高血压并发低血钾与肾上腺疾病15例临床分析

目的:总结我院15例高血压并低血钾患者的临床表现与诊治结果,提高继发性高血压的诊疗水平。方法:对15例患者的临床表现、激素水平、CT定位诊断及术后病理进行回顾分析。结果:15例患者中原发性醛固酮增多症13例(醛固酮瘤11例、双侧肾上腺增生2例),腺瘤型皮质醇增多症2例。结论:顽固性高血压并发低血钾应高度怀疑肾上腺疾病,诊断依靠临床表现及内分泌功能测定,定位诊断依靠CT,腺瘤型手术效果好。     

单侧性原发性醛固酮增多症的预测模型建立及价值评估

原发性醛固酮增多症(PA)是继发性高血压常见的病因之一, 其病因分型诊断的金标准为肾上腺静脉采血(AVS)。本文回顾性分析了2018年7月至2021年8月在南京鼓楼医院内分泌科诊断为PA并行AVS或单侧肾上腺切除手术患者的数据, 通过多元logistic回归分析确定了与单侧醛固酮优势分泌相关的因素, 并基于这些因素建立了诊断单侧原发性醛固酮增多症(UPA)的预测模型:年龄<40岁, 血浆醛固酮浓度(PAC)>15 ng/dL, 肾上腺CT示单侧典型腺瘤, 自发性低钾血症。该预测模型可使14%的PA患者避免非必要的AVS。     

406例原发性醛固酮增多症患者手术预后及影响因素分析

目的评估单侧原发性醛固酮增多症(简称原醛症)术后生化和临床缓解率, 分析相关影响因素。方法回顾性纳入2013年11月至2022年3月在重庆医科大学附属第一医院内分泌科明确分型并接受肾上腺切除术且完成随访的406例原醛症患者, 记录基线和术后的临床资料及生化指标。根据原发性醛固酮增多症手术预后(Primary Aldosteronism Surgical Outcome, PASO)标准进行临床和生化疗效评估。采用多因素logistic回归分析评估影响原醛症术后临床缓解的主要因素。结果 406例原醛症患者术后的生化完全缓解率为96.31%(391/406), 生化部分缓解率为0.99%(4/406), 生化未缓解率为2.71%(11/406);临床完全缓解率为53.45%(217/406), 临床部分缓解率为46.55%(189/406)。相比于临床部分缓解组, 临床完全缓解组年龄较小, 女性占比更大, 体重指数较低, 高血压病程更短, 降压药的限定日剂量更低, 估算的肾小球滤过率(eGFR)更高, 高血压家族史和糖尿病病史所占比例较低。多因素logistic回归分析进一步显示, 性别(...     

原发性醛固酮增多症诊断与治疗的新进展

原发性醛固酮增多症（primary aldosteronism．PA）,属于继发性高血压范畴,是一组由于醛固酮不恰当的自主性高分泌而引起的疾病。过多的醛固酮导致血压升高、心血管损害、肾素抑制、钠潴留和钾排出增多。PA主要的两种病理类型为肾上腺醛固酮腺瘤和肾上腺增生。目前PA的具体发病机制不明确,有研究发现肾上腺醛固酮腺瘤中醛固酮合成酶（CYP11B2）的RNA表达增加。     

原发性醛固酮增多症慢性肾损伤的研究进展

<正>原发性醛固酮增多症(primary aldosteronism)是指醛固酮的过量产生,以往被认为是罕见疾病。随着诊断方法的进步,原发性醛固酮增多症已被确定为继发性高血压的最常见原因。高血压患者中原发性醛固酮增多症患病率为5%～10%,在难治性高血压患者中患病率甚至更高^[1-2]。醛固酮过量会导致许多问题,包括高血压、电解质失衡以及结构和功能性靶器官变化^[3]。早在20世纪五六十年代就有学者研究醛固酮与肾脏之间的关系。后来,动物实验和临床研究表明,醛固酮水平升高与肾脏疾病的进展有关,甚至有研究发现醛固酮水平与肾小球滤过率呈负相关。     

肾上腺疾病性高血压

肾上腺疾病是继发性高血压的重要病因,大部分肾上腺疾病性高血压可通过服用药物准备后行手术治疗,使高血压获得好转或治愈,因此正确认识及治疗肾上腺疾病性高血压有重要意义。嗜铬细胞瘤和原发性醛固酮增多症为较常见的肾上腺疾病性高血压,其患病率在近年来有上升趋势,本文对这两种疾病的临床表现、实验室检查、定性、定位诊断、治疗及预后进行了较详细的综合介绍。     

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目的评价原发性醛固酮增多症(PA)诊断中多项临床试验方法的作用。方法收集1995～2000年上海第二医科大学附属瑞金医院104例PA患者的临床资料,统计分析生化检查、体位激发试验、影像学检查与肾上腺静脉插管在诊断中的阳性率及符合率。结果(1)血醛固酮升高为筛选PA阳性率最高的检测指标。(2)醛固酮腺瘤患者生化异常较明显。(3)与手术病理比较,B超在醛固酮腺瘤和双侧肾上腺增生中的诊断符合率分为95.77%及73.33%;CT为98.51%及31.03%;体位激发试验以升幅30%为标准时在醛固酮腺瘤和双侧肾上腺增生中的符合率分别为61.11%及57.14%,以50%为标准时为72.22%及42.86%;肾上腺静脉插管的符合率为83.33%及100%。结论PA的诊断中,典型患者经血钾、血尿醛固酮及血浆肾素活性等筛查可明确诊断,但部分患者上述生化改变并不典型。体位激发试验结果在醛固酮腺瘤及双侧肾上腺增生中有部分重叠。影像学未能发现明显占位灶者可行肾上腺静脉插管检查。     

肾上腺醛固酮瘤术后持续高血压的多因素分析

目的 探讨肾上腺醛固酮瘤患者术后血压的变化和影响术后血压恢复的相关因素。方法 收集上海交通大学医学院附属瑞金医院2000-2005年行手术治疗的76例醛固酮瘤患者，分为术后血压正常组和术后高血压组，分析比较2组间术前、术后的临床资料；用Logistic回归分析各项指标在预测术后血压方面的作用。结果 60．5％患者术后血压恢复正常；39．5％仍有持续高血压，但血压较术前明显改善。术后高血压组的患者年龄大，高血压病程长，有高血压家族史者较多，血肌酐、尿素氮和内生肌酐清除率等反映肾功能的指标，在2组间差异均有显著性。结论 醛固酮瘤患者高血压病程较长，术前肾损害较严重者，术后持续高血压的可能性较大，提示这类患者应该早期诊治。     

肾上腺醛固酮瘤术后持续高血压的多因素分析

目的探讨肾上腺醛固酮瘤患者术后血压的变化和影响术后血压恢复的相关因素。方法收集上海交通大学医学院附属瑞金医院2000—2005年行手术治疗的76例醛固酮瘤患者,分为术后血压正常组和术后高血压组,分析比较2组间术前、术后的临床资料;用Logistic回归分析各项指标在预测术后血压方面的作用。结果60.5%患者术后血压恢复正常;39.5%仍有持续高血压,但血压较术前明显改善。术后高血压组的患者年龄大,高血压病程长,有高血压家族史者较多,血肌酐、尿素氮和内生肌酐清除率等反映肾功能的指标,在2组间差异均有显著性。结论醛固酮瘤患者高血压病程较长,术前肾损害较严重者,术后持续高血压的可能性较大,提示这类患者应该早期诊治。     

醛固酮瘤260例临床分析

目的 提高醛固酮瘤的诊治水平。方法 回顾性分析郑州大学第一附属医院1986-2005年所有病理诊断为醛固酮瘤的260例患者的临床资料。结果 左侧肾上腺腺瘤132例，右侧119例，双侧5例，多发腺瘤4例。260例患者均有高血压症状。生化检查中，低血钾206例，糖耐量减低26例。血浆肾素、血管紧张素、醛固酮测定中，207例高醛固酮伴低肾素，19例高醛固酮伴高肾素。182例患者行体位激发试验，93例患者直立位时醛固酮水平较卧位时降低，89例醛固酮升高。260例患者均经手术治疗。术后血压恢复正常236例，其余24例患者血压较术前下降。结论 完善检查手段可提高醛固酮瘤的检出率，确诊需病理检查，手术是根本的治疗方法。     

Progression of chronic kidney disease: can it be prevented or arrested?

Chronic kidney disease constitutes a highly prevalent health problem worldwide. Left untreated, it progresses inexorably to greater levels of severity at variable rates. The morbid impact of chronic kidney disease is heightened by its role as risk factor for cardiovascular disease. In the past two decades, considerable gains have been realized in retarding progression of chronic kidney disease by emphasizing blood pressure control and blockade of the renin-angiotensin system. Notwithstanding, the therapeutic goal of preventing or arresting chronic kidney disease progression remains unfulfilled. Currently attainable rates of decrease in glomerular filtration rate remain at 2 to 8 mL/min/y depending on the underlying disease. It is now believed that to achieve optimal therapeutic targets (proteinuria of <500 mg/day and decrease in glomerular filtration rate of 1 mL/min/y, the average age-related decline) we must introduce novel strategies and a multifaceted approach to treatment that interrupts multiple mechanisms of progression. To this end, and wherever relevant, new approaches to cause-specific treatment must be applied, such as targeted immunosuppression, intensive glycemic control, gene therapy, and enzyme replacement therapy. Furthermore, in all chronic kidney disease, we must interfere more effectively with the multitude of common mechanisms of progression. Established or putative, such approaches include aggressive blood pressure control; advanced renin-angiotensin system blockade; cytokine modulation and antifibrotic therapy; aldosterone blockade; endothelin blockade, nitric oxide modulation and vasopeptidase inhibition; antioxidant therapy; statin therapy; glycosaminoglycan therapy; anemia therapy; dietary restrictions; lifestyle changes; and pharmacogenomic profiling. Such a concerted, multifaceted approach to management might indeed prevent or arrest progression of chronic kidney disease, or even achieve regression of chronic kidney disease.     

Niere und Hypertonie

In patients with chronic kidney disease elevated blood pressure is a common finding, but primary hypertension can also damage healthy kidneys. Renal outcome is strictly dependent on blood pressure, no matter whether the kidneys are cause or consequence of hypertension. Furthermore, hypertension and kidney disease are strong cardiovascular risk factors. In every patient diagnosed with hypertension glomerular filtration rate has to be checked. Proteinuria and structural abnormalities of the kidneys should be ruled out. Patients with a decreased glomerular filtration rate, proteinuria or pathologic ultrasound should be seen by a nephrologist. A strict antihypertensive therapy (blood pressure <130/80 mmHg) can substantially improve the prognosis of hypertensive renal patients. In patients with kidney damage, inhibitors of the renin-angiotensin-system are preferred. To avoid adverse events a close monitoring of antihypertensive therapy is warranted.     

Primary aldosteronism: diagnosis and treatment

Recent studies have indicated a higher prevalence of primary aldosteronism (PA) than reported historically. Aldosterone excess induces sodium and fluid retention with consequential increases in blood pressure. Patients with PA are at an increased risk of developing left ventricular hypertrophy, chronic kidney disease, and endothelial dysfunction. Measurement of the plasma aldosterone/plasma renin activity ratio is an effective screening test for PA. The majority of patients with PA do not have a discernable aldosterone-producing adenoma (APA), and the aldosterone excess is considered idiopathic in etiology and/or attributed to adrenal hyperplasia. Treatment of PA includes medical therapy with mineralocorticoid receptor antagonists and adrenalectomy for patients with a unilateral APA. A reasonable treatment strategy is to attempt medical therapy in all patients with a high plasma aldosterone/PRA ratio and reserve the extensive workup needed to identify an APA for those patients whose hypertension or hypokalemia cannot be controlled medically.     

Blood pressure outcome of adrenalectomy in patients with primary hyperaldosteronism with or without unilateral adenoma

OBJECTIVE: To assess blood pressure outcome in patients with primary aldosteronism, who were operated on the basis of a unilateral adenoma detected by computed tomography or a lateralized aldosterone hypersecretion detected by adrenal venous sampling, and to analyze the hormonal and nonhormonal factors associated with the outcome. METHODS: A retrospective study of 168 patients with primary aldosteronism undergoing surgery: 109 patients with a unilateral adenoma detected by computed tomography and 59 without a unilateral adenoma who underwent surgery because of an aldosterone to cortisol ratio at least five times higher on the dominant side than on the nondominant side. RESULTS: Patients with a unilateral adenoma were more likely to be women, had a shorter history of hypertension and had lower blood pressure levels and treatment scores than patients without a unilateral adenoma. The mean systolic blood pressures of patients with and without unilateral adenomas at follow-up were 133 +/- 16 and 137 +/- 16 mmHg, respectively. Hypertension cure or improvement was observed in 77% (95% confidence interval 69-85%) and 68% (95% confidence interval 56-80%) of patients, respectively. Using a linear regression model, baseline urinary aldosterone was positively associated, and baseline serum potassium was negatively associated, with decrease in systolic blood pressure. CONCLUSION: Adrenalectomy improves blood pressure control in patients with primary aldosteronism operated on the basis of either unilateral adenoma detected by computed tomography or a lateralized aldosterone hypersecretion. A high urinary aldosterone excretion and a low serum potassium level predict a more favorable outcome of surgery.     

Aldosterone in the Pathogenesis of Chronic Kidney Disease and Proteinuria

There has been much recent interest in the role of aldosterone as an independent contributor to the progression of chronic kidney disease. Despite treatment with agents such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, many studies have shown that there is incomplete blockade of the renin-angiotensin cascade evidenced by persistent or rising plasma aldosterone levels despite therapeutic renin-angiotensin blockade. This phenomenon is commonly referred to as “aldosterone escape” and is thought to be one of the main contributors to chronic kidney disease progression despite conventional therapeutics. Animal models of the effects of exposure to exogenous aldosterone demonstrate the development of inflammation and fibrosis in both the myocardium and renal parenchyma. In limited human studies, aldosterone receptor antagonism is associated with decreased proteinuria and improved glomerular filtration rate. Although data support the addition of an aldosterone antagonist to conventional therapy when treating patients with chronic kidney disease, more studies are needed to determine the precise clinical indications and the appropriate safety monitoring.     

Use of the converting enzyme inhibitor enalapril in renovascular hypertension. Effect on blood pressure, renal function, and the renin-angiotensin-aldosterone system

Thirteen patients were entered into a protocol to assess the safety and efficacy of enalapril (MK 421), 5 to 20 mg b.i.d., and hydrochlorothiazide, 50 to 100 mg daily, for the treatment of renovascular hypertension. Specifically monitored were the effects of therapy on blood pressure and pulse, renal function, and the renin-angiotensin-aldosterone axis. Enalapril and hydrochlorothiazide therapy produced excellent control of blood pressure with no adverse side effects. After approximately 8 weeks of therapy, renal vascular resistance was decreased and no adverse effects on glomerular filtration rate or renal blood flow were noted, except in one patient with a functional unilateral stenotic kidney. Patients receiving enalapril and hydrochlorothiazide showed stimulation of plasma renin activity and suppression of plasma angiotensin II, although the initial degree of suppression was not sustained in all patients during prolonged therapy. Although plasma aldosterone concentration was initially suppressed, the degree of suppression was not sustained. Nine patients have been followed for an additional 6 months; none have experienced further progression of renal disease, as assessed by repeated measurements of glomerular filtration and effective renal plasma flow. These results suggest that combined enalapril and hydrochlorothiazide therapy is safe and effective in the medical management of renovascular hypertension and that blood pressure control may be achieved in the absence of sustained interruption of the renin-angiotensin-aldosterone system.     

Bilateral adrenal tumours in primary aldosteronism: localization of a unilateral aldosteronoma by dexamethasone suppression scan

In a patient with primary aldosteronism, in which the postural endocrine tests suggested the presence of an aldosteronoma rather than hyperplasia, bilateral adrenal tumours were found by computer tomography. Adrenal scintigraphy using 6-131I-iodomethyl-19-norcholesterol (NP59) during dexamethasone suppression showed early unilateral adrenal visualization on the left side. After removal of the left adrenal gland, which contained a 2 x 2 x 2 cm adenoma, the blood pressure and aldosterone levels returned to normal. A CT-scan, performed 1 year after the pre-operative CT-scan, showed no change in size of the right adrenal tumour, consistent with a non-functioning adenoma. In this patient, the NP59 scan adequately distinguished a non-functioning from an aldosterone-producing adrenal tumour.     

Visit‐to‐Visit Variability of Blood Pressure and Renal Function Decline in Patients With Diabetic Chronic Kidney Disease

The authors previously reported that the visit‐to‐visit variability of blood pressure is correlated with renal function decline in nondiabetic chronic kidney disease. Little is known about the association between visit‐to‐visit variability and renal function decline in patients with diabetic chronic kidney disease. The authors retrospectively studied 69 patients with diabetic chronic kidney disease stage 3a, 3b, or 4. The standard deviation and coefficient of variation of blood pressure in 12 consecutive visits were defined as visit‐to‐visit variability of blood pressure. The median observation period was 32 months. In univariate correlation, the standard deviation and coefficient of variation of blood pressure were not significantly associated with the slope of estimated glomerular filtration rate. There was no significant association between the visit‐to‐visit variability of blood pressure and renal function decline in patients with diabetic chronic kidney disease, in contrast with our previous study of nondiabetic patients with chronic kidney disease.     

FALSE LOCALIZATION OF AN ALDOSTERONOMA BY DEXAMETHASONE-SUPPRESSED ADRENAL SCINTIGRAPHY

A patient with primary aldosteronism had bilateral adrenal tumours on computed tomography. Selenocholesterol scintigraphy showed uptake by the larger right adrenal gland and a tumour in the gland was also visualized by venography. In contrast, measurements of aldosterone concentrations in adrenal venous blood lateralized to the left side. At surgery the left adrenal gland contained an aldosteronoma and the right adrenal gland a large non-functioning adenoma. Thus, selenocholesterol scintigraphy incorrectly localized the functioning adrenal tumour.     

Molecular Mechanisms Involved in Intrarenal Renin-Angiotensin and Alternative Pathways in Diabetic Nephropathy - A Review

Uncontrolled or chronic hyperglycemia causes kidney failure induced by the dysfunction of biomolecules and upregulation of inflammatory cytokines and growth factors. The reninangiotensin system (RAS) is incorporated in the regulation of renal hemodynamics. In a healthy state, local RAS is independent of systemic RAS. However, in pathological conditions such as chronic hyperglycemia, angiotensin II (Ang II) increases locally and causes tissue damage, mainly through the induction of oxidative stress, inflammation, and upregulation of some growth factors and their receptors. Such tissue events may cause disruption of the glomerular filtration barrier, thickening and hypertrophy of the glomerular basement membrane, microvascular hyperpermeability, proteinuria, and finally decrease in the glomerular filtration rate (GFR). Reduced GFR causes the kidney to sense falsely a low blood pressure condition and respond to it by stimulating systemic and local RAS. Therefore, patients with diabetic nephropathy (DN) suffer from chronic hypertension. In contrast to local RAS, there are alternative pathways in the kidney that act protectively by reducing tissue Ang II. Such autoregulatory and protective mechanisms are weakened in chronic kidney disease. Previously, it was presumed that systemic RAS inhibitors such as ACE inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) could prevent renal damage by controlling blood pressure and proteinuria. However, the progression of renal failure to end-stage renal disease (ESRD), despite such treatments, indicates the presence of factors other than Ang II. This review highlights the molecular mechanism in renal disease and discusses pharmaceutical and therapeutic approaches.