠心病组70例;冠心病组又分为单支病变组80例,双支病变组56例,三支病变组62例。分别检测各组研究对象血尿酸含量,同时记录年龄、性别、吸烟、高血压、糖尿病、血尿酸及冠状动脉造影结果,分析血尿酸与已知冠心病主要危险因素、冠状动脉病变程度的相关性。结果:冠心病组血尿酸水平(395.35±84.40)μmol/L,显著高于非冠心病组(282.20±66.68)μmol/L(P<0.05)。单支病变组(338.48±77.36)μmol/L、双支病变组(399.62±84.36)μmol/L、三支病变组(445.16±92.20)μmol/L,血尿酸水平呈递增趋势,各组之间的差异有统计学意义。结论:血尿酸水平可反映冠状动脉病变严重程度。降尿酸治疗有望成为心血管疾病防治的一种新途径。     

2型糖尿病患者血糖波动与糖尿病视网膜病变的相关性分析

目的:探讨2型糖尿病(T2DM)患者血糖波动与糖尿病视网膜病变(DR)的关系.方法:T2DM患者进行眼底照相或眼底荧光造影,根据DR程度分为糖尿病背景期视网膜病变(BDR)组、糖尿病增殖期视网膜病变(PDR)组、无视网膜病变(NDR)组,记录年龄、性别、体重指数、病程、测量血压、糖化血红蛋白、空腹胰岛素、餐后2h胰岛素、空腹C-肽、餐后2hC-肽、血脂指标.选取三组中上述基线指标具有可比性的病例共106例(BDR组38例,PDR组35例,NDR组33例)纳入观察.采用动态血糖监测系统(CGMS)连续监测患者血糖72 h.结果:各组间平均血糖水平(MBG)、血糖标准差(SDBG)、平均血糖波动幅度(MAGE)及血糖波动最大幅度(LAGE)相比较有统计学差异(P＜0.05).Spearman相关分析显示,糖尿病视网膜病变(DR)与MBG、SDBG、MAGE及LAGE呈正相关(P＜0.05).校正MBG后,糖尿病视网膜病变(DR)与SDBG、MAGE及LAGE的相关系数分别为0.297、0.396、0.284(P＜0.01).结论:血糖波动与糖尿病视网膜病变(DR)的发生发展有关,应尽早干预.     

IL-6与2型糖尿病关系的研究进展

2型糖尿病(T2DM)已成为全世界危害人类健康的主要疾病,且患病率逐年增加.虽然T2DM确切的发病机制尚未完全阐明,但越来越多的证据提示T2DM的发生同炎症密切相关.IL-6是参与炎症反应的重要的细胞因子,研究发现IL-6在T2DM及其并发症的发生发展中起重要的作用.通过阻断炎症因子及其受体的抗炎治疗明显降低糖尿病的发生率或延迟其发展.这将有望给T2DM的防治提供新途径,为临床早发现及治疗提供更多的科学依据.     

低血糖与2型糖尿病

糖尿病（DM）是一种慢性终身性疾病,目前已成为严重威胁人类健康的世界性公共卫生问题,2型糖尿病患者也逐渐增加。流行病学调查显示,目前全球大约有近2亿糖尿病患者,其中2型糖尿病占90%～95%。2型糖尿病发病机理是胰岛素分泌的相对或绝对不足伴有或不伴有胰岛素抵抗,持续的高血糖可严重抑制胰岛功能。严格的血糖控制能够延缓糖尿病慢性并发症的发生和发展,延长了患者的预期寿命。但是随着血糖控制达标,发生低血糖的危险性增加了,低血糖不仅严重阻碍了良好血糖控制,而且严重低血糖还是2型糖尿病致死、致残的重要原因。本文探讨2型糖尿病患者治疗中低血糖发生的原因、诱发因素以及可能的解决方案。     

Visfatin 与2 型糖尿病研究新进展

Visfatin是Fukuhara等发现的一种蛋白质细胞因子,由内脏脂肪细胞分泌,受多种因素调节,有烟酰胺磷酸核糖转移酶活性,类胰岛素作用,促炎作用等多种生物学作用。2型糖尿病是一种内分泌代谢性疾病,由多基因遗传因素、环境因素综合作用引起,visfatin与其有密切的关系。Visfatin对于寻找糖尿病新的药物靶点,开发新的疾病生物标志物有非常重要临床意义。     

内脂素与2型糖尿病关系的研究进展

内脂素是新近被发现的主要由内脏脂肪合成的一种脂肪细胞因子,它具有类胰岛素样作用,能降低血糖和促进脂肪组织的分化与合成。内脂素还可以调节血管平滑肌的成熟和影响胰岛细胞的胰岛素的分泌,亦具有调节炎症反应和免疫功能的作用。随着研究的发展,人们对内脂素的结构特性、分布、表达调控及其生物学功能有了更加深入的认识。2型糖尿病是以胰岛素抵抗和糖代谢紊乱为特征的代谢性疾病,研究发现内脂素与2型糖尿病密切相关,其中与肥胖、胰岛素抵抗及胰岛素分泌方面的关系尤为显著,深入研究内脂素的生理和病理生理作用将会有力地促进对2型糖尿病的进一步认识、治疗与预防。     

BNP及NT-proBNP与2型糖尿病关系的研究进展

BNP及NT-proBNP是诊断心衰的重要指标。近年来BNP及NT-proBNP与2型糖尿病关系的研究有了新的进展。我们收集近年来国内外关于2型糖尿病中BNP及NT-proBNP的相关文献并进行研究。结果显示2型糖尿病合并冠心病、高血压、糖尿病肾病患者BNP或NT-proBNP有升高趋势。单纯2型糖尿病及糖尿病视网膜病变患者以及低血糖患者BNP或NT-proBNP差异无统计学意义。高血压、年龄、性别、体重指数、肾功能及心脏结构功能改变是2型糖尿病患者BNP及NT-proBNP的影响因素。降糖药物对2型糖尿病患者BNP及NT-proBNP水平的研究尚少,糖尿病病程、FPG以及HbA1c对BNP及NT-proBNP的影响尚存在争议。BNP及NT-proBNP升高对2型糖尿病合并冠心病、高血压、糖尿病肾病患者病情评估,预后判断及诊治具有非常重要的意义。降糖药物、糖尿病病程、FPG以及HbA1c对BNP及NT-proBNP的影响需要进一步研究。     

2型糖尿病下肢血管病变的危险因素分析

目的:探讨2型糖尿病合并下肢血管病变的主要危险因素.方法:选择2011年2月至2012年2月我院收治的220例2型糖尿病患者为研究对象,采用彩色多普勒超声对其双下肢血管进行检查,根据检查结果将患者分为下肢血管病变组与无下肢血管病变组,对两组患者的年龄、性别、腰围、体质量指数(BMI)、收缩压(SBP)、舒张压(DBP)、空腹血糖(FBG)、餐后2h血糖(2hBG)、糖化血红蛋白(HbA1c)、胰岛素抵抗指数(HOMA-IR)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)进行测定及分析.结果:220例患者中,152例患者合并下肢血管病变,发生率69.1％.单因素分析表明年龄、SBP、2hBG、HbA1c、HOMA-IR、TC、LDL-C等因素与合并下肢血管病变有关.而多因素分析表明年龄、TC、合并神经病变是引起2型糖尿病下肢血管病变的独立危险因素.结论:2型糖尿病患者下肢血管病变的发生较高,临床应根据上述危险因素进行积极干预及预防.     

High Prevalence of Lower Extremity Peripheral Artery Disease in Type 2 Diabetes Patients with Proliferative Diabetic Retinopathy

Little is known about the relationship between lower extremity peripheral arterial disease (PAD) and proliferative diabetic retinopathy (PDR) in type 2 diabetes (T2D). Here, we explored the relationship between sight-threatening PDR and PAD. We screened for diabetic retinopathy (DR) and PAD in hospitalized patients with T2D. Patients with a diabetic duration of more than 10 years, HbA1c ≥7.5%, eGFR ≥60mL/min/1.73m2 and with PDR or with no diabetic retinopathy (NDR) were eligible for this cross-sectional study. Severities of DR were graded by digital retinal photographs according to the Early Treatment Diabetic Retinopathy Study (ETDRS) scale. We assessed PAD by measuring Ankle Brachial Index (ABI), Toe Brachial Index (TBI) and Doppler ultrasound. Statistical analyses were performed using SPSS 17.0 software. Of the 1544 patients, 169 patients with extreme eye (57 PDR and 112 NDR) phenotypes met the inclusion criteria. Patients with PDR had a significantly higher proportion of low ABI (≤0.99) and high ABI (≥1.3) than patients with NDR (28.1% and 15.8% vs. 14.3% and 6.2% respectively, P<0.05). PDR patients also had lower TBI than NDR patients (0.56±0.09 vs. 0.61±0.08, P<0.01). The proportion of patients with abnormal duplex ultrasound was higher in PDR than in NDR (21.1% vs. 9.8%, P<0.001). This showed that PDR associated with PAD could be defined in multiple ways: abnormal ABI (≤0.9) (OR = 3.61, 95% CI: 1.15–11.26), abnormal TBI (OR = 2.84, 95% CI: 1.19–6.64), abnormal duplex (OR = 3.28, 95% CI: 1.00–10.71), and critical limb ischemia (OR = 5.52, 95% CI: 2.14–14.26). Moreover, PDR was a stronger independent correlation factor for PAD than a diabetic duration of 10 years. In conclusion, PAD is more common in PDR than in NDR. It implies that PDR and PAD are mostly concomitant in T2D. We should focus on screening PAD in patients with PDR in clinical practice.     

Angiogenic Potential of Vitreous from Proliferative Diabetic Retinopathy and Eales' Disease Patients

Purpose

Proliferative Diabetic Retinopathy (PDR) and Eales'' Disease (ED) have different aetiologies although they share certain common clinical symptoms including pre-retinal neovascularization. Since there is a need to understand if the shared end-stage angiogenic pathology of PDR and ED is driven by common stimulating factors, we have studied the cytokines contained in vitreous from both patient groups and analyzed the angiogenic potential of these samples in vitro.

Material and Methods

Vitreous samples from patients with PDR (n = 13) and ED (n = 5) were quantified for various cytokines using a cytokine biochip array and sandwich ELISA. An additional group of patients (n = 5) with macular hole (MH) was also studied for comparison. To determine the angiogenic potential of these vitreous samples, they were analyzed for their ability to induce tubulogenesis in human microvascular endothelial cells. Further, the effect of anti-VEGF (Ranibizumab) and anti-IL-6 antibodies were studied on vitreous-mediated vascular tube formation.

Results

Elevated levels of IL-6, IL-8, MCP-1 and VEGF were observed in vitreous of both PDR and ED when compared to MH. PDR and ED vitreous induced greater levels of endothelial cell tube formation compared to controls without vitreous (P<0.05). When VEGF in vitreous was neutralized by clinically-relevant concentrations of Ranibizumab, tube length was reduced significantly in 5 of 6 PDR and 3 of 5 ED samples. Moreover, when treated with IL-6 neutralizing antibody, apparent reduction (71.4%) was observed in PDR vitreous samples.

Conclusions

We have demonstrated that vitreous specimens from PDR and ED patients share common elevations of pro-inflammatory and pro-angiogenic cytokines. This suggests that common cytokine profiles link these two conditions.     

Chronic Kidney Disease and Diabetic Retinopathy in Patients with Type 2 Diabetes

Purpose

To explore the relationship between chronic kidney disease (CKD) and diabetic retinopathy (DR) in a representative population of type 2 diabetes mellitus (DM2) patients in Catalonia (Spain).

Methods

This was a population-based, cross-sectional study. A total of 28,344 patients diagnosed with DM2 who had recorded ophthalmologic and renal functional examinations were evaluated. Data were obtained from a primary healthcare electronic database of medical records. CKD was defined as an estimated glomerular filtration ratio (eGFR) of <60 ml/min/1.73m² and/or urine albumin to creatinine ratio (UACR) ≥30 mg/g. DR was categorized as non-vision threatening diabetic retinopathy and vision threatening diabetic retinopathy.

Results

CKD was associated with a higher rate of DR [OR], 95% confidence interval [CI], 1.5 (1.4–1.7). When we analyzed the association between different levels of UACR and DR prevalence observed that DR prevalence rose with the increase of UACR levels, and this association was significant from UACR values ≥10 mg/g, and increased considerably with UACR values ≥300mg/g (Odds ratio [OR], 95% confidence interval [CI], 2.0 (1.6–2.5). This association was lower in patients with eGFR levels 44 to 30 mL/min/1.73m² [OR], 95% confidence interval [CI], 1.3 (1.1–1.6).

Conclusions

These results show that CKD, high UACR and/or low eGFR, appear to be associated with DR in this DM2 population.     

Growth Factors in Proliferative Diabetic Retinopathy

Many growth factors are implicated in the pathogenesis of proliferative diabetic retinopathy. Alteration of growth factors and their receptors in diabetes has been shown in both experimental and clinical studies. Sustained hyperglycemia resulting from long-standing diabetes leads to several biochemical abnormalities that consequently result in retinal hypoxia. Retinal oxygenation state regulates various growth factors that promote angiogenesis in order to meet the oxygen demands of the tissue. However, unregulated expression of these growth factors and induction of complex cascades leading to augmentation of other proangiogenic factors, which may not be regulated by tissue oxygenation, leads to uncontrolled retinal neovascularization and blindness in diabetic patients.     

Neurotrophins and Neurotrophin Receptors in Proliferative Diabetic Retinopathy

Neurotrophins (NTs) are emerging as important mediators of angiogenesis and fibrosis. We investigated the expression of the NTs nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4) and their receptors TrkA, TrkB, and TrkC in proliferative diabetic retinopathy (PDR). As a comparison, we examined the expression of NTs and their receptors in the retinas of diabetic rats. Vitreous samples from 16 PDR and 15 nondiabetic patients were studied by Western blot analysis and enzyme-linked immunosorbent assay (ELISA). Epiretinal membranes from 17 patients with PDR were studied by immunohistochemistry. Rats were made diabetic with a single high dose of streptozotocin and retinas of rats were examined by Western blot analysis. Western blot analysis revealed a significant increase in the expression of NT-3 and NT-4 and the shedding of receptors TrkA and TrkB in vitreous samples from PDR patients compared to nondiabetic controls, whereas NGF and BDNF and the receptor TrkC were not detected with the use of Western blot analysis and ELISA. In epiretinal membranes, vascular endothelial cells and myofibroblasts expressed NT-3 and the receptors TrkA, TrkB and TrkC in situ, whereas NT-4 was not detected. The expression levels of NT-3 and NT-4 and the receptors TrkA and TrkB, both in intact and solubilized forms, were upregulated in the retinas of diabetic rats, whereas the receptor TrkC was not detected. Co-immunoprecipitation studies revealed binding between NT-3 and the receptors TrkA and TrkB in the retinas of diabetic rats. Our findings in diabetic eyes from humans and rats suggest that the increased expression levels within the NT-3 and NT-4/Trk axis are associated with the progression of PDR.     

The Effects of Pleiotrophin in Proliferative Diabetic Retinopathy

Pleiotrophin (PTN), a secreted, multifunctional cytokine, is involved in angiogenic, fibrotic and neurodegenerative diseases. However, little is known about its effects on diabetic retinopathy, a neurovascular disease. To investigate the role of PTN in proliferative diabetic retinopathy (PDR), PTN concentration in the vitreous was evaluated in PDR patients and non-diabetic controls. PTN expression was observed in epiretinal membranes from patients. PTN knockdown was performed using small interfering (si)RNA, and the effects on retinal pigment epithelium (RPE) cells and human umbilical vascular endothelia cells (HUVECs) were observed in vitro under hyperglycemic and hypoxic conditions. Cell attachment, proliferation, migration, tube formation, cell cycle, apoptosis, extracellular signal-regulated kinase 1/2 (ERK 1/2) phosphorylation, and VEGF levels were studied. The vitreous PTN concentration in PDR patients was higher than that in non-diabetic controls, and PTN was highly expressed in the fibrovascular membranes of PDR patients. Under hyperglycemic and hypoxic conditions, PTN knockdown reduced cell attachment, proliferation, migration, and tube formation and induced cell cycle arrest and apoptosis in vitro. Mechanically, PTN depletion decreased ERK 1/2 phosphorylation. Recombinant PTN up regulated the concentration of VEGF in vitro, which can be attenuated by the ERK 1/2 inhibitor. Taken together, our results implied that elevated PTN in PDR patients might participate in the critical processes of the development of PDR, most likely playing roles in angiogenesis and proliferation, possibly by activating the ERK 1/2 pathway and regulating VEGF secretion. These findings provide new insight into the roles of PTN in PDR and suggest that PTN may become a new target for therapeutic intervention in PDR.     

冠心病合并2型糖尿病的冠脉病变特征及危险因素分析

目的:探讨冠心病合并2型糖尿病的冠状动脉病变特征及其相关危险因素.方法:选择2010年1月至2012年1月我院经冠状动脉造影确诊为冠心病合并2型糖尿病的患者227例(DM组)和同期不合并2型糖尿病的冠心病患者229例(NDM组)为研究对象,回顾性分析其血脂、血糖及冠状动脉造影结果,比较两组患者冠状动脉病变的特点,探讨血糖水平对糖尿病合并冠心病患者冠状动脉病变的影响.结果:DM组患者总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)显著高于NDM组(P＜0.05),高密度脂蛋白胆固醇(HDL-C)显著低于NDM组(P＜0.05);DM组患者三支血管病变、弥漫性病变以及狭窄程度大于75％的血管的病例数百分率显著高于NDM组(P＜0.05);在DM患者中,血糖水平控制理想组(A组)的冠状动脉血管狭窄程度大于75％以及发生弥漫性病变的病例数百分率均显著低于血糖控制较差组(B组,P＜0.05).结论:2型糖尿病合并冠心病患者冠状动脉多表现为弥漫和多支病变,狭窄程度严重;血糖和血脂水平异常是其冠脉病变的危险因素;控制患者的血糖水平于正常范围可改善其冠状动脉病变程度并减小其病变范围.     

Adiponectin Multimers and ADIPOQ T45G in Coronary Artery Disease in Caribbean Type 2 Diabetic Subjects of African Descent

Ethnic differences may affect the association of adiponectin (Ad) multimers with coronary artery disease (CAD). We analyzed the associations of total Ad, Ad multimers, and T45G polymorphism of ADIPOQ gene with pre‐existing CAD. We carried out a cross‐sectional study of 216 Afro‐Caribbean type 2 diabetic (T2D) subjects. Levels of total Ad, high molecular weight (HMW), middle molecular weight (MMW), and low molecular weight (LMW) isoforms were measured. Subjects were genotyped. Of the subjects studied, 57 had pre‐existing CAD, 77% of whom have had myocardial infarction. Subjects with CAD had lower Ad levels (total and multimers) and a higher frequency carried the minor allele 45G, GG/TG, (18% vs. 8%, P = 0.03) than subjects without CAD. In logistic regression analysis, the models used evaluate Ad in the context of adjustment for metabolic syndrome characteristics. The adjusted odds ratio (OR) of CAD was increased significantly (by factors of 1.05–3.27) for males, older subjects, low high‐density lipoprotein cholesterol (HDL‐C), high triglycerides (TGs), and carriers of the 45 G allele. For Ad, in model 1 (including only total Ad) the adjusted OR was 2.30; P = 0.03 and, in model 2 (including the three multimers, but not total Ad), the adjusted ORs were 0.73; P = 0.52 (HMW), 2.90; P = 0.01 (MMW), and 2.08; P = 0.09 (LMW). The T45G polymorphism in the ADIPOQ gene and hypoadiponectinemia were associated with CAD in our T2D subjects of predominantly African background. This effect of Ad level was mainly related to the MMW Ad form.     

The 5-Year Onset and Regression of Diabetic Retinopathy in Chinese Type 2 Diabetes Patients

Purpose

To determine the rate and risk factors of diabetic retinopathy (DR) onset and regression in Chinese type 2 diabetes mellitus patients.

Methods

This is a 5-year community-based prospective study. The demographic information, systemic examination results and ophthalmological test results of each participant were collected. The study outcomes were DR incidence, defined as the onset of DR in at least one eye, and DR regression, defined as full regression from existing DR to no retinopathy without invasive treatments. The associations between each potential risk factor and the outcomes were studied.

Results

In total, 778 participants were enrolled. There were 322 patients without DR at baseline, of which 151 participants developed DR during follow-up (DR incidence rate = 46.89%). Baseline hyperglycemia and high blood pressure were two independent risk factors associated with DR incidence. Among the 456 participants with existing DR at entry, 110 fully recovered after 5 years (DR regression rate = 24.12%). Low baseline glucose and low serum triglyceride were two independent factors associated with DR regression.

Conclusions

DR incidence occurred more frequently in patients with hyperglycemia and high blood pressure. DR regression occurred mostly in patients with lower glucose and lower serum triglyceride levels among Chinese type 2 diabetes patients.     

Renal Artery Stenosis Predicts Coronary Artery Disease in Patients with Hypertension

In hypertensive patients with indication of renal arteriography to investigate renal artery stenosis (RAS) there are no recommendations regarding when to investigate coronary artery disease (CAD). Moreover, the predictors of CAD in patients with RAS are not clear. We aimed to evaluate the frequency and the determinants of CAD in hypertensive patients referred to renal angiography. Eighty-two consecutive patients with high clinical risk suggesting the presence of RAS systematically underwent renal angiography and coronary angiography during the same procedure. Significant arterial stenosis was defined by an obstruction≥70% to both renal and coronary territories. Significant CAD was present in 32/82 (39%) and significant RAS in 32/82 (39%) patients. Both CAD and RAS were present in 25.6% from the 82 patients. Patients with severe CAD were older (63±12 vs. 56±13 years; p = 0.03) and had more angina (41 vs. 16%; p = 0.013) compared to patients without severe CAD. Significant RAS was associated with an increased frequency of severe CAD compared to patients without significant RAS (66% vs. 22%, respectively; p<0.001). Myocardial scintigraphy showed ischemia in 21.8% of the patients with CAD. Binary logistic regression analysis showed that RAS≥70% was independently associated with CAD≥70% (OR: 11.48; 95% CI 3.2–40.2; p<0.001), even in patients without angina (OR: 13.48; 95%CI 2.6–12.1; p<0.001). Even considering a small number of patients with significant RAS, we conclude that in hypertensive patients referred to renal angiography, RAS≥70% may be a strong predictor of severe CAD, independently of angina, and dual investigation should be considered.