原发性高血压肾病患者红细胞ATP酶活性检测的临床意义

目的 探讨原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶活性的改变参与原发性高血压肾病的可能机制。方法 按Reilni制膜法测定32例原发性高血压无肾病和40例原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶含量,并与35名正常健康人作比较。结果 原发性高血压无肾病组和肾病组细胞膜Na^＋、K＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶活性均显著地低于正常人组（P〈0.01）。原发性高血压肾病组与无肾病组亦有显著性差异（P〈0.05）。结论 原发性高血压肾病的发生和发展与细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP的活性有密切的关系。     

原发性醛固酮增多症患者诊断试验护理

原发性醛固酮增多症(简称原醛症),由肾上腺皮质分泌过多的醛固酮而导致高血压、低血钾、低血浆肾素活性及高醛固酮水平为主要特征的临床综合症[1]。由于原发性醛固酮增多症的类型不同,治疗方法及预后不尽相同,所以其筛查、定性、定位诊断尤其重要,现将我科1985~2005年6月间收治的134例原发性醛固酮增多症患者各种试验性诊断方法的护理报告如下:1资料与方法1.1资料1995年6月~2005年6月间收治的134例原发性醛固酮增多症患者中,男性64例,女性70例,平均年龄(39.2±10.8)岁,平均病程(50±68.4)个月。134例患者均有高血压,平均血压为(184.31±21.3…     

原发性醛固酮增多症误诊2例

原发性醛固酮增多症(简称原醛症,PA)是由肾上腺皮质球状带病变致醛固酮分泌异常增多所致,属于不依赖肾素-血管紧张素的盐皮质激素过多症,是一种以高血压、低血钾或正常血钾、低血浆肾素、高血浆醛固酮为主要特点的继发性高血压。我国以往对高血压伴低血钾者进行检查,原醛症患病率占高血压患者的0.4%~2.0%,近年采用血浆醛固酮/血浆肾素活性比值对血钾正常的高血压病患者进行筛查,发现近10%以上为原发性醛固酮增多症[1]。作     

原发性醛固酮增多症高血压的临床特点分析

目的：通过临床观察探讨原发性醛固酮增多症高血压患者的临床主要特征。方法原发性醛固酮增多症高血压患者31例作为观察组,并以同期接收的35例原发性高血压患者作为对照组。两组患者均开展临床相关检测,通过结果比较分析观察组患者的临床特征。结果两组患者的基本情况比较差异无统计学意义（P〉0.05）,但观察组血压水平略高于对照组;观察组患者在卧位与站立位下肾素活性（PRA）、血醛固酮（PAC）以及醛固酮-肾素比值（ARR）水平与对照组比较,差异均具有统计学意义（P〈0.05）。结论原发性醛固酮增多症高血压患者具有PRA、PAC与ARR水平异常等临床特征,经上述指标检验可避免诊断误区,提高准确程度。     

黄芪注射液对盐水负荷模型大鼠的利尿作用研究

目的:研究黄芪注射液对盐水负荷模型大鼠的利尿作用。方法:取大鼠ig给予去离子水(2.5 ml/100 g)复制水负荷模型,取水负荷模型大鼠随机分为模型(生理盐水)组、阳性对照(呋塞米0.01 g/kg)组和黄芪注射液低、中、高剂量[2.5、5、10 g(生药)/kg]组,每组10只。各组大鼠ig给予1%氯化钠溶液(4 ml/100 g)复制盐水负荷模型,复制模型20 min后ig给予相应的药物。给药后收集6 h内的尿液,每1 h收集1次;检测各组大鼠尿液中Na+、K+、Cl-量及尿液p H;腹主动脉取血,采用酶联免疫吸附(ELISA)法测定各组大鼠血浆中醛固酮(ALD)、心房钠尿肽(ANP)与抗利尿激素(ADH)的含量。结果:与模型组比较,黄芪注射液高剂量组和阳性对照组大鼠的总尿量均增加;黄芪注射液中、高剂量组和阳性对照组大鼠尿液中Na+、Cl-量均增加,K+量仅阳性对照组大鼠增加;黄芪注射液中、高剂量组大鼠血浆中ALD含量均减少、ANP含量均增加,以上差异均具有统计学意义(P<0.05)。各组大鼠尿液p H和血浆中ADH含量均未见明显变化。结论:黄芪注射液可明显增加盐水负荷模型大鼠的尿量,其机制可能与增加血中ANP和减少ALD的分泌,进而促进尿液中Na+、Cl-的排泄有关。     

原发性醛固酮增多症30例诊治分析

目的 提高原发性醛固酮增多症的诊治水平.方法 分析1987～2005年收治的原发性醛固酮增多症30例,其中肾上腺瘤者24例（80%）,肾上腺皮质增生者6例（20%）,均经手术和病理证实.结果 术后肾上腺瘤者24例,血钾均恢复正常,21例血压恢复正常,3例仍高,肾上腺皮质增生者6例,血钾恢复正常5例.结论 原醛症定性诊断主要靠症状和生化测定,定位靠B超、CT,开放性或腹腔镜手术是主要治疗手段.     

探讨血浆醛固酮肾素活性比值(ARR)在原发性醛固酮增多症(PA)诊断中的临床价值

目的 探讨血浆醛固酮肾素活性比值(ARR)在原发性醛固酮增多症(PA)诊断中的临床价值.方法 选择我院2013年1月~2015年1月收治的高血压疑似PA的患者250例,收集所有患者的基本资料,对患者进行原发性醛固酮增多症的筛查,患者采取卧位或者立位,检查指标包括血浆醛固酮(PAC)、血浆肾素(PRA)等,经确诊分为PA组100例和EH(原发性高血压)组150例,对比两组基本资料情况和不同体位的血浆醛固酮活性比值、血浆醛固酮、血浆肾素水平.结果 ①与EH组对比,PA组年龄明显更小,高血压病程明显更长,舒张压和收缩压明显更高,血钾水平明显更低,尿钾含量明显更高,P<0.05;两组患者的性别比较差异不具有统计学意义,P>0.05.②与EH组对比,PA组卧位和立位PAC明显更高,卧位和立位PRA明显更低,卧位和立位ARR明显更高,P<0.05.结论 血浆醛固酮肾素活性比值(ARR)在原发性醛固酮增多症(PA)诊断中具有较高的准确度,可作为可靠的筛查指标,值得临床广泛应用.     

原发性醛固酮增多症患者浦肯野细胞蛋白4表达与细胞凋亡关系研究

目的 探讨原发性醛固酮增多症(primary aldosteronism,PA)的两种主要亚型——醛固酮瘤(aldosterone-producing adenoma,APA)及特发性醛固酮增多症(idiopathic hyperaldosteronism,IHA)患者组织中浦肯野细胞蛋白(Purkinje cell ...     

原发性醛固酮增多症患病率调查

目的在高血压人群中进行原发性醛固酮增多症（原醛症）患病率的筛查。方法抽取就诊患者立位2d,时静脉血查血浆醛固酮与血浆。肾素之比（ARR）,若ARR大于30,进一步行肾上腺CT检查或卡托普利试验,以确定原醛症的诊断。结果817例患者中,诊断为原醛症的31例,占3．8％,伴有低钾者占65％,血钾正常者占35％。结论ARR是针对高血压人群进行原醛症筛查的有效指标,可提高原醛症的检出率,我国原醛症患者仍以低钾占多数。     

不同体位醛固酮/肾素比值对鉴别诊断原发性醛固酮增多症的意义

目的:研究不同体位醛固酮/肾素比值(ARR)对鉴别诊断原发性醛固酮增多症(PA)的两个主要亚型肾上腺皮质醛固酮瘤(APA)和特发性醛固酮增多症(IHA)的意义。方法:在40例临床确诊的PA患者中进行卧立位试验。结果:①IHA组立位醛固酮较卧位明显升高(P<0.05)②APA组立位较IHA组醛固酮及肾素都显著升高(P<0.05)③立位ARR≥100结合立位血浆醛固酮水平>200ng/dL鉴别APA及IHA敏感性和特异性分别为77.27%和78.26%。结论:立位ARR结合立位血醛固酮水平在APA及IHA鉴别诊断中价值有限。     

高血压患者中原发性醛固酮增多症的检出率及特点

【摘要】目的探讨高血压患者中原发性醛固酮增多症（PA）的检出率及临床特点。方法197例高血压患者检测PA及其他相关指标,排除其他继发性高血压。将研究对象分PA组及原发性高血压组（EH组）。对2组患者行卧、立位试验,卡托普利试验或静脉高钠试验,血钾及肾上腺薄层CT,部分患者行午夜地塞米松抑制试验、促肾上腺皮质激素（ACTH）及性激素测定,主要指标为血醛固酮、肾素活性及醛固酮与肾素活性比值（ARR）。结果（1）197例高血压患者中确诊PA38例（19.29%）,13例经病理诊断证实,醛固酮腺瘤6例,单侧肾上腺增生7例,未发现无功能腺瘤。（2）2组患者的高血压病程及体质指数（BMI）的差异无统计学意义,PA组及EH组男性均多于女性。（3）与EH组比较,PA组的起病年龄相对年轻,收缩压与舒张压水平更高,但差异均无统计学意义;PA组卧位、立位血醛固酮水平及ARR均显著升高,血肾素活性均显著下降（均P＜0.01）,血钾水平差异无统计学意义。结论同期住院的高血压患者中PA的检出率较高,其中醛固酮腺瘤和单侧肾上腺增生的比例相近,低钾血症不常见。     

Is Primary Aldosteronism Underdiagnosed In Clinical Practice?

1. Primary aldosteronism is a syndrome consisting of hypertension, suppressed renin activity or concentration and high aldosterone levels in plasma or urine. The main steps in diagnosis are the determination of renin and aldosterone levels, the demonstration of renin-aldosterone dissociation and discrimination between idiopathic hyperplasia and Conn's adenoma, with only Conn's adenoma amenable to surgery. 2. Patients with resistant hypertension and/or hypokalaemia should be screened for primary aldosteronism with simple, redundant hormonal tests. The aldosterone to renin ratio is a logical initial screening test, a high ratio demonstrating renin-aldosterone dissociation. Criteria for a high ratio should be determined in each laboratory. 3. In patients with documented primary aldosteronism, computed tomography scan and adrenal vein sampling help to distinguish between idiopathic hyperplasia and Conn's adenoma. 4. Patients with low renin hypertension, idiopathic hyperplasia and Conn's adenoma have overlapping values for plasma concentrations of potassium, renin and aldosterone and the aldosterone to renin ratio. Because primary aldosteronism subtypes are quantitative diseases, the true prevalence of primary aldosteronism cannot be defined. 5. The use of sensitive screening tests (e.g. aldosterone to renin ratio) gives a higher prevalence of diagnosed cases of primary aldosteronism, but not of surgically correctable forms. Therefore, there is no clinical evidence that primary aldosteronism is underdiagnosed. 6. There is a need for tests to predict the postoperative blood pressure outcome of surgery in subjects with Conn's adenoma.     

The effect of amiloride on the renin-aldosterone system in primary hyperaldosteronism and Bartter's syndrome

Amiloride is a potassium-sparing diuretic which has been advocated for the treatment of hypokalemic disorders. This agent was prospectively evaluated in hypokalemic patients with either primary hyperaldosteronism (ten patients) or Bartter's syndrome (five patients). Vital signs, electrolytes, and ambulatory hormonal studies were assessed during a control period and treatment period with amiloride therapy at 10 to 40 mg/day over two to 24 weeks. During the treatment period the systolic and diastolic blood pressure fell significantly in primary hyperaldosteronism but remained unchanged in Bartter's syndrome. In summary, amiloride therapy (1) increased plasma potassium in both diseases; (2) increased plasma renin activity (PRA) in primary hyperaldosteronism but decreased PRA in Bartter's syndrome; and (3) increased plasma aldosterone in both diseases. Since potassium is known to suppress renin production and stimulate aldosterone secretion, correction of the hypokalemia in this study probably accounts for the decreased PRA and increased plasma aldosterone observed in Bartter's syndrome. The increase in both PRA and plasma aldosterone in primary hyperaldosteronism, however, may be evidence of either a direct activation of the renin-aldosterone system or, alternatively, may be due to the mild natriuretic effects of amiloride.     

IS ALDOSTERONE/RENIN RATIO USEFUL TO SCREEN A HYPERTENSIVE POPULATION FOR PRIMARY ALDOSTERONISM?

The ratio of aldosterone to renin in plasma was measured in samples collected from 79 hypertensive patients. Eighteen patients with primary aldosteronism had ratios ranging from 25 to 677 (mean 183) when measured on 34 occasions, while 16 normal subjects had ratios of 3.3-21 (mean 11.3). Of the remaining 61 patients with ratios ranging from 1.8 to 184, 15 patients have ratios greater than 25 and are under investigation for primary aldosteronism, which appears highly likely in five and has been excluded in two. The aldosterone/renin ratio appears promising as a screening test for primary aldosteronism. Consistency and the effects of sodium and potassium balance and of antihypertensive medications require further study.     

A case report of aldosterone producing adenoma with masked hyperaldosteronemia

A 50-year old female with primary aldosteronism and masked hyperaldosteronemia is reported. Her blood pressure was 176/110 mmHg with no paralysis of hypokalemia. Serum potassium, aldosterone and renin activity were 4.3 mEq/L, 17 ng/dl and 0.6ng/ml/h, respectively. Following a stimulation test by sodium loading and furosemide plus standing, neither aldosterone nor renin activity responded. Adrenal computed tomographic scanning, ultrasonography and cortical scintiscanning failed to reveal the tumor mass. A definite diagnosis of aldosterone producing adenoma was made after adrenal venous sampling in which the concentration of aldosterone was 15-fold greater in the right adrenal vein than in the left. The diagnosis of right adrenal cortical adenoma was confirmed by surgery. Thus, this case indicates the usefulness of the sampling technique in making an accurate diagnosis for primary aldosteronism with normo-kalemia, normo-aldosteronemia and normo-reninemia.     

FAMILIAL HYPERALDOSTERONISM TYPE II: FIVE FAMILIES WITH A NEW VARIETY OF PRIMARY ALDOSTERONISM

1. Thirteen patients from five families had Familial Hyperaldosteronism Type II (FH-II), a new variety of familial primary aldosteronism not suppressible with dexamethasone that often involves adrenocortical adenoma formation. 2. Five patients had solitary aldosterone-producing adenomas, three had bilateral autonomous overproduction of aldosterone, and in five the subtype is yet to be determined. 3. Comparing FH-II patients with 88 patients with primary aldosteronism of other causes revealed no differences in mean age at presentation or at onset of hypertension, sex incidence, lowest recorded serum potassium, plasma aldosterone, plasma renin activity or adenoma size. 4. Analysis of DNA in peripheral blood of patients with FH-II, their affected and unaffected relatives, and in removed tumours is in progress in order to determine the underlying genetic defect(s) in FH-II, perhaps an abnormality in the P-450_aldo gene (CYP11B2). 5. It is recommended that hypertensive relatives of patients with primary aldosteronism should have measurements of the aldosterone/renin ratio.     

HIGH INCIDENCE OF PRIMARY ALDOSTERONISM IN 199 PATIENTS REFERRED WITH HYPERTENSION

1. This study sought to assess the incidence of primary aldosteronism in 199 hypertensives who were normokalaemic and in whom the question of primary aldosteronism had never been raised. 2. The screening test applied was the aldosterone to renin ratio in plasma, which was raised in 40 and normal in 159 patients. A second ratio was normal in 14 of these 40. 3. Twenty-two patients with two further raised ratios required fludrocortisone suppression testing. This has been completed in 17, and failure to suppress led to a diagnosis of primary aldosteronism in all. 4. A dexamethasone suppression test (DST) excluded ACTH-dependent hyperaldosteronism and laterality of aldosterone production was determined by adrenal vein sampling. 5. Unilaterality in five patients led to adrenalectomy in four and spironolactone in one. Bilaterality in six patients led to spironolactone. 6. This study so far provides a proven (minimum) incidence for primary aldosteronism of 8.5%, a probable incidence of 12.0% (including two raised ratios) and a possible (maximum) incidence of 13.0% (leaving out those with second ratio normal). Exclusion of hypokalaemic hypertensives will lead to an underestimation of the true incidence of primary aldosteronism. 7. Based on this and other evidence, it is estimated that the incidence of primary aldosteronism in the ‘essential hypertensive’ population is between 5 and 15%, and is probably around 10%.     

CLINICAL AND PATHOLOGICAL DIVERSITY OF PRIMARY ALDOSTERONISM, INCLUDING A NEW FAMILIAL VARIETY

1. Of 93 patients with primary aldosteronism seen during a 20 year period, 52 had an aldosterone-producing adenoma (APA) removed (five more await surgery), 14 had bilateral adrenal hyperplasia (BAH), three had glucocorticoid-suppressible hyperaldosteronism (GSH), one had adrenal carcinoma and 18 are yet to be categorized. 2. Seventy-three presented with hypertension and hypokalaemia. Others had markedly suppressed renal venous plasma renin activity (PRA) or elevated plasma aldosterone (PA)/PRA ratio, in new or resistant hypertensives. 3. The PA/PRA ratio was the most reliable screening test. 4. Diagnosis depended on the failure of suppression of aldosterone by salt loading and fludrocortisone. 5. Differentiation of BAH from APA depended on adrenal venous sampling comparing adrenal and peripheral venous PA/cortisol ratios. 6. A new familial variety of primary aldosteronism is described, with two affected members in each of three families. 7. Primary aldosteronism should be looked for in resistant and low-renin hypertension as well as in hypertension with hypokalaemia, and other family members should have PA/PRA measured if they are hypertensive.     

原发性醛固酮增多症的诊治(附120例报告)

对１２０例经手术、病理证实为原发性醛固酮增多症（ＰＡ）患者的临床资料进行回顾性分析。结果显示：皮质腺瘤 ９８例（８１．７％），皮质增生２２例（１８．３％）。手术前血清钾降低者 １１４例（９５．０％），最低者达 １．６ ｍｍｏｌ／Ｌ。测定１０３例血浆醛固酮均高于正常，测定９１例血浆肾素活性５４例低于正常（５９．３％）。Ｂ超检查１０６例，阳性７２例（６７．９％），ＣＴ检查１１０例，阳性１０５例（９５．５％）。手术后１２０例血清钾均恢复正常。说明ＰＡ的定性诊断主要依赖患者的血清钾降低及血浆醛固酮升高，Ｂ超及ＣＴ定位诊断较为准确。治疗方法以开放性手术切除肿瘤侧肾上腺为主。     

Selection of patients for surgery for primary aldosteronism

1. Primary aldosteronism is a condition characterized by renin suppression and various degrees of hypertension and hypokalemia caused by aldosterone hypersecretion. 2. The adoption of the aldosterone-to-renin ratio determination as a screening test has led to an increase in the prevalence of diagnosed cases of primary aldosteronism. 3. Primary aldosteronism is confirmed by the demonstration of either sustained absolute aldosterone hypersecretion, or non-suppressible aldosterone hypersecretion. 4. Computed tomography and adrenal vein sampling can then be used to distinguish between idiopathic primary aldosteronism and the surgically remediable forms: aldosterone-producing adenoma and primary adrenal hyperplasia. 5. In patients with aldosterone-producing adenoma or primary adrenal hyperplasia, unilateral adrenalectomy generally results in the normalization of aldosterone secretion and kalemia, but normotension is achieved in only half of the cases. Nevertheless, in many cases without hypertension cure, adrenalectomy leads to an improvement in hypertension control with lower blood pressure levels and/or less antihypertensive medication.