两种腹腔镜肾上腺切除术式治疗原发性醛固酮增多症效果评价

目的：比较腹腔镜肾上腺全切术与部分切除术治疗原发性醛固酮增多症的效果。方法：对152例原发性醛固酮增多症分别采用肾上腺全切术（A组82例）和肾上腺部分切除术（B组70例）进行治疗,测量并比较两组患者手术时间、手术失血量、住院时间以及术后一月内血压恢复者比例。结果：两组患者性别、年龄、高血压和低血钾在组间情况无统计差异,具备可比性（P〉0．05）。A组患者手术时间、术后一月内血压恢复比例高于B组（P〈0．05）,而失血量和住院时间无组间差异（P〉0．05）。结论：在腹腔镜肾上腺切除手术中,肾上腺全切取得了较好的效果,具有较高的临床应用价值。     

原发性醛固酮增多症与睡眠呼吸暂停关系的研究现状

近年来,随着筛查技术的提高,原发性醛固酮增多症的检出大大提高,并且在抵抗性高血压中的检出也比普通人群中高出很多,原发性醛固酮增多症的发病率从不到1%增加到5%-15%。研究发现,在高危险的睡眠呼吸暂停低通气综合症症状的患者中,原发性醛固酮增多症的检出高于低危险的睡眠呼吸暂停低通气综合症症状组。由此我们了解到睡眠呼吸暂停低通气综合症与原发性醛固酮增多症之间存在着某种必然的联系,其病理生理的联系,以及都可以导致继发性高血压和严重的心、脑并发症等。原发性醛固酮增多症其超生理的醛固酮或是睡眠呼吸暂停低通气综合症患者中低氧和高碳酸血症引起的醛固酮的增高都可以导致高血压及高血压的心脏,肾脏等靶器官的损害。然而,睡眠呼吸暂停低通气综合症与原发性醛固酮增多症之间的关系还不是很清楚,需要我们进一步的研究。     

分侧肾上腺静脉取血与肾上腺CT对原发性醛固酮增多症诊断的价值比较研究

摘要 目的：研究原发性醛固酮增多症（PA）患者行分侧肾上腺静脉取血（AVS）、肾上腺CT诊断的效果。方法：数据遴选本院2018年1月-2021年11月收治的70例原发性醛固酮增多症患者,所有患者均行肾上腺CT、AVS诊断,对最终诊断结果比较分析。结果：收缩压、舒张压、空腹血糖、总胆固醇在单双侧间无差异（P＞0.05）,双侧肾素活性、血清醛固酮肾素比值较单侧存在差异（P＜0.05）;肾上腺CT与AVS诊断的符合率情况：肾上腺CT显示为单侧异常、双侧异常及双侧正常患者,AVS符合率分别为65.00 %、31.25 %、50.00 %;单独肾上腺CT诊断：灵敏度为57.1 %,特异度为25.7 %,肾上腺静脉采血诊断：灵敏度为74.3 %,特异度为42.9 %;并联联合诊断灵敏度为100.0 %,特异度为26.3 %,串联诊断灵敏度为19.5 %,特异度为100.0 %。结论：PA是临床常见疾病,具有患病率高、预后差等特点,临床依靠临床表现、血液生化检查诊断PA疾病,但仅借助血液生化检验进行诊断治疗较困难,功能定位是治疗关键。实际工作中,可以临床通过CT检查及AVS检查功能定位诊断,但对于PA患者来说,仅借助肾上腺CT诊断结果制定治疗方案,可能导致手术侧选择错误,建议愿意接受肾上腺手术治疗者,推荐先行AVS,正确选择治疗方案,达到改善预后作用,效果较理想、值得临床借鉴推广。     

培哚普利联合螺内酯治疗非腺瘤型原发性醛固酮增多症的临床疗效研究

目的:研究培哚普利联合螺内酯治疗非腺瘤型原发性醛固酮增多症患者的临床效果及安全性。方法:选取在我院进行诊治的62例非腺瘤型原发性醛固酮增多症患者并将其随机分为对照组和观察组,每组31例。对照组患者在常规治疗方案的基础上给予20 mg螺内酯口服,一天3次;观察组患者在对照组的基础上加用4 mg培哚普利口服,一天1次。所有患者均治疗3个月,观察和比较两组的临床疗效,治疗前后血压、心功能、血钾、6分钟步行试验结果的变化。结果:(1)治疗后,对照组临床总有效率为74.2%(23/31),较观察组[93.5%(29/31)]显著降低(P0.05);(2)治疗后,两组患者收缩压和舒张压、LVESD(左室收缩末期内径)、LVEDD(左室舒张末期内径)均显著低于治疗前(P0.05),而LVEF(左室射血分数)、血清钾浓度、6分钟步行距离均显著高于治疗前(P0.05),且观察组患者收缩压和舒张压、LVEDD、LVESD均明显低于对照组,而LVEF、血清钾浓度、6分钟步行距离均显著高于对照组(P0.05);(3)治疗过程中,对照组患者不良反应发生率为6.5%(2/31),观察组为12.9%(4/31),两组之间比较差异无统计学意义(P0.05)。结论:培哚普利联合螺内酯治疗非腺瘤型原发性醛固酮增多症患者可显著提高其临床疗效,改善患者心功能,并有效降低血压,且安全性高。     

心脏磁共振成像诊断原发性醛固酮增多症患者左室重构价值研究

摘要 目的：探讨心脏磁共振成像（CMRI）诊断原发性醛固酮增多症（PA）患者左室重构的价值。方法：选取2017年10月-2022年12月在辽宁省金秋医院诊断为PA的患者82例作为研究组，另选取同时期内在我院就诊的原发性高血压（EH）患者82例作为对照组。对比研究组和对照组临床资料、CMRI参数、生化及激素指标水平。根据研究组患者有无左室重构分为PA且有左室重构亚组（PA1组，n=38）和PA但无左室重构亚组（PA2组，n=44），对比PA1组和PA2组患者CMRI参数。采用多因素Logistic回归分析 PA患者左室重构的因素，建立回归方程及ROC曲线评价CMRI对PA患者左室重构的诊断效能。结果：研究组患者血清K、肾素活性低于对照组，醛固酮显著高于对照组（P＜0.05）。研究组患者EDVi、ESVi、Massi、初始T1 mapping值和ECV均高于对照组，增强后T1 mapping值低于对照组（P＜0.05）。多因素Logistic回归分析结果显示，ESVi、Massi、增强后T1 mapping值、ECV均与PA患者左室重构密切关联（P＜0.05）。ROC分析结果显示，ESVi、Massi、增强后T1 mapping值、ECV各指标及其联合诊断PA患者左室重构时的AUC分别为0.623、0.677、0.736、0.675、0.779，说明联合诊断效能较高。结论：CMRI可定量评估PA患者的左室重构情况，其诊断效能较高，可为临床治疗、监测进展等提供参考依据。     

ST段抬高型心肌梗死患者血钾水平与原发性恶性室性心律失常的相关研究

目的:探讨ST段抬高型心肌梗死(STEMI)患者与冠状动脉造影阴性的对照组血钾水平以及低血钾发病率的差异;探讨STEMI患者中原发性恶性室性心律失常组和非原发性恶性室性心律失常组血钾水平的差异.方法:选取2007年1月至2009年11月间STEMI并行直接经皮冠状动脉介入术(直接PCI)患者371例,其中男303例,女68例,平均年龄(56.1±11.7)岁.同时选取冠状动脉造影阴性患者(对照组)161例,其中男性131人,女性30人,平均年龄(56.8±10.3)岁.两组基线资料无显著性差异.将血钾含量＜3.5mmol/l定义为低血钾,比较2组间血钾含量及低血钾发病率.根据直接PCI之前是否发生原发性室颤和持续性室速,将STEMI患者分为原发性恶性室性心律失常组和非原发性恶性室性心律失常组,本组数据所指原发性恶性室性心律失常仅包括直接PCI之前发生的原发性室颤和持续性室速,其中原发性室颤24例,持续性室速11例.比较2组间血钾水平.结果:血钾含量STEMI患者(3.81±0.49)低于对照者(4.03+0.41)mmol/L,差异有统计学意义(t=5.08,P＜0.001).低血钾发病率STEMI(22.6%)高于对照者(6.83%),差异有统计学意义(X2=19.13,P＜0.001).STEMI患者中原发性恶性室性心律失常组和非原发性恶性室性心律失常组的血钾水平差异无统计学意义.结论:STEMI患者急性期存在血钾的下降,我们需要积极纠正低血钾,但低血钾与原发性恶性室性心律失常有无必然联系仍需更深入的研究.     

原发性醛固酮增多症大鼠自主活动和学习记忆行为的影响

摘要 目的：探讨原发性醛固酮增多症(primary aldosteronism,PA)大鼠其自主活动和对学习记忆行为的影响。方法：8周龄健康雄SD(Sprague-Dawley)大鼠(n=30)随机分为对照组与模型组各15只。两组都皮下埋置微量渗透泵,模型组泵内灌注醛固酮,对照组泵内灌注等量的生理盐水,记录大鼠自主活动和学习记忆行为的变化情况。结果：所有大鼠均存活,模型组都造模成功,切口愈合良好。模型组造模后的收缩压高于对照组(P<0.05),也高于造模前(P<0.05),两组造模前后心率对比差异无统计学意义(P>0.05)。模型组造模后的逃避潜伏期与穿台次数少于对照组(P<0.05),也少于造模前(P<0.05)。模型组造模后的自主活动次数高于对照组(P<0.05),也高于造模前(P<0.05)。造模后模型组的鼠双微基因2(Mouse Double Microgene 2,MDM2)蛋白相对表达水平高于对照组(P<0.05)。造模后模型组的血清醛固酮含量都高对照组(P<0.05),血清钾离子、钠离子、肾素活性低于对照组(P<0.05)。结论：原发性醛固酮增多症大鼠伴随有血清钾离子、钠离子含量降低与MDM2蛋白的高表达,从而导致大鼠出现自主活动和学习记忆行为障碍。     

高原红细胞增多症患者肠道菌群变化研究

目的探究高原红细胞增多症患者肠道菌群变化及相关意义。方法招募西藏那曲地区血红蛋白(hemoglobin, HB)含量高于210 g/L的高原红细胞增多症患者12人,对照组(170 g/LHB210 g/L)42人,采集粪便、血液等样本。从中选取高原红细胞增多症患者9人,对照组16人粪便样本提取DNA,进行16S rRNA测序分析。结果高原红细胞增多症患者的血红蛋白水平以及红细胞比容显著高于对照组。红细胞增多症患者的肠道菌群整体结构改变不明显,多样性没有显著差异。红细胞增多症患者的粪便菌群出现厚壁菌门中梭状芽胞杆菌BB60属、纺锤链杆菌属、厌氧棒杆菌属、霍氏真杆菌,变形菌门中假单胞菌属,拟杆菌门中副拟杆菌属丰度的显著增高。这些菌属改变经KEGG预测分析显示与代谢紊乱相关。斯皮尔曼分析显示多种菌群改变与血红蛋白水平以及红细胞比容正相关。结论高原红细胞增多症患者肠道菌群出现紊乱,菌群变化与代谢紊乱和红细胞增多相关。     

血S100B蛋白和尿乳酸/肌酐比值对门静脉高压症术后肝性脑病发生的早期预测价值

目的评价血S100B蛋白和尿乳酸/肌酐对乙肝肝硬化门脉高压症术后肝性脑病发生的早期预测价值。方法回顾性分析65例乙肝肝硬化门脉高压症患者的临床资料,动态检测术后24、48和72h的血S100B蛋白和尿乳酸/肌酐比值水平,根据是否发生术后肝性脑病将受试者分为肝性脑病组与非肝性脑病组,并对肝性脑病组患者进行临床分度。结果乙肝肝硬化门脉高压症患者术后发生肝性脑病组72h内血S100B蛋白含量和24 h内尿乳酸/肌酐比值水平明显高于非肝性脑病组(P<0.001);72h内血S100B蛋白含量和24 h内尿乳酸/肌酐比值之间及与肝性脑病的临床分度呈正相关(P<0.001);当血S100B水平在28ng/L,尿乳酸/肌酐比值在0.47时,单独检测72h血S100B蛋白的敏感度、特异度分别为91.2%、93.6%;尿乳酸/肌酐比值预测肝性脑病的敏感度和特异性度以术后24h最高,分别为89.3%和91.7%;如检测72h血S100B蛋白的同时监测术后24h尿乳酸/肌酐比值可显著提高肝性脑病诊断的准确性,联合应用两项指标进行检测,诊断的敏感度和特异度分别为95.7%和98.6%,较两种方法单独应用敏感度和特异度均提高。结论对门静脉高压症患者术后以临床表现为基础,同时监测72h内血S100B蛋白和24h尿乳酸/肌酐比值,对提高术后肝性脑病的早期诊断和临床分度具有一定应用价值。     

维持性血液透析患者高钾血症的相关因素分析及环硅酸锆钠散辅助干预效果研究

摘要 目的：分析维持性血液透析（MHD）患者高钾血症的相关因素,并观察环硅酸锆钠散辅助干预效果。方法：纳入我院2020年3月~2022年3月期间收治的MHD患者134例,通过本院病历系统收集患者资料,以是否出现高钾血症作为分组标准：分为血钾正常组（n=49）和高钾血症组（n=85）,多因素Logistic回归分析MHD患者发生高钾血症的相关因素。采用随机数字表法将高钾血症组患者分为对照组（接受MHD治疗）和观察组（MHD治疗基础上接受环硅酸锆钠散干预,比较两组高钾血症干预前后相关指标和不良反应发生情况。结果：134例MHD患者中血钾正常49例（36.57%）纳入血钾正常组,高钾血症85例（63.43%）纳入高钾血症组。单因素分析结果显示,MHD患者高钾血症与甲状旁腺激素（PTH）、合并糖尿病、既往高钾血症史、透析前血钾检验次数、超滤量、血流量、血红蛋白（Hb）、超敏C反应蛋白（hs-CRP）、尿素、尿酸、血肌酐、血钠、白蛋白、血磷有关（P<0.05）。多因素Logistic回归分析结果显示：尿素偏高、血钠偏高、血磷偏高、白蛋白偏高、Hb偏高、合并糖尿病、透析前血钾检验次数偏少是MHD患者高钾血症发生的危险因素（P<0.05）。对照组与观察组干预后血钾均降低,且观察组低于对照组（P<0.05）。对照组、观察组不良反应发生率组间对比无统计学差异（P>0.05）。结论：MHD患者高钾血症的相关因素主要有尿素、血钠、血磷、白蛋白、Hb、合并糖尿病、透析前血钾检验次数。应用环硅酸锆钠散辅助干预高钾血症患者,可有效改善其血钾水平,安全有效。     

The PI3K/AKT/mTOR Signaling Pathway Is Overactivated in Primary Aldosteronism

Background

To date, the available non-invasive remedies for primary aldosteronism are not satisfactory in clinical practice. The phosphoinositide 3-kinase (PI3Ks)/protein kinase B (PKB or AKT)/mammalian target of rapamycin (mTOR) signaling pathway is essential for tumorigenesis and metastasis in many types of human tumors, including renal cancer, adrenal carcinoma and pheochromocytoma. The possibility that this pathway is also necessary for the pathogenesis of primary aldosteronism has not yet been explored. To answer this question, we investigated the activity of the PI3K/AKT/mTOR signaling pathway in normal adrenal glands (NAGs), primary aldosteronism (PA) patients and NCI-H295R cells.

Methodology/Principal Findings

Between January 2005 and December 2011, we retrospectively reviewed the records of 45 patients with PA. We compared clinical characteristics (age, gender and biochemical data) and the expression of phospho-AKT (p-AKT), phospho-mTOR (p-mTOR), phospho-S6 (p-S6) and vascular endothelial growth factor (VEGF) by immunohistochemical staining and western blotting, analyzing 30 aldosterone-producing adenomas (APAs), 15 idiopathic hyperaldosteronism (IHA) tissues and 12 NAGs following nephrectomy for renal tumors (control group). Compared with the control group, most of the PA patients presented with polydipsia, polyuria, resistant hypertension, profound hypokalemia, hyperaldosteronemia and decreased plasma renin activity. Compared with normal zona glomerulosa, the levels of p-AKT, p-mTOR, p-S6 and VEGF were significantly upregulated in APA and IHA. No significant differences were found between APA and IHA in the expression of these proteins. Additionally, positive correlations existed between the plasma aldosterone levels and the expression of p-AKT and p-mTOR. In vitro studies showed that mTOR inhibitor rapamycin could inhibit cell proliferation in NCI-H295R cells in a dose- and time-dependent manner. Furthermore, this inhibitor also decreased aldosterone secretion.

Conclusions

Our data suggest that the PI3K/AKT/mTOR signaling pathway, which was overactivated in APA and IHA compared with normal zona glomerulosa, may mediate aldosterone hypersecretion and participate in the development of PA.     

Clinical characteristics of primary hyperaldosteronism due to adrenal microadenoma

An increasing number of patients are being diagnosed with primary aldosteronism (PA) due to aldosterone-producing macroadenoma (APA). However, there are only limited data available on the clinical characteristics of PA that are associated with adrenal microadenoma. Of the 55 patients that were diagnosed with PA in our study, 22 patients showed a unilateral adrenal over-production of aldosterone. The histopathology of the surgically removed adrenal tissues led to six patients being diagnosed with microadenoma, and the clinical features of microadenoma, macroadenoma and idiopathic hyperaldosteronism (IHA) were studied. The expression levels of CYP11B2, CYP17, CYP21 and 3β-hydroxysteroid dehydrogenase 2 (HSD3B2) mRNA in the adrenal cortices (n = 5 and 6, respectively) that remained attached to the adrenal microadenomas or macroadenomas were examined by real time-PCR and then compared to the expression levels in the adrenal cortices (n = 5) of non-functioning adrenal adenomas (NF). The patients with microadenoma (n = 6) had significantly higher diastolic blood pressure than the patients with macroadenoma (n = 16) or IHA (n = 33) (p < 0.05). The systolic blood pressure, plasma aldosterone concentration, serum potassium level and renal function did not differ between the PA sub-groups. The levels of CYP11B2 and CYP17 mRNA were significantly increased in the adjacent tissues of microadenomas, as compared with macroadenomas or NF (p < 0.05), whereas no significant differences in the CYP21 and HSD3B2 mRNA levels were found between the PA sub-groups. The tumor size did not influence the clinical characteristics of APA. The non-tumor portions of the microadenomas showed marked and sustained CYP11B2 mRNA expression under the suppressed renin-angiotensin system. We suggest that an increased number of microadenomas should be sampled, and the immunohistochemistry for steoridogenic enzymes should be investigated to clarify the etiology of microadenoma.     

Hydrochlorothiazide-amiloride versus hydrochlorothiazide alone for essential hypertension: effects on blood pressure and serum potassium level

In a double-blind randomized controlled trial the effects on the blood pressure and the serum potassium concentration of hydrochlorothiazide-amiloride hydrochloride (Moduret) and hydrochlorothiazide alone were compared in 266 adults who were normokalemic and had a diastolic blood pressure greater than 95 mm Hg at the time of entry into the study. The mean ages (52.2 and 53.8 years) and the proportions of men (66% and 56%) in the groups given the combination drug and hydrochlorothiazide alone respectively were similar. In the group given the combination drug the mean blood pressure, measured while the patients were supine, and the mean serum potassium level fell significantly, from 156/99 to 138/88 mm Hg and from 4.23 to 3.91 mmol/L, after 8 weeks of treatment. In the other group both measures also fell significantly, the blood pressure from 157/99 to 138/87 mm Hg and the potassium level from 4.16 to 3.69 mmol/L. The proportions of patients in the two groups with hypokalemia (14% and 29% respectively), defined as a serum potassium level below 3.5 mmol/L, differed significantly (p = 0.0026), whereas the proportions with a potassium level exceeding 4.5 mmol/L (4.5% and 3.9% respectively) were similar. Thus, the combination drug reduced the blood pressure to the same extent as hydrochlorothiazide alone but significantly less often caused hypokalemia. In light of growing concerns about the cardiovascular complications of hypokalemia, hydrochlorothiazide-amiloride appears preferable to hydrochlorothiazide alone for the treatment of some patients with hypertension.     

Regulations of plasma aldosterone in young hyperkalemic patients with stable chronic renal failure.

In a group of four young patients with stable chronic renal failure and hyperkalemia sodium restriction induced a remarkable increase in plasma renin activity (PRA) and plasma aldosterone (PA), a decrease in the elevated serum potassium (SK) and a rise in potassium excretion. During high sodium intake the levels of PRA and PA were lower than those found in the healthy control group suggesting that enhanced suppressibility of the renin-angiotensin-aldosterone system (RAAS) was the main cause of hyperkalemia. During sodium restriction despite a marked increase in PRA and PA levels poor correlations were found between these variables indicating disorganisation within the RAAS and probably a diminished role for renin-angiotensin in the regulation of aldosterone production in three hyperkalemic patients with chronic glomerulonephritis. On the other hand, in the same patients significant correlations were found between fluctuations of SK and PA on constant normal and low sodium diets supporting the concept of an (at least) equal role of potassium and RAAS in the acute regulation of PA. A prominent role for SK was found in an unusual hyperkalemic patient with interstitial nephritis when PRA was suppressed and the elevated SK showed a definite postural rise inducing dramatic increases in PA in the upright posture. Reversion of the postural SK rise masked again the governing role of SK.     

Fecal and salivary electrolytes in the diagnosis of primary aldosteronism

Fecal and salivary sodium and potassium concentrations were measured in 22 hypertensive patients with hypokalemia who were undergoing investigation for primary aldosteronism due to an adrenocortical adenoma (Conn''s syndrome). Of eight patients with a high aldosterone secretion rate, five had clearly low fecal Na/K ratios, (including all four patients with Conn''s syndrome), in three the ratios were equivocal. Of 14 patients with hypertension and a normal aldosterone secretion rate, none had a sufficiently low fecal Na/K ratio strongly to suggest hyperaldosteronism, although two were borderline. Salivary electrolyte concentrations were not as consistent an indicator of mineralocorticoid hormone excess. Estimation of fecal sodium and potassium concentrations may be useful in the diagnosis of mineralocorticoid hormone excess and in assessing the results of therapy.     

Mineralocorticoid Receptor Antagonists Decrease the Rates of Positive Screening for Primary Aldosteronism

Objective: Mineralocorticoid receptor antagonists (MRAs) are effective in patients with resistant hypertension and/or primary aldosteronism (PA). Screening for PA should ideally be conducted after stopping medications that might interfere with the renin-angiotensin-aldosterone system, but this is challenging in patients with recalcitrant hypertension or hypokalemia. Herein, we aimed to evaluate the impact of MRAs on PA screening in clinical practice.Methods: We conducted a retrospective cohort study of patients with hypertension who had plasma aldosterone and renin measurements before and after MRA use in a tertiary referral center, over 19 years.Results: A total of 146 patients, 91 with PA, were included and followed for up to 18 months. Overall, both plasma renin and aldosterone increased after MRA initiation (from median, interquartile range: 0.5 [0.1, 0.8] to 1.2 [0.6, 4.8] ng/mL/hour and from 19.1 [12.9, 27.7] to 26.4 [17.1, 42.3] ng/dL, respectively; P<.0001 for both), while the aldosterone/renin ratio (ARR) decreased from 40.3 (18.5, 102.7) to 23.1 (8.6, 58.7) ng/dL per ng/mL/hour (P<.0001). Similar changes occurred irrespective of the MRA treatment duration and other antihypertensives used. Positive PA screening abrogation after MRA initiation was found in 45/94 (48%) patients. Conversely, 17% of patients had positive PA screening only after MRA treatment, mostly due to correction of hypokalemia. An initially positive screening test was more likely altered by high MRA doses and more likely persistent in patients with confirmed PA or taking beta-blockers.Conclusion: MRAs commonly reduce ARR and the proportion of positive PA screening results. When PA is suspected, screening should be repeated off MRAs.Abbreviations: ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; ARR = aldosterone/renin ratio; DRC = direct renin concentration; MRA = mineralocorticoid receptor antagonist; PA = primary aldosteronism; PAC = plasma aldosterone concentration; PRA = plasma renin activity; RAAS = renin-angiotensin-aldosterone system     

Comparison of 24-h Urinary Aldosterone Level and Random Urinary Aldosterone-to-Creatinine Ratio in the Diagnosis of Primary Aldosteronism

Background

Historically, urinary aldosterone level measurement was a commonly employed confirmatory test to detect primary aldosteronism (PA). However, 24-h urine collection is inconvenient and cumbersome. We hypothesized that random urinary aldosterone measurements with correction for creatinine concentration might be comparable to 24-h urinary aldosterone levels (Uald-24 h) in the diagnosis of PA.

Methods

The non-concurrent prospective study was conducted between June 2006 and March 2008 in patients admitted for confirmation of aldosteronism by salt loading test. A 24-h urine sample, which was collected during hospitalization on the day before saline infusion testing after restoration of serum hypokalemia, was collected from all subjects. Moreover, participants were asked to collect a first bladder voiding random urine sample during clinic visits. Uald-24 h and the random urinary aldosterone-to-creatinine ratio (UACR) were calculated accordingly.

Results

A total of 102 PA patients (71 patients diagnosed of aldosterone-producing adenoma, 31 with idiopathic hyperaldosteronism) and 65 patients with EH were enrolled. The receiver operating characteristic curve showed comparable areas under the curves of UACR and Uald-24 h. The Bland-Altman plot showed mean bias but no obvious heteroscedasticity between the two tests. When using random UACR >3.0 ng/mg creatinine as the cutoff value, we obtained a specificity of 90.6% to confirm PA from essential hypertension.

Conclusions

Our study reinforce that the diagnostic accuracy of random UACR was comparable to that of Uald-24 h in PA patients. With the quickness and simplicity of the UACR method and its equivalence to Uald-24 h, this assay could be a good alternative diagnostic tool for PA confirmation.     

Prevalence,Subtype Classification,and Outcomes of Treatment of Primary Aldosteronism: A Prospective Study in China

ObjectiveTo investigate the prevalence of primary aldosteronism (PA) among participants with hypertension, evaluate the concordance of PA classification between adrenal computed tomography and adrenal venous sampling, and compare the outcomes of surgery and medication for unilateral PA.MethodsA prospective study was conducted among all inpatients with hypertension (n = 7594) at the National Center for Cardiovascular Diseases, China, from May 2016 to April 2018.ResultsOf the 7594 participants, 8.12% (n = 617) with plasma aldosterone-renin ratio ≥3.7 were possible PA cases. Three hundred sixty-seven cases with plasma aldosterone-renin ratio ≥3.7 and plasma aldosterone concentration ≥10 ng/dL were confirmed using the recumbent saline infusion test (69.20%, 182 of 263) or the captopril challenge test (66.5%, 69 of 104, P > .05). The prevalence of PA was 3.31% (n = 251). Of the 251 patients with PA, all of them had multiple comorbidities, and 49.40% (n = 124) had spontaneous hypokalemia. The concordance of PA classification between adrenal computed tomography and adrenal venous sampling was only 47.11%. The patients’ blood pressure declined to normal ranges in the adrenalectomy (85.71%, 30 of 35) and spironolactone (63.04%; 29 of 46) groups (P < .05). Furthermore, hypokalemia was normalized in the adrenalectomy (100.00%; 26 of 26) and spironolactone (94.74%; 18 of 19) groups.ConclusionIt is necessary to incorporate PA screening into routine practice for those with hypertension in the Chinese population. This will assist in ensuring that the best therapeutic schedule based on PA subtypes is devised. Additionally, as a result, it may contribute to restoring the blood pressure levels and reducing the prevalence of comorbidities in these patients with PA.     

Renin-dependency of glycyrrhizin-induced pseudoaldosteronism

A prospective study was carried out on 12 patients with chronic hepatitis who were taking 546 mg/day of glycyrrhizin for 4 weeks in order to identify the factors responsible for the development of hypertension and hypokalemia. In 5 patients, blood pressure increased and serum potassium decreased after the treatment (responders). In the remaining 7 patients, these values were unchanged (nonresponders). There were no significant differences in age, plasma aldosterone, the catecholamine concentrations or serum transaminases. The basal plasma renin activity (PRA) in the responders was more than 1.5 ng/m/h (2.5 +/- 0.3 ng/m/h), while that in the non-responders was less than 1.5 ng/m/h (0.7 +/- 0.1 ng/ml/h). Furthermore, a positive correlation between the basal RPA and the changes in blood pressure, and a negative correlation between the basal PRA and the changes in potassium were found. These results suggest that patients with higher PRA levels are more likely to develop hypertension and hypokalemia when treated with glycrrhizin.     

Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.