老年高尿酸血症肾损害19例临床分析

本文介绍了１９９０￣１９９３年我院住院的１９例老年高尿酸肾病患者。除血尿酸升高外，全部患者伴有不同程度的高血压和肾损害。往往伴有关节痛和肾结石。老年患者常因饮酒过量、高嘌呤饮食、受凉、劳累诱发。以下几点有助于诊断：①本病老年患者并不少见；②肾功能减退进展缓慢，早期以肾小管功能损害为主；③血尿酸升高与肌酐不成比例，血尿酸／升高与肌酐不成比例，血尿酸／血肌酐可〉２．５；④痛风肾病有典型临床表现，而原发     

探析造影剂肾病患者尿胱抑素C及血尿酸水平变化的意义

目的探析造影剂肾病患者尿胱抑素C及血尿酸水平变化的意义。方法以血肌酐水平变化为据将60例造影剂肾病患者分为a组和b组,其中a组为重型造影剂肾病组,b组为轻型造影剂肾病组。两组患者均进行造影检查,分别于检查前后留取患者6h尿和患者晨起空腹状态的静脉血,检测并比较患者的血肌酐、血胱抑素C、血尿酸、尿肌酐、尿胱抑素C水平。结果造影前,两组患者的血肌酐、血胱抑素C、血尿酸、尿肌酐、尿胱抑素C水平比较差异无统计学意义(P0.05)。造影后,两组患者的血肌酐、尿胱抑素C及血尿酸水平均较造影前有所升高,且造影前后的差异有统计学意义(P0.05)。造影后,a组患者的尿胱抑素C及血尿酸水平显著高于b组,差异有统计学意义(P0.05)。结论造影后,造影剂肾病患者的尿胱抑素C、血尿酸水平越高,其肾损伤程度越严重,高尿胱抑素C水平及高血尿酸水平可作为重型造影剂肾病的预测指标。     

苏州地区305例血尿酸升高实验结果探讨

目的了解苏州地区70岁以上老年人健康体检群体血尿酸水平及其相关项目结果,分析这一群体血尿酸及其相关项目升高原因,为今后开展这方面工作提供参考。方法采用上海科华东菱诊断用品公司生产试剂,分别用酶法测定血尿酸、三酰甘油和肌酐。结果 70岁以上老年男性1 136例,血尿酸升高202例,占17.78%,女性1 156例,血尿酸升高103例,占8.91%。在305例血尿酸升高同时伴有三酰甘油升高168例,占55.08%,伴有肌酐升高44例,占14.43%。结论 70岁以上老年人血尿酸水平比70岁以下人群血尿酸水平高,而且是随着年龄增加而升高,男性高于女性,女性与男性比较差异有统计学意义(P<0.01)。     

别嘌醇降低血尿酸延缓慢性肾衰竭进展的观察

目的:应用别嘌醇降低血尿酸水平,观察其对延缓慢性肾衰竭进展的作用.方法:选择轻中度慢性肾衰竭伴有轻度高尿酸血症患者61例,随机分为别嘌醇治疗组29例和对照组32例.给予别嘌醇治疗组患者别嘌醇100～3mg/d,控制血尿酸于正常范围内.慢性肾衰竭药物治疗方案两组相同.观察期限12个月,比较两组患者慢性肾衰竭进展的差异.观察终点为:血肌酐较基线翻倍,进入终末期肾病(透析治疗或血清肌酐>707μmmol/L),全因死亡.结果:两组患者血肌酐和尿素氮水平均有升高,但别嘌醇治疗组肌酐和尿素氮水平上升幅度低于对照组(t=2.331,P=0.023和t=3.673,P=0.001).别嘌醇治疗组有8例患者达观察终点,时照组有18例患者达观察终点,别嘌醇治疗组终点事件发生率低于对照组(27.59%比56.25%.X2=5.111,P=0.024).结论:别嘌醇通过降低血尿酸水平,可明显延缓轻中度慢性肾衰竭的进展.     

血尿酸水平与新发心血管疾病及糖尿病肾病的相关性

目的探讨Ⅱ型糖尿病患者血尿酸水平与新发心血管疾病及糖尿病肾病的相关性。方法筛选西安市中心医院2014年11月~2016年11月280例糖尿病患者,以血尿酸水平为基准分为高尿酸组和正常尿酸组,各140例,检测两组患者心血管相关指标和肾损害指标,评价血尿酸水平与新发心血管疾病及糖尿病肾病的关系。结果高尿酸组患者的颈动脉内-中膜厚度、尿白蛋白/肌酐比值及甘三油酯高于正常尿酸组,差异有统计学意义（P<0.01）;高尿酸组高血压、冠状动脉粥样硬化及糖尿病肾病的发生率高于正常尿酸组（P<0.05）;高尿酸组冠状动脉粥样硬化和糖尿病肾病的发生时间分别为12.58±2.36月和11.75±1.96月,短于正常尿酸组（P<0.05）;多元回归分析显示血尿酸水平是颈动脉内-中膜厚度、尿白蛋白/肌酐比值的主要影响因素。结论Ⅱ型糖尿病患者血尿酸水平与新发心血管疾病及糖尿病肾病呈正相关,随着血尿酸水平升高新发心血管疾病及糖尿病肾病的概率更高、发病时间更早。     

慢性肾病患者检测血尿酸的意义

目的探讨慢性肾病患者检测血尿酸的意义。方法 40例慢性肾病组与30例健康对照组同时检测肌酐(Cr)、尿素氮(BUN)和血尿酸(UA),进行相关的统计学分析。结果慢性肾病组的Cr、BUN和UA值分别高于对照组,组间比较差异有统计学意义(P<0.01)。慢性肾病组患者的血尿酸异常阳性率与健康对照组比较差异有统计学意义(P<0.01)。结论高尿酸血症是慢性肾病的危险因素之一。     

高尿酸血症与老年高血压患者尿微量白蛋白排泄率及颈动脉内膜中层厚度的关系

目的:探讨高尿酸血症与老年高血压患者尿微量白蛋白排泄率(UAER)及颈动脉内膜中层厚度(CMT)的关系。方法:检测341例老年高血压患者的空腹血糖、甘油三酯、胆固醇、HDL-C、LDL-C、血清肌酐、血尿酸,计算尿白蛋白排泄率(UAER)。分析患者血尿酸水平与各项临床指标的相关性及影响UAER和CMT的相关因素。结果:血尿酸水平与UAER相关,在校正内血清肌酐的影响后,相关性仍然存在(男性r=0.27,P<0.01;女性r=0.29,P<0.01)。女性患者血尿酸水平与CMT相关(r=0.23,P<0.01)。血尿酸是老年高血压患者UAER(男性β=0.19,P<0.01;女性β=0.23,P<0.05)及老年女性高血压患者(β=0.16,P<0.05)CMT的独立相关因素。结论:血尿酸在老年高血压患者肾损害及心血管疾病的发病中起一定作用,控制血尿酸可能在防治高血压导致靶器官损伤中有着重要作用,     

血尿酸、β2微球蛋白、脂蛋白(a)和C反应蛋白在老年高血压患者早期肾损伤的诊断价值

目的 探讨血尿酸(SUA)、β2微球蛋白(β2-MG)、脂蛋白(a)[Lp(a)]和C反应蛋白(CRP)在老年高血压患者引起早期肾损伤中的临床应用价值。方法 根据临床诊断将210例原发性老年高血压患者作为研究对象和50例健康老年人作为健康对照,分别测定其SUA、β2-MG、Lp(a)和CRP水平并进行统计分析;根据内生肌酐清除率(Cr)将这210例高血压患者又分单纯高血压组和高血压肾病组,观察这4项指标的变化情况。结果 高血压组SUA、β2-MG、Lp(a)和CRP水平明显升高且高于对照组,差异有统计学意义(P<0.05)。根据血压升高程度分组研究:高血压1级,高血压2级,高血压3级组的SUA、β2-MG、Lp(a)和CRP水平呈趋势性升高,差异有统计学意义(P<0.05);高血压肾病组与单纯高血压组比较:SUA、β2-MG、LP(a)和CRP水平显著升高,差异有统计学意义(P<0.05)。结论 监测老年高血压患者SUA、β2-MG、LP(a)和CRP水平,可有效监测老年高血压患者肾功能的早期受损,可更快地、更有效发现其患者的肾脏病变,有利于临床医生早期对其进行诊治。     

伴有肉眼血尿的IgA肾病患者临床特点分析

目的 研究伴有肉眼血尿的IgA肾病患者临床及病理特点,指导临床治疗.方法 经肾活检病理诊断为IgA肾病的患者76例,根据患者病程中是否出现肉眼血尿分为研究组和对照组,研究组22例,病程中均伴有肉眼血尿;对照组54例,不伴有肉眼血尿.应用Katafuchi半定量积分法分析患者肾脏病变程度,结合患者临床特点比较两组患者病理学改变及临床特点.结果 ①研究组患者前驱感染发生率显著高于对照组,高血压发生率低于对照组,血肌酐低于对照组,平均病程短于对照组(P<0.05).两组患者24 h尿蛋白排泄量无统计学差异(P>0.05).②研究组患者肾脏病理积分、血管积分、球硬化积分及血管壁增厚积分低于对照组(P<0.05).结论 伴有肉眼血尿的IgA肾病患者发病期多伴有前驱感染,病程中高血压发生率、血肌酐水平较不伴有肉眼血尿的IgA肾病患者低.病理改变较不伴有肉眼血尿的IgA肾病轻,预后相对较好.     

原发性膜性肾病患者外周血CysC补体C3补体C4水平及临床意义

目的 了解原发性膜性肾病患者外周血胱抑素C、补体C3、补体C4水平,并分析其临床意义。方法 检测并比较90例原发性膜性肾病患者(观察组)和90名健康体检者(对照组)的血清胱抑素C、补体C3、补体C4、肌酐、尿素氮、白蛋白、血尿酸及24 h尿蛋白定量水平。分析血清胱抑素C、补体C3、补体C4与血清肌酐、尿素氮、白蛋白、血尿酸及24 h尿蛋白定量的相关性,以及其对原发性膜性肾病患者预后的诊断价值。观察组给予激素+他克莫司治疗6个月,比较治疗前后两组上述实验室指标水平变化情况。结果 观察组血清胱抑素C、24 h尿蛋白定量水平显著高于对照组(P<0.01),血清白蛋白、补体C3、补体C4水平显著低于对照组(P<0.01);两组血清肌酐、尿素氮、血尿酸水平比较差异无统计学意义(P>0.05)。不同病理分期患者血清胱抑素C、补体C3、补体C4、肌酐、尿素氮、血尿酸、白蛋白及24 h尿蛋白定量水平比较差异无统计学意义(P>0.05)。原发性膜性肾病患者血清胱抑素C水平与血清肌酐、尿素氮及24 h尿蛋白定量水平呈显著正相关(P<0.01),与血尿酸及血清白蛋白水平无显著相...     

Hyperuricemia as a risk factor of nephropathy in gout

Among 196 patients with primary gout examined in hospital or earlier stable or transient hyperuricemia was noted in 160 (81.6%). These patients were entered into the study group. The control group included 36 persons in whom the level of blood uric acid did not exceed normal values. The familial pattern of disease was established in the patients of the study group. Urolithic, proteinuric and hypertensive types of nephropathy as well as chronic renal insufficiency were more frequently observed in hyperuricemia patients. Alongside with severe tubular, interstitial and vascular changes, glomeruli in the form of mesangioproliferative or mesangiocapillary glomerulonephritis were regularly involved in the pathological process. In the rest of the patients vascular lesions were less marked and less frequent, renal glomerular changes reminded the picture of mesangioproliferative glomerulonephritis only; urolithiasis in them took a more favorable course. Thus, a high level of blood uric acid is one of the risk factors of renal affection in gout determining in many ways prognosis of disease.     

中老年高尿酸血症预防知识与行为状况的调查研究

[目的]通过对中老年高尿酸血症的预防知识与行为状况的调查,分析预防护理知识缺乏的原因。[方法]2003年1月—2005年2月来我院查体与就诊者年龄在40岁以上的中老年人685例,分为高尿酸组123例,非高尿酸组562例,进行血压(BP)、血尿酸(URIC)、体重指数(BMI)、空腹血糖(GLU)、血清胆固醇(CHOL)、三酰甘油(TG)、血尿素氮(BUN)、肌酐(CREA)等指标对比观察。同时采用问卷调查方法,对123例高尿酸血症者进行预防护理知识与行为状况的调查分析。[结果]在685例调查者中有123例(17.96%)血尿酸高,在高尿酸血症组中,有半数以上人员对血尿酸高的相关知识认识不足,有近半数人员对高尿酸血症发展预后了解不足,自我护理行为缺乏,另与高尿酸血症同时并存的还有肥胖、高血压、高血脂、高血糖。[结论]中老年高尿酸血症发生率在升高,疾病知识缺乏,自我护理意识不强,应加大对高尿酸血症发生发展的教育力度,以使其建立健康的生活习惯,减少痛风的发生。     

Gout: current views. Stage oriented treatment

Gout is a common disease arising due to abnormal purin metabolism and excessive accumulation of uric acid in the blood (hyperuricemia) and manifesting with attacks of acute gouty arthritis. In long duration of gout uric acids accumulate in the bones and periarticular tissues as tophuses. Repeat attacks lead to development of chronic gouty arthritis. Purins restriction diet is an important component of gout treatment. Treatment of acute arthritis should be started early, in initial pains before the development of the attacks. Gouty arthritis in the presence of continuous hyperuricemia, tophyses and urolithiasis is treated with allopurinol. Its intake should be long and controlled by the blood level of uric acid. Balneotherapy is recommended for patients with chronic gouty arthritis associated with cardiovascular diseases, urolithiasis.     

Asymptomatic hyperuricemia: to treat or not to treat

Treatment of asymptomatic hyperuricemia is not necessary in most patients, unless perhaps they have very high levels of uric acid or are otherwise at risk of complications, such as those with a personal or strong family history of gout, urolithiasis, or uric acid nephropathy.     

Gout: an update

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.     

Rasburicase (Fasturtec)

Rasburicase (Fasturtec) is an enzyme that transforms uric acid to the more water soluble allantoin to be excreted by the kidneys. Rasburicase fulfills an unmet clinical need in the treatment of hyperuricemia in that it produces a more rapid action of controlling serum uric acid compared with allopurinol. Tumours with high proliferative rate and sensitive to chemotherapy such as hematological malignancies (mainly) solid tumours (occasionally) may lead to a tumor lysis syndrome. In this situation rasburicase can effectively lower serum uric acid concentrations with a secondary improvement in renal function. Hyperuricemia is the hallmark of severe gout with tophi formation. Rasburicase represents an interesting new option in controlling serum uric acid in patients with severe tophaceous gout.     

基于DECT分析高尿酸血症患者尿酸盐结晶的相关因素

目的:探讨高尿酸血症患者尿酸盐结晶的相关因素。方法:选择328例高尿酸血症患者作为研究对象,均行双侧足踝部DECT扫描,收集患者的临床资料、完善相关实验室检查,记录尿酸盐结晶分布情况,根据DECT检测有无尿酸盐结晶将所有研究对象分为两组,即无尿酸盐结晶的高尿酸血症组和有尿酸盐结晶的高尿酸血症组,分析两组尿酸盐结晶情况、一般人口统计学资料、生化指标以及发生尿酸盐结晶的风险因素。结果:328例高尿酸血症患者检出尿酸盐结晶者185例,215例伴发痛风。DECT检查发现有尿酸盐结晶组伴痛风发生率(93.0%)远高于无尿酸盐结晶组(30.1%),P<0.05。有尿酸盐结晶组患者BMI、高血压、高脂血症、伴发痛风率均高于无尿酸盐结晶组(P<0.05)。有尿酸盐结晶组的生化指标中SUA、TC及Scr水平均高于无尿酸盐结晶组(P<0.05),HDL-C水平低于无尿酸盐结晶组(P<0.05)。Logistics回归分析显示痛风、体重指数、高血压、高脂血症为高尿酸血症患者尿酸盐结晶的危险因素。结论:DECT可检测高尿酸血症患者尿酸盐结晶情况,提示临床对出现尿酸盐结晶的患者及早干预。对于肥胖、伴有高血压、高脂血症的高尿酸血症患者,需临床积极干预相关因素,有望使高尿酸血症患者止步于尿酸盐结晶形成之前。     

Severity of a female gout course

AIM: Comparison of a gout course in males and females. MATERIAL AND METHODS: The trial enrolled 34 patients (17 females and 17 males). The patients were matched by age and the disease duration. Severity of a gout course was assessed by the disease history, articular syndrome, concomitant diseases, blood biochemistry. Statistical processing was made with a computer program "Statistica 6.0". RESULTS: Events predisposing to purin metabolism disturbances and, therefore, to development of gout occur more frequently in females than in males. For the most part this concerns arterial hypertension and intake of diuretics. Women often have endocrine pathology (artificial menopause, dysmenorrhea, euthyroid goiter). In women gout runs a more severe course manifesting in early chronization, polyarticularity, lingering arthritis, rapid formation of tophuses. Both groups demonstrated marked polymorbidity with accumulation of the diseases related to atherosclerosis. Distinct group differences by content of uric acid seem to arise from early onset of chronic renal failure in women. CONCLUSION: In the absence of sex- and age-related differences, a more severe course of gout is observed in women. This may be due to hyperuricemia and a trend to the disease chronization, high prevalence of arterial hypertension and renal failure.     

河北蔚县地区人群痛风和高尿酸血症现状调查

目的：调查河北省蔚县居民高尿酸血症与痛风的流行情况,并观察高尿酸血症与体重指数、收缩压、血浆胆固醇、甘油三脂和空腹血糖的相关性。方法采用随机、分层、整群抽样的方法,调查了该县各地区7,083名20岁以上居民的高尿酸血症和痛风的患病情况。结果①血尿酸水平及高尿酸血症情况：总体血尿酸水平为（345.43±68.52）μmol/L,其中男性为（371.82±78.22）μmmol/L,女性为（315.28±73.67）μmmol/L;高尿酸血症患病率为15.40%,男性患病率为16.88%,女性为10.83%;②痛风患病率：痛风125例,痛风患病率为1.76%,其中男113例（2.11%）,女12例（0.70%）;③与血尿酸正常组比较,高尿酸血症组体重指数、收缩压、血浆甘油三酯、胆固醇和空腹血糖水平均明显升高,差异有统计学意义。结论河北省蔚县人群高尿酸血症及痛风患病率均呈现升高趋势。高尿酸血症患者易合并高血压、高脂血症、糖尿病等疾病,表明作为心血管疾病的危险因素,高尿酸血症患病率仍在继续升高,高尿酸血症已经成为危胁人类健康的重要隐患。     

Primary hyperuricemia due to decreased renal uric acid excretion

Hyperuricemia reflects extracellular fluid supersaturation for uric acid. Although dietary, genetic, or disease-related excesses in urate production underlie hyperuricemia in some cases, impaired renal excretion of uric acid is the dominant cause of hyperuricemia. This type of hyperuricemia may be primary (idiopathic) and unassociated with an identifiable disorder. Two important candidates that may affect renal urate excretion were identified recently. One is an organic anion transporter (OAT) family member called urate transporter (URAT) 1. URAT1 has highly specific urate transport activity, exchanging this anion with others including most of the endogenous organic anions and drug anions that are known to affect renal uric acid transport. Another is uromodulin (UMOD), which is the key protein for the pathogenesis of familial juvenile hyperuricemic nephropathy that is characterized by early onset of hyperuricemia and renal failure. The role of these proteins in the cause of hyperuricemia is under investigation.