高原地区高血压患者红细胞指标和血清高迁移率族蛋白2与颈动脉粥样硬化的相关性

目的:探讨高原地区高血压患者红细胞指标和血清高迁移率族蛋白2(HMGB2)与颈动脉粥样硬化的相关性。方法:本研究共纳入244例高原地区高血压患者,通过检测颈动脉内膜中层厚度(IMT)分三组:内膜正常组(0.8 mm≤IMT1.0 mm);内膜增厚组(1.0 mm≤IMT1.2 mm);斑块形成组(IMT≥1.2 mm)。收集患者的临床资料,检测患者红细胞指标和血清HMGB2水平及其他生化指标。通过分析IMT与各项指标之间的相关性,评价颈动脉硬化的相关因素。结果:三组间红细胞压积(HCT)、红细胞计数(RBC)、红细胞分布宽度(RDW)、血清HMGB2水平差异均具有统计学意义(均P0.05)。相关分析结果显示,RBC(r=0.368)、HCT(r=0.409)、RDW(r=0.596)、HMGB2(r=0.291)与IMT呈正相关(均P0.05)。多因素Logistic回归分析显示RBC、HCT、RDW、HMGB2是颈动脉硬化的独立危险因素。结论:高原地区高血压患者RBC、HCT、RDW、HMGB2水平与IMT密切相关,且RBC、HCT、RDW、HMGB2水平升高是颈动脉硬化发生的危险因素,可作为动脉硬化早期预测因子。     

红细胞分布宽度与ICU院内感染的相关性研究

目的:探索红细胞分布宽度(RDW)与ICU院内感染的相关性。方法:根据2001年卫生部颁布的医院感染诊断标准,筛选出2011年1月至2013年12月在ICU住院发生院内感染的224例患者,与同期在ICU住院未发生院内感染的患者232例,收集相关临床资料[年龄、性别、既往合并高血压、冠心病史、慢性病(APACHEⅡ)评分、住院时间、预后]及RDW等实验室指标(连续收集入ICU前三天的实验指标取平均值),分析RDW与院内感染发生的相关性。结果:与对照组RDW(12.18±1.08)%相比,院内感染组RDW(13.52±2.01)%明显升高,差异有统计学意义(P0.01)。多因素logistic回归分析显示,RDW是院内感染的独立预测因素(OR=4.75,95%CI:3.27~6.91,P0.01)。RDW界值为12.81%,RDW的ROC曲线下面积为(0.76±0.02)%,95%CI:0.71~0.80,诊断院内感染的敏感性为56.65%,特异性为85.75%。结论:RDW与ICU院内感染独立相关,是ICU院内感染的独立预测因素。     

红细胞分布宽度、中性粒细胞与淋巴细胞比值与晚期非小细胞肺癌患者临床病理特征及预后的关系研究

目的:探讨红细胞分布宽度(RDW)、中性粒细胞与淋巴细胞比值(NLR)与晚期非小细胞肺癌(NSCLC)患者临床病理特征及预后的关系。方法:选择2017年5月至2019年5月我院收治的106例确诊为晚期NSCLC患者(NSCLC组)和门诊接诊的102例体检正常者(对照组)作为研究对象。检测RDW、NLR,分析RDW、NLR与NSCLC患者临床病理特征以及预后的关系。结果:NSCLC组RDW、NLR高于对照组(P<0.05),年龄≥60岁、淋巴结转移NSCLC患者RDW高于年龄<60岁、无淋巴结转移NSCLC患者(P<0.05),TNM分期为Ⅳ期、淋巴结转移NSCLC患者NLR高于TNM分期为Ⅲ期、无淋巴结转移患者(P<0.05)。Kaplan-Meier生存曲线分析结果显示高RDW组、高NLR组NSCLC患者生存率低于低RDW组、低NLR组(P<0.05)。单因素COX回归分析显示分化程度、TNM分期、淋巴结转移、RDW、NLR与NSCLC预后有关(P<0.05),多因素COX回归分析显示淋巴结转移、RDW、NLR与NSCLC患者预后相关(P<0.05)。结论:晚期NSCLC患者RDW、NLR较高,RDW与年龄、淋巴结转移有关,NLR与TNM分期和淋巴结转移有关,高水平RDW、NLR预示着NSCLC预后不良,可作为预后评估的辅助指标。     

红细胞体积分布宽度对心力衰竭患者病情及预后转归的评估价值

目的:研究红细胞体积分布宽度(RDW)对心力衰竭患者病情及预后转归的评估价值。方法:将我院心内科收治的110例心力衰竭患者(研究组)根据病情分为NYHAⅡ级30例、Ⅲ级46例、Ⅳ级34例,另选择同期健康体检者110例作为对照组。同时根据患者6个月内预后情况分为存活组(91例)和死亡组(19例)。比较分析各组患者RDW水平、死亡率,采用单因素和多因素logistic回归分析心力衰竭预后的影响因素。结果:研究组中,NYHAⅢ~Ⅳ级患者RDW水平明显高于对照组,且随着NYHA分级的增加,RDW水平明显升高(P0.05)。NYHAⅣ级患者死亡率明显高于NYHAⅡ、Ⅲ级患者(P0.05)。与死亡组比较,存活组年龄明显较小,入院时Hcy、CRP、GLU、RDW、NT-pro BNP明显降低,Hb、RBC、LVEF水平明显升高(P 0.05)。年龄、入院时NT-pro BNP和RDW是心力衰竭的独立危险因素,而LVEF水平是独立保护因素(P0.05)。结论:RDW可反映心力衰竭患者的病情严重程度,对于预后转归评估具有重要指导意义。     

红细胞分布宽度对NSTE-ACS患者行PCI术植入DES长期生存率的影响

本研究旨在评价红细胞分布宽度(red blood cell distribution width,RDW)对植入药物洗脱支架(drugeluting stents,DES)的非ST段抬高急性冠脉综合征患者(non-ST elevation myocardial infarction,NSTE-ACS)远期预后的影响。研究纳入南方医科大学珠江医院2013年2月1日至2014年1月31日在心内科行经皮冠状动脉介入术(percutaneous coronary intervention,PCI)并植入DES的NSTE-ACS患者共181名,其中男性136例,女性45例,按照入院时的RDW的中位数分为2组;RDW≥13.3%为高RDW组,RDW13.3%为低RDW组。收集患者的相关临床资料采用门诊、电话等形式进行随访,比较两组患者之间长期生存率。纳入符合条件的患者181例,完成随访177例(97.8%),随访时间(14.67±5.78)月。2组患者基线资料中RDW血小板,受体阻滞剂(BETA BLOCK)比较,差异有统计学意义。高、低RDW两组患者随访结果显示,高RDW组全因死亡率及主要心脏不良事件(major adverse cardiac events(MACE))发生率与低RDW组比较有统计学差异,随访期间内靶血管再次血运重建的概率两组有统计学差异。Cox多元回归分析显示RDW升高是全因死亡和MACE发生率的预测因子,高RDW和LVEF≤40%与病死率相关。Kaplan-Meier曲线显示两组间全因死亡率和MACE事件发生率差异有统计学意义(Log-rank p=0.025,p=0.005)。本研究结果显示RDW升高是植入药物洗脱支架的NSTE-ACS患者不良临床预后的独立预测因子。     

小儿重症肺炎红细胞体积分布宽度与患儿近期预后的相关性分析

目的:探讨小儿重症肺炎红细胞体积分布宽度(RDW)与患儿近期预后的相关性。方法:选择107例重症肺炎患儿为研究对象,检测患儿入院时RDW水平,记录相关实验室检查指标及住院后28d的转归情况,将患者分为死亡组和存活组,高RDW组和正常RDW组,分析各组之间相关指标的差异,并探讨RDW与患儿近期预后的关系。结果:死亡组患儿的入院急性病生理学和长期健康评价评分Ⅱ(APACHEⅡ)评分、降钙素原(PCT)、超敏C-反应蛋白(hs-CRP)、白细胞计数(WBC)、中性粒细胞百分比(PMN)、血沉(ESR)高于存活组(P0.05),RDW水平亦高于存活组(P0.05);高RDW组患儿APACHEⅡ评分、PCT、hs-CRP、WBC、PMN、ESR高于正常RDW组,死亡率亦高于正常RDW组(P0.05)。Logistic回归分析显示RDW水平是重症肺炎患儿近期死亡的独立危险因素(OR=2.025,95%CI:1.252~4.243,P0.05);ROC曲线分析显示:RDW水平预测重症肺炎患儿死亡的ROCAUC为0.801,灵敏度为82.0,特异度为74.4,最佳诊断截点为16.35%。结论:RDW水平可能是重症肺炎患儿近期预后不良的独立危险因素,并对患儿预后可能具有较好的预测价值。     

qSOFA评分、血乳酸及红细胞分布宽度与急性上消化道出血病情严重程度的关系及其预测患者预后的效能分析

摘要 目的：探讨快速序贯器官功能衰竭评估（qSOFA）评分、血乳酸（Lac）及红细胞分布宽度（RDW）与急性上消化道出血（AUGIB）病情严重程度的关系及其预测患者预后的效能。方法：选取2017年6月～2022年6月我院收治的230例AUGIB患者为研究对象,根据病情严重程度分为低危组44例、中危组140例、高危组36例、极高危组10例,且根据其入院28 d内生存情况分为死亡组（n=31）和存活组（n=199）。收集AUGIB患者临床资料,检测血Lac、RDW水平并计算qSOFA评分。采用多因素Logistic回归分析AUGIB患者预后不良的影响因素,受试者工作特征（ROC）曲线分析qSOFA评分和血Lac、RDW对AUGIB患者预后不良的预测价值。结果：低危组、中危组、高危组、极高危组qSOFA评分和血Lac、RDW水平依次升高（P＜0.05）。230例AUGIB患者入院28 d内死亡率为13.48％（31/230）。多因素Logistic回归分析显示,年龄增加、GBS评分≥6分及休克指数、qSOFA评分、血尿素氮、血Lac、RDW水平升高为AUGIB患者预后不良的独立危险因素（P＜0.05）。ROC曲线分析显示,qSOFA评分、血Lac及RDW联合预测AUGIB患者预后不良的曲线下面积大于qSOFA评分、血Lac及RDW单独预测。结论：AUGIB患者qSOFA评分、血Lac及RDW水平升高与病情加重和预后不良密切相关,qSOFA评分、血Lac及RDW联合预测AUGIB患者预后不良的效能较高。     

血清白蛋白、降钙素原联合红细胞分布宽度对重型颅脑损伤患者住院期间死亡风险的预测价值研究

摘要 目的：探讨血清白蛋白（Alb）、降钙素原（PCT）联合红细胞分布宽度（RDW）对重型颅脑损伤（sTBI）患者住院期间死亡风险的预测价值。方法：选取2019年1月～2022年2月长沙市第一医院收治的120例sTBI患者,根据住院期间预后情况分为死亡组和存活组。收集sTBI患者临床资料并检测其血清Alb、PCT、RDW水平。采用多因素Logistic回归分析sTBI患者住院期间预后的影响因素,受试者工作特征（ROC）曲线分析血清Alb、PCT、RDW对sTBI患者住院期间死亡风险的预测价值。结果：120例sTBI患者住院期间死亡率为45.83％（55/120）。体温升高、糖尿病、瞳孔散大、基底池异常、中线移位≥5 mm、蛛网膜下腔出血和PCT、RDW升高为sTBI患者住院期间死亡的独立危险因素,Alb升高、格拉斯哥昏迷量表（GCS）评分增加为独立保护因素（P＜0.05）。血清Alb、PCT、RDW联合预测sTBI患者住院期间死亡风险的曲线下面积大于Alb、PCT、RDW单独预测。结论：临床应重视sTBI患者住院期间预后的影响因素,并采取对应措施进行干预。血清Alb、PCT、RDW联合预测sTBI患者住院期间死亡风险的价值较高,可作为sTBI患者住院期间死亡风险的预警指标。     

甘油三酯葡萄糖乘积指数、红细胞分布宽度、血清尿酸、降钙素原与冠心病患者冠状动脉狭窄程度和短期预后的关系分析

摘要 目的：探讨甘油三酯葡萄糖乘积（TyG）指数、红细胞分布宽度（RDW）、血清尿酸（UA）、降钙素原（PCT）与冠心病患者冠状动脉狭窄程度和短期预后的关系。方法：选取2017年1月至2021年12月我院收治的150例冠心病患者,均行冠状动脉造影并以Gensini积分系统评估冠状动脉狭窄程度,分为轻度组、中度组和重度组,比较各组的TyG指数、RDW、UA、PCT水平,以Pearson相关系数分析上述指标与Gensini积分的相关性。患者出院后均随访6个月,根据有无发生主要心血管不良事件（MACE）分为预后良好组和预后不良组,以多因素Logisitc回归分析预后的影响因素,以受试者工作特征（ROC）曲线分析对预后的预测效能。结果：不同冠状动脉狭窄程度患者的TyG指数、RDW、UA、PCT水平差异均表现为,从轻度到重度依次升高（P＜0.05）。Pearson相关性分析显示,冠心病患者的TyG指数、RDW、UA、PCT水平与Gensini积分均呈正相关（P＜0.05）。预后不良组的甘油三酯（TG）、Gensini积分、TyG指数、RDW、UA、PCT水平均高于预后良好组（P＜0.05）;多因素Logistic回归分析显示,TG≥3.5 mmol/L、Gensini积分≥30分、TyG指数≥5、RDW≥12.8%、UA≥380 μmol/L、PCT≥35 μg/L是冠心病患者预后不良的危险因素（P＜0.05）。ROC曲线分析显示,TyG指数、RDW、UA、PCT单独及联合预测冠心病患者预后不良的曲线下面积分别为0.786、0.793、0.794、0.789和0.948,联合预测效能明显更高。结论：冠心病患者的TyG指数、RDW、血UA、PCT水平与冠状动脉狭窄程度呈正相关,其均为患者短期预后的影响因素,联合检测上述指标对患者短期预后有一定预测价值。     

血清hs-CRP及红细胞分布宽度与急性冠脉综合征患者危险分层及预后的相关性研究

目的:探讨血清超敏C反应蛋白(hs-CRP)及红细胞分布宽度(RDW)与急性冠脉综合征(ACS)患者危险分层及预后的相关性。方法:将132例ACS患者按照全球急性冠状动脉事件注册(GRACE)危险评分分为低、中、高危三组;检测各组的血清hs-CRP、RDW、肌钙蛋白I(c Tn I)、B型脑钠肽(BNP)水平;并记录入院后心脏超声检查中左室射血分数(LEVF)及住院期间有无发生主要不良心脏时间(MACE)等情况。结果:低、中、高危三组间血清hs-CRP、RDW、BNP、c Tn I、LEVF比较具有统计学差异(P0.05),高危组患者血清hs-CRP、RDW、BNP、c Tn I高于低危组及中危组(P0.05),中危组高于低危组(P0.05);血清hs-CRP水平与GRACE评分呈正相关(rs=0.490,P0.05),RDW水平与GRACE评分亦呈正相关(rs=0.401,P0.05);与非MECE组比较,MECE组患者hs-CRP、RDW较高(P0.05);血清高水平hs-CRP及RDW是ACS患者发生近期住院MACE相关高危因素。结论:血清hs-CRP及RDW水平随着ACS患者危险分层的增加而增加,高水平hs-CRP及RDW是近期发生MACE的高危因素,对临床评估ACS患者病情及预后具有重要价值。     

Endothelial function and cardiovascular disease: effects of quercetin and wine polyphenols

Endothelial dysfunction is an early pathophysiological feature and independent predictor of poor prognosis in most forms of cardiovascular diseases. Epidemiological studies report an inverse association between dietary flavonoid consumption and mortality from cardiovascular diseases. In the present paper, we review the effects of flavonoids, especially quercetin and wine polyphenols, on endothelial function and dysfunction and its potential protective role in hypertension, ischemic heart disease and stroke. In vitro studies show that flavonoids may exert multiple actions on the NO-guanylyl cyclase pathway, endothelium-derived hyperpolarizing factor(s) and endothelin-1 and protect endothelial cells against apoptosis. In vivo, flavonoids prevent endothelial dysfunction and reduce blood pressure, oxidative stress and end-organ damage in hypertensive animals. Moreover, some clinical studies have shown that flavonoid-rich foods can improve endothelial function in patients with hypertension and ischemic heart disease. Altogether, the available evidence indicates that quercetin and wine polyphenols might be of therapeutic benefit in cardiovascular diseases even though prospective controlled clinical studies are still lacking.     

Endothelial function and cardiovascular disease: Effects of quercetin and wine polyphenols

Endothelial dysfunction is an early pathophysiological feature and independent predictor of poor prognosis in most forms of cardiovascular diseases. Epidemiological studies report an inverse association between dietary flavonoid consumption and mortality from cardiovascular diseases. In the present paper, we review the effects of flavonoids, especially quercetin and wine polyphenols, on endothelial function and dysfunction and its potential protective role in hypertension, ischemic heart disease and stroke. In vitro studies show that flavonoids may exert multiple actions on the NO-guanylyl cyclase pathway, endothelium-derived hyperpolarizing factor(s) and endothelin-1 and protect endothelial cells against apoptosis. In vivo, flavonoids prevent endothelial dysfunction and reduce blood pressure, oxidative stress and end-organ damage in hypertensive animals. Moreover, some clinical studies have shown that flavonoid-rich foods can improve endothelial function in patients with hypertension and ischemic heart disease. Altogether, the available evidence indicates that quercetin and wine polyphenols might be of therapeutic benefit in cardiovascular diseases even though prospective controlled clinical studies are still lacking.     

microRNA在常见致死性心脏病中的改变

微小RNA(micro RNA,mi RNA)是一类真核生物内源性非编码单链的小RNA分子,长度大约为19-23个核苷酸,拥有高度的保守性,不编码蛋白质,也是近年来研究最热门的一个新领域,通过与靶m RNA特异性结合来调节基因表达,且表达都具有组织特异性。最近,许多研究表明mi RNA在心血管系统疾病和肿瘤疾病方面的相关研究都取得了突破性的进展,mi RNA在肿瘤疾病中是通过调节癌基因及抑癌基因而调控肿瘤的生物学过程,在心血管系统疾病中与心肌肥厚及心肌再生等过程有密切的关系,包括冠状动脉疾病、心肌肥大、心肌梗死、心律失常、高血压和心力衰竭等疾病,且在心脏病学中扮演着及其重要的角色。Mi RNA的表达量增加或者减少对心血管疾病都有影响,该文对新近有关的mi RNA在心血管系统疾病中的研究进展、诊断、治疗以及预后予以综述。     

维生素D与高血压关系的研究进展

众所周知维生素D(VitD)在钙、磷代谢及骨重建中具有重要的作用。而近年来许多研究发现VitD与高血压、心力衰竭、缺血性心脏病和脑卒中等心血管事件的发生呈负相关,其具体机制尚不完全清楚,经过补充VitD可以预防或治疗高血压,VitD缺乏参与了高血压的形成,成了最近争论的焦点。故本文将对VitD和高血压相互关系的研究进展做一综述,为高血压的防治提供新的理论依据。     

Red Cell Distribution Width in Relation to Incidence of Stroke and Carotid Atherosclerosis: A Population-Based Cohort Study

BackgroundIncreased red cell distribution width (RDW) has been related to poor prognosis in patients with cardiovascular disease, and is a predictor of cardiovascular mortality in the general population. The purpose of the present study was to investigate if RDW is associated with increased incidence of stroke and its subtypes in individuals from the general population.MethodsRed cell distribution width was measured in 26,879 participants (16,561 women and 10,318 men aged 45–73 years) without history of coronary events or stroke, from the population-based Malmö Diet and Cancer Study. Incidences of total stroke and stroke subtypes over a mean follow-up of 15.2 years were calculated in relation to sex-specific quartiles of RDW. The presence of carotid plaque and intima–media thickness, as assessed by ultrasound, was studied in relation to RDW in a randomly selected subcohort (n = 5,309).ResultsIncidences of total stroke (n = 1,869) and cerebral infarction (n = 1,544) were both increased in individuals with high RDW. Hazard ratios (HRs) in the highest compared to the lowest quartile were 1.31 for total stroke (95% confidence interval [CI]: 1.11–1.54, p for trend = 0.004) and 1.32 for cerebral infarction (95% CI: 1.10–1.58, p for trend = 0.004) after adjustment for stroke risk factors and hematological parameters. The adjusted HR for intracerebral hemorrhage (n = 230) was 1.44 (95% CI: 0.90–2.30) and the HR for subarachnoid hemorrhage (n = 75) was 0.94 (95% CI: 0.43–2.07), in the highest compared to the lowest quartile of RDW. Red cell distribution width was positively associated with intima–media thickness of the common carotid artery (p for trend = 0.011).ConclusionsRed cell distribution width in the highest quartile was associated with increased incidence of total stroke and cerebral infarction. There was no significant association between RDW and incidence of intracerebral or subarachnoid hemorrhage.     

Mineralocorticoid receptors in immune cells: Emerging role in cardiovascular disease

Mineralocorticoid receptors (MRs) contribute to the pathophysiology of hypertension and cardiovascular disease in humans. As such, MR antagonists improve cardiovascular outcomes but the molecular mechanisms remain unclear. The actions of the MR in the kidney to increase blood pressure are well known, but the recent identification of MRs in immune cells has led to novel discoveries in the pathogenesis of cardiovascular disease that are reviewed here. MR regulates macrophage activation to the pro-inflammatory M1 phenotype and this process contributes to the pathogenesis of cardiovascular fibrosis in response to hypertension and to outcomes in mouse models of stroke. T lymphocytes have recently been implicated in the development of hypertension and cardiovascular fibrosis in mouse models. MR activation in vivo promotes T lymphocyte differentiation to the pro-inflammatory Th1 and Th17 subsets while decreasing the number of anti-inflammatory T regulatory lymphocytes. The mechanism likely involves activation of MR in antigen presenting dendritic cells that subsequently regulate Th1/Th17 polarization by production of cytokines. Alteration of the balance between T helper and T regulatory lymphocytes contributes to the pathogenesis of hypertension and atherosclerosis and the associated complications. B lymphocytes also express the MR and specific B lymphocyte-derived antibodies modulate the progression of atherosclerosis. However, the role of MR in B lymphocyte function remains to be explored. Overall, recent studies of MR in immune cells have identified new mechanisms by which MR activation may contribute to the pathogenesis of organ damage in patients with cardiovascular risk factors. Conversely, inhibition of leukocyte MR may contribute to the protective effects of MR antagonist drugs in cardiovascular patients. Further understanding of the role of MR in leukocyte function could yield novel drug targets for cardiovascular disease.     

Prognostic Value of Red Blood Cell Distribution Width for Patients with Heart Failure: A Systematic Review and Meta-Analysis of Cohort Studies

Aims

Multiple studies have investigated the prognostic role of red blood cell distribution width (RDW) for patients with heart failure (HF), but the results have been inconsistent. The aim of the present study was to estimate the impact of RDW on the prognosis of HF by performing a systematic review and meta-analysis.

Methods and Results

The Embase, PubMed, and Web of Science databases were searched up to November 16, 2013 to identify eligible cohort studies. The quality of each study was assessed using the Newcastle-Ottawa Scale (NOS). The association between RDW, either on admission or at discharge, and HF outcomes (all-cause mortality [ACM], heart transplantation, cardiovascular mortality, and rehospitalization, etc.) were reviewed. The overall hazard ratio (HR) for the effect of RDW on ACM was pooled using a random-effects model, and the publication bias was evaluated using funnel plots and Eggers'' tests. Seventeen studies, with a total of 18288 HF patients, were included for systematic review. All eligible studies indicated that RDW on admission and RDW at discharge, as well as its change during treatment, were of prognostic significance for HF patients. The HR for the effect of a 1% increase in baseline RDW on ACM was 1.10 (95% confidence interval: 1.07–1.13), based on pooling of nine studies that provided related data. However, publication bias was observed among these studies.

Conclusions

HF patients with higher RDW may have poorer prognosis than those with lower RDW. Further studies are needed to explore the potential mechanisms underlying this association.     

Relationship Between Hyperuricemia and Chronic Kidney Disease

Because approximately 70% of uric acid is excreted from the kidney, hyperuricemia occurs when renal function deteriorates. Until now, it has not been clear if the hyperuricemia seen in such renal diseases plays a role in the progression of renal disease. However, recent clinical studies show that the serum uric acid value is closely associated with hypertension in hyperuricemic patients (cross-sectional study), and also with the onset of hypertension (longitudinal study). Furthermore, one interesting report shows that treatment of hyperuricemia with allopurinol lowers blood pressure in juvenile essential hypertension patients with hyperuricemia. In addition, it is well known that hyperuricemia is closely associated with chronic kidney disease (CKD), is a risk factor for renal insufficiency in general populations, and is a poor prognostic factor of renal function in patients who also have IgA nephropathy. On the other hand, in intervention studies on hyperuricemia, the treatment of hyperuricemia with allopurinol in CKD has resulted in a fall in blood pressure and inhibition of the progression of renal damage. Conversely, the cessation of allopurinol treatment in CKD was followed by a rise in blood pressure and the development of renal damage. Furthermore, the rise of blood pressure and development of renal damage following cessation of allopurinol treatment are only seen in patients not receiving angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB). This suggests that the renin angiotensin (RA) system plays an important role in the development of hypertension and renal damage from hyperuricemia.     

Relationship between hyperuricemia and chronic kidney disease

Because approximately 70% of uric acid is excreted from the kidney, hyperuricemia occurs when renal function deteriorates. Until now, it has not been clear if the hyperuricemia seen in such renal diseases plays a role in the progression of renal disease. However, recent clinical studies show that the serum uric acid value is closely associated with hypertension in hyperuricemic patients (cross-sectional study), and also with the onset of hypertension (longitudinal study). Furthermore, one interesting report shows that treatment of hyperuricemia with allopurinol lowers blood pressure in juvenile essential hypertension patients with hyperuricemia. In addition, it is well known that hyperuricemia is closely associated with chronic kidney disease (CKD), is a risk factor for renal insufficiency in general populations, and is a poor prognostic factor of renal function in patients who also have IgA nephropathy. On the other hand, in intervention studies on hyperuricemia, the treatment of hyperuricemia with allopurinol in CKD has resulted in a fall in blood pressure and inhibition of the progression of renal damage. Conversely, the cessation of allopurinol treatment in CKD was followed by a rise in blood pressure and the development of renal damage. Furthermore, the rise of blood pressure and development of renal damage following cessation of allopurinol treatment are only seen in patients not receiving angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB). This suggests that the renin angiotensin (RA) system plays an important role in the development of hypertension and renal damage from hyperuricemia.