卧位时长对ARR诊断原发性醛固酮增多症的影响

目的 探讨不同时长卧位及立位血浆醛固酮水平、血浆肾素活性及醛固酮/肾素比值（ARR）在原发性醛固酮增多症（PA）诊断中的价值。方法 选取疑似PA的患者103例,分别测定立位2 h、卧位4 h和卧位2 h血浆肾素活性、血浆醛固酮水平,计算ARR。根据临床诊断结果将患者分为PA组（44例）和非PA组（59例）。采用受试者工作特征（ROC）曲线评价ARR诊断PA的价值。结果 PA组与非PA组比较,立位2 h、卧位4 h和卧位2 h的血浆醛固酮水平、血浆肾素活性、ARR差异均有统计学意义（P<0.01）。PA组立位2 h血浆醛固酮水平、血浆肾素活性与卧位4 h、卧位2 h比较,差异均有统计学意义（P<0.05）。PA组和非PA组组内比较,立位2 h、卧位4 h、卧位2 h ARR差异均无统计学意义（P>0.05）,卧位4 h与卧位2 h血浆醛固酮水平、血浆肾素活性、ARR差异均无统计学意义（P>0.05）。ROC曲线分析结果显示,立位2 h ARR、卧位4 h ARR、卧位2 h ARR诊断PA的曲线下面积（AUC）分别为0.821、0.779、0.787。结论 立位2...     

醛固酮与肾素活性比值对原发性醛固酮增多症的诊断价值

目的 评价醛固酮与肾素活性比值(ALD/PRA,ARR)对原发性醛固酮增多症(PA)的诊断价值.方法 回顾性收集44例PA、9例嗜铬细胞瘤、8例无功能性瘤、12例库欣综合征、4例肾动脉狭窄及13例原发性高血压患者的ALD、PRA结果,计算ARR,采用受试者操作特性(ROC)曲线评价各项指标的诊断价值.结果 卧位ALD ROC曲线下面积为0.947,临界值(cut-off值)为174.1 ng/L时,敏感度为86.4%,特异度为91.3%.立位ALDROC曲线下面积为0.889,cut-off值为209.8 ng/L时,敏感度为84.1%,特异度为87.0%.卧位ARR ROC曲线下面积为0.978,cut-off值为40.8 ng·dl-1/ng·ml-1·h-1时,敏感度为95.5%,特异度为95.7%;立位ARR ROC曲线下面积为0.981,cut-off值为35.26 ng·dl-1/ng·ml-1·h-1时,敏感度为95.5%,特异度为93.5%;联合立位ARR和立位ALD,其诊断价值明显优于单一指标,当立位ALD>275 ng/L,立位ARR ROC曲线下面积为0.989,cut-off值为23.73 ng·dl-1/ng·ml-1·h-1时,特异度为100%,敏感度为95.7%.结论 ARR诊断PA的价值高于ALD、PRA,立位ARR优于卧位,当联合立位AID>275ng/L,则诊断价值更大.     

血浆醛固酮/肾素浓度比值诊断原发性醛固酮增多症的价值

目的探讨血浆醛固酮/肾素浓度比值(ADRR)对原发性醛固酮增多症(PA)的诊断价值及最佳临界值。方法选取高血压患者222例,其中PA临床确诊患者33例(CPA组)。采用化学发光法检测血浆醛固酮及肾素浓度,并计算ADRR。采用受试者工作特征(ROC)曲线评价ADRR对PA的诊断价值,并确定最佳临界值。结果高血压患者中PA患者的比例为14.86%(33/222)。PA组卧位和立位的血浆肾素浓度均明显低于高血压组(P0.05),ADRR则明显高于高血压组(P0.05)。ROC曲线分析显示,血浆ADRR诊断PA卧位和立位的曲线下面积(AUC)分别为0.906和0.908;ADRR卧位的最佳临界值为31.32,敏感性和特异性分别为96.97%和73.54%;立位的最佳临界值为27.57,敏感性和特异性分别为81.82%和86.77%。结论血浆ADRR是筛查PA的有效指标。建议在PA初筛时采用25作为立位ADRR筛查的最佳临界值。     

卡托普利肾动态显像诊断肾血管性高血压及血浆肾素的影响分析

目的 探讨卡托普利肾动态显像（CRS）诊断肾血管性高血压（RVH）的效能及血浆肾素活性（PRA）的影响。方法 回顾性分析35例接受立、卧位外周血浆PRA、血管紧张素Ⅱ（AngⅡ）、醛固酮（ALD）水平检测及基础、CRS的RVH患者，按CRS结果分为阳性组和阴性组。比较2组激素水平，以ROC曲线分析2组血浆立位PRA，得出PRA的最低阈值。结果 阳性组24例，阴性组11例。阳性组立位PRA较阴性组升高（Z=3.11，P<0.001）；2组卧位PRA、立卧位AngⅡ及ALD差异均无统计学意义（P均>0.05）。ROC曲线分析显示2组立位PRA的AUC为0.84，PRA为2.47 ng/（ml·h）时，CRS诊断RVH阳性的灵敏度为83.33%，特异度为81.82%。结论 立位PRA是影响CRS诊断RVH敏感度的重要因素。联合测定血浆PRA可提高CRS对RVH的诊断效能。     

醛固酮肾素定量比值筛查原发性醛固酮增多症的探讨

目的探讨醛固酮肾素定量比值(PAC/PRC以下简称AARR)筛查原发性醛固酮增多症(以下简称为原醛症)的价值。方法使用化学发光方法检测32例原醛症和88例原发性高血压患者立、卧位醛固酮和肾素浓度,计算醛固酮肾素浓度比值(AARR),构建AARR对原醛症的ROC曲线,确定AARR筛查原醛症的最佳切点。结果原醛症患者组立位肾素浓度为4.55(15.67)pg/ml,卧位为2.85(5.34)pg/ml,立位醛固酮浓度为213.70(237.38)pg/ml,卧位为207.52(137.90)pg/ml, 立位AARR为61.53(182.84),卧位为100.69(254.03)。原发性高血压患者组立位肾素浓度为6.80(11.90)pg/ml,卧位为4.79(8.36)pg/ml,立位醛固酮浓度为121.20(31.94)pg/ml,卧位为112.47(23.99)pg/ml,立位AARR为17.49(28.57),卧位为22.67(37.43)。立位AARR筛查原醛症的ROC曲线AUC为0.802,Youden’s指数提示最佳切点为54.40 pg/ml,灵敏度为0.719,特异度为0.852;卧位AARR筛查原醛症的ROC曲线AUC为0.848,最佳切点为64.18 pg/ml,灵敏度为0.750,特异度为0.818。卡方检验提示立、卧位AARR筛查原醛症的诊断效果差异无统计学意义(P>0.05)。结论临床上采用醛固酮肾素定量比值对原发性醛固酮增多症进行筛查有一定的应用价值,且立、卧位AARR诊断效果相当。     

血浆醛固酮/肾素活性比值与血清钾在原发性醛固酮增多症诊断中的临床意义

目的探讨血浆卧位ARR比值与血清钾浓度在原发性醛固酮增多症(PA)疾病中的临床诊断价值。方法以PA患者66例作为疾病组,非PA高血压患者58例为对照组,采用放射免疫法测定血醛固酮(SAC)及肾素活性(PRA),采用离子选择电极法测定血清钾,并计算ARR比值(SAC/PRA)。结果 PA组中ARR比值和血清钾浓度分别为203.47±50.23和2.76±0.72mmol/L,与对照组间的差异均达到显著水平(P0.01)。以卧位ARR比值为112.0作为临界值,诊断PA的灵敏度为92.42%,特异性为87.93%,诊断符合率为90.32%;卧位ARR比值与血清钾浓度联合进行诊断时,灵敏度为98.48%,特异性为86.20%,诊断符合率为92.74%。结论血浆卧位ARR比值与血清钾浓度联合测定可用于PA疾病的临床诊断,但将卧位ARR比值与血清钾浓度指标联合检测时具有更高的诊断符合率,可提高PA的检出率。     

原发性醛固酮增多症术前鉴别诊断分析

目的提高对原发性醛固酮增多症(PA)中腺瘤(APA)和特发性醛固酮增多症(IHA)患者的诊断水平。方法对近5年临床确诊的52例PA患者的生化检查、体位试验、影像学检查与术后病理结果进行分析。结果APA患者血钾低于IHA组,尿钾、尿PH高于IHA组;体位试验结果:17例APA患者中立位血醛固酮较卧位升高11例,下降的6例,35例IHA患者立位血醛固酮均较基础升高;影像学检查:APA患者B超、CT、MR I诊断符合率分别为50%、90%和91.6%。IHA患者符合率则为68%、93.75%和90.48%。结论APA患者部分生化异常程度较IHA患者明显;体位试验在APA和IHA中有部分重叠,立位血醛固酮升高者者不能排除APA,而血醛固酮下降者可确诊APA;CT与MR I诊断符合率基本相似。     

血浆ARR筛查原发性醛固酮增多症的应用分析

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)的应用分析。方法选取2016年1月至2017年12月在驻马店市中心医院治疗的PA患者78例(PA组),同时选取疑似PA但确诊为原发性高血压(EH)患者120例(EH组),比较两组临床一般资料以及卧位、立位ARR水平。方法 PA组收缩压、舒张压和尿钾分别为(162.20±20.03)mmHg、(103.20±12.23)mmHg和(37.18±9.39)mmol/L,明显高于EH组(P0.05),而血钾为(3.02±0.55)mmol/L,明显低于EH组(P0.05);PA组卧位、立位ARR分别为73.01(42.23,120.03)ng·dl-1/ng·ml-1·h-1和60.10(30.12,220.43)ng·dl-1/ng·ml-1·h-1,明显高于EH组(P0.05);卧位ARR和立位ARR诊断PA的ROC曲线下面积分别为0.910和0.946(P0.05),卧位ARR和立位ARR截断值分别为15.96ng·dl-1/ng·ml-1·h-1和32.96ng·dl-1/ng·ml-1·h-1,灵敏度分别为94.90%和100.00%,特异度分别为80.83%和81.67%。结论血浆ARR筛查PA有重要作用,其中立位ARR筛查诊断的价值可能较高,值得进一步研究。     

肾性高血压患者肾素、血管紧张素及醛固酮测定的临床价值

目的探讨肾性高血压患者肾素(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)测定对临床诊断与治疗价值。方法收集2014年4月至2016年10月来该院就诊肾性高血压患者134例,其中肾实质性高血压患者114例,肾血管性高血压患者20例,健康体检正常志愿者50例(对照组),均在普通饮食下卧位、立位时采血测定血浆中PRA、AngⅡ、ALD水平。结果肾实质性高血压组卧位、立位血浆PRA、AngⅡ、ALD水平均高于对照组,两组比较,差异有统计学意义(P0.05);肾血管性高血压组卧位、立位血浆PRA、AngⅡ、ALD水平明显高于对照组,两组比较,差异有统计学意义(P0.05);肾血管性高血压组卧位、立位血浆PRA、AngⅡ、ALD水平高于肾实质性高血压组,两组比较,差异有统计学意义(P0.05)。结论肾性高血压患者血浆PRA、AngⅡ及ALD的测定有一定的临床诊断治疗价值。     

白大衣高血压患者血浆肾素活性和血管紧张素Ⅱ及醛固酮水平变化及意义

目的探讨白大衣高血压(white-coat hypertension,WCH)患者血浆肾素活性(plasma renin activity,PRA),血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)、醛固酮(aldosterone,ALD)水平变化及WCH与肾素-血管紧张素-醛固酮系统的关系。方法 WCH患者150例为WCH组,轻中度原发性高血压患者161例为高血压组,同期体检健康者167例为对照组,比较3组诊室血压及24h平均血压;采用ELISA法检测3组血浆三酰甘油(triacylglycerol,TG)、总胆固醇(total cholesterol,TC)、高密度脂蛋白胆固醇(high density lipoprotein-cholesterol,HDL-C)、低密度脂蛋白胆固醇(low density lipoprotein-cholesterol,LDL-C)水平;采用离子交换层析法检测3组糖化血红蛋白水平;采用化学发光免疫分析法检测3组卧位、立位血浆PRA及AngⅡ、ALD水平。结果WCH组诊室血压[(159±17)/(98±10)mm Hg]高于对照组[(123±16)/(78±12)mm Hg](P0.05),与高血压组[(154±11)/(99±10)mm Hg]比较差异无统计学意义(P0.05);WCH组24h平均血压[(119±20)/(78±10)mm Hg]低于高血压组[(138±10)/(86±12)mm Hg](P0.05),与对照组[(115±16)/(76±11)mm Hg]比较差异无统计学意义(P0.05);3组血浆TG、TC、HDL-C、LDL-C、糖化血红蛋白水平比较差异均无统计学意义(P0.05);WCH组血浆PRA、AngⅡ、ALD水平[立位:(3.70±2.36)ng/(mL·h)、(87.89±40.86)ng/L、(325.49±124.56)ng/L,卧位:(3.08±2.21)ng/(mL·h)、(85.57±42.81)ng/L、(295.69±138.47)ng/L]均高于高血压组[立位:(2.56±2.18)ng/(mL·h)、(72.12±17.16)ng/L、(299.44±111.23)ng/L,卧位:(2.25±2.02)ng/(mL·h)、(73.68±19.08)ng/L、(279.57±121.68)ng/L]和对照组[立位:(1.87±1.37)ng/(mL·h)、(58.73±18.23)ng/L、(247.95±76.83)ng/L;卧位:(1.79±1.32)ng/(mL·h)、(59.68±20.43)ng/L、(251.57±77.69)ng/L],且高血压组高于对照组(P0.05)。结论 WCH患者血浆PRA及AngⅡ、ALD水平均增高,肾素-血管紧张素-醛固酮系统可能参与WCH发病机制的调节。     

Aldosterone in primary hypertension relationship to plasma renin activity and urinary electrolytes and a comparison with normotensive subjects

Plasma aldosterone (PA) and urinary aldosterone (Aldo-U) concentrations were studied in 123 patients with primary (essential) hypertension during basal (1 h supine rest), upright and frusemide (80 mg orally) stimulated conditions, and were related to urinary sodium and potassium excretions, supine and sitting blood pressure (BP) and the relationship to plasma renin activity (PRA). As controls, 120 normotensive subjects, matched for age and sex, were investigated identically during strictly defined out-patient conditions. No differences regarding the different mean PA levels, urinary electrolyte excretion or the urinary sodium: potassium ratio were observed between the hypertensive and the normotensive populations. However, the hypertensive subjects had significantly higher mean Aldo-U excretions than the controls. Correlations between PA and the corresponding PRA were consistently significant in the normotensive control group but weak to non-existent in the hypertensive subjects. No relationships at all could be found between the different PRA and Aldo-U values in the hypertensive population but significant correlations were noted in the control group. These findings point to a disturbed function of the renin-angiotensin-aldosterone (RAA) system even in primary hypertension.     

The influence of autonomic diabetic neuropathy and human atrial natriuretic peptide on adrenal gland function in postural changes]

To investigate the influence of postural changes on plasma renin activity (PRA), plasma levels of human atrial natriuretic peptide (hANP) and on aldosterone in diabetes mellitus and autonomic neuropathy, ten patients with diabetes mellitus and autonomic neuropathy and ten patients with diabetes mellitus but without autonomic neuropathy were studied. Ten healthy subjects served as controls. Patients and controls were in supine position for 60 minutes, then changed posture sequentially to sitting (90 minutes) and to upright position (15 minutes). In controls, PRA was increased upon sitting and in the upright position, while hANP was decreased. Patients with autonomic neuropathy differed from controls in impaired renin stimulation, whereas in patients without autonomic neuropathy PRA responses to postural changes were only slightly decreased. In both groups of patients, the normal hANP responsiveness to postural changes was lacking. There were no differences in aldosterone levels between patients and controls. In patients with high basal hANP levels due to elevated systolic blood pressure renin responses to postural changes were decreased in comparison to those patients with low basal hANP levels. Thus, in patients with diabetes mellitus increased hANP levels which are not decreased in response to upright standing may contribute to the development of hyporeninism and its sequelae.     

Sequential responses of the renin-angiotensin-aldosterone axis to acute postural change: effect of dietary sodium.

The simultaneous levels of plasma renin activity (PRA), angiotensin II (A II), and aldosterone (PA) were frequently assessed in 13 normal subjects following acute postural change (assumption of upright posture or returning to the supine position) on low (10 mEq.) and high (200 mEq.) sodium (Na+) intakes. The rate of response of aldosterone secretion was also correlated with changes in the metabolic clearance rate (MCR) of aldosterone. Significant increments of PRA and A II on either sodium intake occurred within 5 to 20 minutes; the peak values occurred within 90 minutes and tended to plateau until the end of the study (240 minutes). The mean absolute peak levels were approximately 2 to 3.5-fold greater than control. Increments of PA were initially delayed 20 to 30 minutes, but peak levels also were achieved by 90 minutes. The secretion rate of aldosterone increased 4-fold on the 10 mEq. Na+ and 2-fold on the 200 mEq. Na+ intake even though MCR declined 30 to 40 per cent in the upright posture. Sodium restriction enhanced the rate and magnitude of response of all parameters. Specifically, the slope of the regression relationship between PRA and PA was more than 4-fold steeper in the sodium-restricted than sodium-loaded subjects. From the rate of decline in PRA following resumption of supine posture, the half-life of PRA was estimated to be 14 to 15 minutes. The present study demonstrates that acute changes in posture are associated with closely correlated changes in PRA or A II. To varying degrees, it appeared that sympathetic activity, intravascular volume, diurnal secretion, and the sodium ion play a role in the sequential responses of these parameters to acute postural alterations.     

Age, blood pressure, renin and urinary electrolytes in primary hypertension and in the normotensive state

One hundred and twenty-three patients, sixty-four men and fifty-nine women, with primary hypertension were studied with regard to supine and sitting blood pressure (BP), plasma renin activity (PRA) during basal and stimulated conditions, and urinary sodium and potassium excretions. The patients ranged in age from 20 to 76 (mean 48) years. A control material of 120 normotensive subjects, forty-nine men and seventy-one women, with an age range 22--78 (mean 47) years were studied during the same strictly standardized conditions. The two populations were compared statistically. The mean basal PRA level, measured after 1 h supine rest, was significantly higher in the hypertensive subjects, while the upright PRA, determined after ambulation for 3--4 h, was the same in the two groups. On the contrary, the stimulated mean PRA, measured 3--4 h after intake of 80 mg frusemide orally was significantly lower in the hypertensive subjects. No relationships could be demonstrated between PRA and the 24 h urinary electrolyte excretions. An age dependent decrease of upright and stimulated PRA was demonstrated only in the hypertensive population. Applying our previously published reference ranges for stimulated PRA, 16% of the hypertensive patients were considered to have low renin hypertension.     

Effects of medroxalol on renal function and the renin-angiotensin-aldosterone axis

Ten subjects with hypertension received medroxalol, which blocks both alpha- and beta-adrenergic receptors, has intrinsic sympathomimetic beta 2-agonist properties and is a direct vasodilator. Renal function tests consisting of inulin clearance and p-amino hippuric acid (PAH) clearance, plasma renin activity (PRA) in recumbent and upright postures, and aldosterone excretion rate were performed. After intravenous medroxalol, inulin clearance and PAH clearance rose, renal vascular resistance fell, recumbent PRA was unchanged, and the rise in PRA with upright posture was blunted. After 1 mo on oral medroxalol, blood pressure was controlled while inulin clearance, PAH clearance, and renal vascular resistance were unchanged. The rise in PRA with upright posture remained blunted. Urinary aldosterone excretion was unchanged after 1 mo on medroxalol.     

Effect of propranolol therapy on aldosterone responses to angiotensin II and adrenocorticotropic hormone in essential hypertension

1. The plasma aldosterone responses to exogenous angiotensin II and adrenocorticotropic hormone (ACTH) were studied before and after 1 month of propranolol therapy (120-240 mg/day) in eight patients with essential hypertension. 2. Basal supine plasma renin activity was decreased (P less than 0.001) after propranolol, whereas plasma aldosterone was unchanged. After 3 h of upright posture the increases in both plasma renin activity and aldosterone were decreased (P less than 0.05) after propranolol. 3. Plasma aldosterone responses to exogenous angiotensin II and ACTH were not significantly different after propranolol. Serum and urinary electrolytes and plasma cortisol were also unaffected by propranolol therapy. 4. It is concluded that changes in adrenal sensitivity are not responsible for maintaining unchanged supine plasma aldosterone concentrations after beta-adrenoceptor antagonism in essential hypertension.     

Effect on Plasma Aldosterone, Renin Activity and Cortisol of Acute Volume Depletion Induced by Ethacrynic Acid under Constant Infusion of Angiotensin II and Dexamethasone in Man

Abstract. The influence on plasma aldosterone of acute volume depletion induced by ethacrynic acid was studied in man. The experiments were performed during the morning in supine healthy males receiving a control infusion of 5 % glucose or an infusion of angiotensin II (All) to suppress endogenous renin production or an infusion of dexamethasone to suppress endogenous ACTH. Ethacrynic acid induced in all circumstances a similar diuresis and volume depletion. The rise of plasma renin activity (PRA) was effectively suppressed by All and the rise of plasma Cortisol by dexamethasone. Plasma aldosterone (PA) rose markedly even when the elevation of PRA or Cortisol were suppressed. Yet when both endogenous renin and ACTH secretion were blocked, PA rose much less after ethacrynic acid. This residual increase could be attributed mainly to a decrease of the metabolic clearance rate (MCR) of aldosterone which had been measured before and after ethacrynic acid administration. The data presented indicate that multiple factors influencing PA after acute volume depletion could be dissected out and that renin, ACTH and a decrease of the MCR each contribute to the elevation of PA.     

Abnormal Adrenal Responsiveness and Angiotensin II Dependency in High Renin Essential Hypertension

Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na(+)/100 meq K(+) diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+/-6 ng/ml per h) and significantly smaller plasma aldosterone increments 47 +/- 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 +/- 1 ng/ml per h; plasma aldosterone = 87 +/- 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 mug/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (-15 +/- 3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3 +/- 2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent hypertension. In these patients, the mechanism responsible for the elevated renin and blood pressure could be a compensatory increase secondary to decreased adrenal responsiveness to AII. In the remainder, the high PRA levels have little, if any, causal role in the pathogenesis of the hypertension but could reflect a marker of other pathophysiologic processes.     

Relationships between blood pressure, age, plasma renin activity and electrolyte excretion in normotensive subjects

Plasma renin activity (PRA), supine and sitting blood pressure (BP) and urinary sodium and potassium excretion were studied in 120 normotensive subjects aged 22--78 years, during strictly standardized conditions. PRA was measured after 1 h supine rest (basal PRA) after ambulation for 3--4 h (upright PRA) and after stimulation with 80 mg frusemide orally (stimulated PRA). PRA was determined with a new, simple, accurate and sensitive radioimmunoassay method. Supine and sitting systolic BP increased with age but no such correlation was found for the diastolic BP. No correlation could be shown between the BP levels and either the sodium or the potassium excretions. PRA levels increased about two-fold from basal to upright levels and about four-fold from basal levels after stimulation. No differences in mean PRA-levels were seen between males and females. We could not demonstrate any correlations between PRA-levels and 24 h sodium or potassium excretions, nor was there any relationship between age and PRA. Reference ranges are given for basal, upright and stimulated PRA in normotensive subjects. From these reference values a rational and clinically useful subdivision into low, normal and high renin groups can be made for hypertensive patients.