钠盐摄入对卡托普利抑制试验和盐水负荷试验一致性的影响

目的:本研究旨在探讨不同水平钠盐摄入对两种原发性醛固酮增多症诊断试验卡托普利抑制试验(CCT)和盐水负荷试验(SIT)结果一致性的影响。方法:本研究回顾了中国医学科学院阜外医院自2016年10月至2018年8月同时行CCT和SIT的298例患者的临床资料。根据试验前24 h尿钠排泄量由低到高三等分将患者分为低钠组(<93 mmol/24 h)、中钠组(93~144 mmol/24 h)、高钠组(>144 mmol/24 h);四等分将患者分为低钠组(<75 mmol/24 h)、中钠组A(75~116 mmol/24 h)、中钠组B(117~164 mmol/24 h)、高钠组(>164 mmol/24 h),通过比较不同组别中CCT和SIT结果一致性的差异来探讨钠盐摄入对两种不同确诊试验的影响。结果:共有145例(48.7%)患者两种确诊试验结果不同,其中103例(34.6%)呈CCT单阳性,42例(14.1%)呈SIT单阳性。三等分时高钠组中CCT单阳性比例较高(高钠组49.0%vs中钠组26.7%vs低钠组28.3%,P<0.001),四等分时结果相似(高钠组48.0%vs中钠组B 36.5%vs中钠组A 25.7%vs低钠组28.0%,P=0.018)。多因素Logistic回归分析显示,24 h尿钠排泄量是影响CCT单阳性患者比例的因素(P=0.006)。结论:高钠组患者CCT结果和SIT结果一致性低于中钠组。进行原发性醛固酮增多症诊断试验前应标准化钠盐摄入而非单纯不限制钠盐摄入。     

尿钠排泄量与动脉弹性指数的关系

目的探讨尿钠排泄量与大小动脉弹性指数(C1,C2)的关系。方法入选体检人群397例(男性195例,女性202例),年龄(53.4±15.1)岁。通过24 h尿钠排泄量测定钠盐摄入量,将入选人群分为低盐组(n=99),低中盐组(n=100),中高盐组(n=99),高盐组(n=99)。C1、C2采用CVProfilor Do-2020动脉脉搏波分析仪测量。使用广义线性模型比较24 h尿钠排泄量与C1、C2的关系,使用多元线性回归分析影响C1、C2的主要因素。结果随着24 h尿钠排泄量的增多,C1、C2逐步降低,其中高盐组较低盐组C1、C2显著降低。多元逐步线性回归分析结果提示24 h尿钠排泄量增高是C1、C2降低的独立危险因素。结论随着24 h尿钠排泄量的增加,反映动脉弹性的指标C1、C2下降。     

老年2型糖尿病患者摄盐量与蛋白尿的相关性

目的探讨老年2型糖尿病患者摄盐量与蛋白尿的相关性。方法选择老年2型糖尿病患者180例,检测患者血糖、糖化血红蛋白(HbA1c)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、尿素氮(BUN)、血肌酐(Scr)、尿钠及尿微量白蛋白。根据患者尿钠水平换算摄盐量分组,比较2型糖尿病患者摄盐量与各指标相关性,并采用Logistic回归分析探讨蛋白尿危险因素。结果根据患者24 h尿钠排泄量分组,其中低钠组54例、中钠组78例、高钠组48例,三组在体重指数(BMI)、收缩压(SBP)、TC及24 h尿蛋白水平上差异有统计学意义(P<0. 05)。24 h尿蛋白与SBP、每日摄盐量均呈显著正相关(P<0. 05)。经多因素Logistic回归分析显示,SBP及每日摄盐量是老年2型糖尿病患者蛋白尿发生的独立危险因素。结论高钠盐摄入量是老年2型糖尿病患者蛋白尿发生的独立危险因素,限制老年2型糖尿病患者纳盐摄入量,可以延缓糖尿病肾病的发生和进展。     

盐敏感性高血压患者血压波动情况与昼夜尿钠排泄量的临床观察

目的探讨盐敏感性高血压患者24h血压变化及尿钠排泄量的变化。方法采用快速静脉输注生理盐水与呋塞米排钠缩容结合的方法判定患者的盐敏感性,并根据盐敏感性判定结果将患者分为盐敏感性组(SS)及非盐敏感性组(NSS),对两组患者的24h血压变化节律进行监测,并测定两组患者的白天、夜间尿钠排泄量。结果 85例患者中出现盐敏感性患者35例,达41.2%。24h动态血压监测结果表明,两组患者的24h收缩压和舒张压、白天收缩压和舒张压差异无统计学意义(P0.05),但SS组患者夜间收缩压、舒张压明显升高,差异具有统计学意义(P0.05)。两组患者24h尿钠量及白天尿钠量差异均无统计学意义(P0.05)。但SS组患者的夜间尿钠量及其在24h尿钠量中所占的比重与NSS组比较均明显上升,差异有统计学意义(P0.01)。结论盐敏感性高血压患者出现夜间尿钠排泄量明显增加,并导致血压出现"非杓型"改变,给予利尿剂可有效缓解患者血压变异性变化。     

原发性高血压24 h尿钠与微量白蛋白尿关系研究

目的探讨原发性高血压患者尿钠与微量白蛋白尿的关系。方法选择2011年11月至2013年10月在第三军医大学附属第三医院住院治疗的原发性高血压患者418例。根据24 h尿钠的四分位数,将入选人群分为低尿钠组、低中尿钠组、中高尿钠组和高尿钠组,用单因素方差分析比较4组的一般临床资料、血清学指标和24 h尿钠、尿微量白蛋白,用多元线性回归分析影响24 h尿微量白蛋白的危险因素。结果随着24 h尿钠的升高,原发性高血压患者24 h尿微量白蛋白随之升高(P0.01)。多元线性回归分析结果提示24 h尿钠是原发性高血压患者微量白蛋白尿的独立危险因素[OR(95%CI):0.437(0.264,0.611),P0.001]。结论 24 h尿钠是原发性高血压患者微量白蛋白尿的独立危险因素,控制钠盐摄入有利于防治高血压肾脏病变。     

尿醛固酮在原发性醛固酮增多症筛查中的价值及钠摄入对其筛查效率的影响

目的探讨尿醛固酮在原发性醛固酮增多症(PA)筛查中的作用并评估钠盐摄入对其筛查效率的影响。方法收集2006-09-2009-07中山大学附属第二医院内分泌科门诊和住院的高血压患者269例,其中包括原发性高血压患者237例(女119例,男118例,平均年龄47.4岁)和PA患者32例(女20例,男12例,平均年龄41.9岁)。所有入组的研究对象均测定立位1h血清醛固酮(SAC)和血浆肾素活性(PRA),并留取24h尿检测尿醛固酮、尿钠和尿钾。通过构建受试者工作特征曲线(ROC),评估尿醛固酮在PA筛查中的效率并确定最佳切点。以尿钠/尿钾作为钠盐摄入的评估方法,以尿钠/尿钾中位数作为切点将原发性高血压组分为高尿钠/尿钾组(n=119)和低尿钠/尿钾组(n=118),分别以这两组高血压人群作为阴性人群,以PA组作为阳性人群进行ROC分析,比较不同钠盐摄入情况对尿醛固酮水平及其PA筛查效率的影响。结果通过构建ROC曲线评估尿醛固酮在PA筛查中的作用,其曲线下面积为0.824(95%CI0.773～0.867,P<0.01),应用Youden’s指数确定尿醛固酮诊断PA的最佳切点值为11.6μg/24h,其敏感性和特异性分别为81.2%(95%CI63.3%～92.7%)和74.3%(95%CI68.2%～79.7%);在原发性高血压患者中,尿醛固酮与尿钠/尿钾呈负相关(r=-0.174,P<0.01)。高尿钠/尿钾组尿醛固酮、SAC和PRA水平明显低于低尿钠/尿钾组。结论尿醛固酮在PA筛查有一定意义,采用11.6μg/24h作为切点可取得较高的筛查效率。钠摄入可影响尿醛固酮水平,但不影响其筛查效率。     

原发性高血压患者24h尿钠与血浆肾素活性、醛固酮水平及血压节律的关系

目的分析原发性高血压患者24h尿钠与血浆肾素活性、醛固酮水平及血压昼夜节律之间的关系。方法回顾性分析2010年1月至2014年12月连续住院的原发性高血压患者1284例。根据24h尿钠排泄量评价患者的盐摄入量,将患者分为3组:低尿钠组(24h尿钠100 mmol)362例,中等尿钠组(24h尿钠100~200 mmol)675例,高尿钠组(24h尿钠200mmol)247例。对各组血浆肾素活性、醛固酮水平及24h动态血压情况进行分析。结果本研究人群平均24h尿钠水平为(145±69)mmol,估算平均每日摄盐量为(8.48±4.04)g。经性别、年龄、体质量指数校正后,与低尿钠组相比,中等尿钠组和高尿钠组的血浆肾素活性明显降低[(2.77±0.08)、(2.49±0.14)比(3.34±0.11)μg/(L·h),均P0.05],高尿钠组的醛固酮水平低于中等尿钠组和低尿钠组[(150.2±5.4)比(161.8±3.2)、(175.2±4.4)ng/L,均P0.05]。高尿钠组的24h、白天及夜间平均收缩压、舒张压较低尿钠组及中等尿钠组均明显升高(均P0.01)。高尿钠组非杓型血压比例高于低尿钠组(P0.05)。非杓型及夜间高血压患者的24h尿钠水平较杓型和非夜间高血压患者高(均P0.05)。结论高盐摄入患者的血浆肾素活性及醛固酮水平较低,血压水平较高,更多表现为非杓型血压及夜间高血压。     

慢性充血性心力衰竭治疗时低钠血症的形成及其对预后的影响

对钠水处理方式不同的７８例充血性心力衰竭（ＣＨＦ）患者血钠浓度的变化进行观察，显示在排钠利尿的基础上严格限钠不限水时，使正常血钠者１６／３５例形成低钠血症，与不限钠水者比较Ｐ＜０．０５；对低钠血症患者行单纯补钠或单纯严格限水时，分别有７／９例和８／１４例血钠浓度恢复正常，与限钠不限水组比较分别Ｐ＜０．００１和Ｐ＜０．０１。认为在排钠利尿基础上严格限钠和（或）忽视对水摄入量的控制是造成低钠血症的一个重要原因。对ＣＨＦ的预后对比，显示合并低钠血症者非好转出院人数与住院期间死亡人数均明显高于不合并低钠血症者（Ｐ＜０．０５），前者死亡原因均与低排综合征有关。表明：ＣＨＦ治疗中低钠血症的形成与应用排钠利尿剂严格限制钠盐的摄入且不限制水的摄入关系密切。     

营养和代谢疾病(911491～911517)

911491 老年人低钠血症/李晓玫…∥中华老年医学杂志.-1990,9(4).-209～211 健康老年组(60～80岁)96例,老年组和青年组内科患者(无心衰,肝硬化及肾脏病)分别为100例及20例,分析结果:老年患者组低钠血症的发生率达25.0％,明显高于健康老年组(4.2%)及青年患者组(10.0％)(P<0.005),其主要类型为缺钠性低血钠,主要原因为胃肠道消化液的丧失以及持续禁食。     

肝硬化腹水患者并发低钠血症30例治疗体会

本文总结了我院肝硬化腹水并发低钠血症 3 0例。临床治疗体会认为临床医师应提高警惕 ,减少该病的发生 ,减轻病人的痛苦 ,延长病人的生命。1　资料与方法对于轻度低钠血症的 9例患者我们给予调整利尿剂 ,适当增加口服钠盐及给予 0 .9%氯化钠注射液深部灌肠。 2 1例中、重度低钠     

Hyponatremia - carbamazepine medication complications

Hyponatremia can be defined like the low sodium concentration, lower that 135 mmol/l. It becomes really serious when the concentration is lower than 120 mmol/l. The most frequent causes of hyponatremia are: the extrarenal loss (GIT, skin, bleeding, sequestration), the renal loss (diuretics, nephritis with the salt loss, osmotical diuresis, the Addison disease), hypothyroidism, the lack of glucocorticoids, emotional stress, pain, pseudohyponatremia (incorrect taking, dyslipoproteinemia). There is fatigue, exhaustion, headache and vertigoes dominating in the clinical record file. By the deficit increasing a patient becomes delirious, comatose even with the shock development. It is necessary to separate sufficient supply of sodium from much more often reason, which is loss of sodium which can be caused by: excessive sweating, vomitting with the metabolical alkalosis development, diarrhoea with the metabolical acidosis development, renal losses (a phase of renal failure). Treatment of hyponatremia: intensive treatment starts at the level of plasmatic concentration of sodium under 120 mmol/l or when neurological symptoms of brain oedema are present. In the therapy it is necessary to avoid fast infusions of hypertonic saline solutions (3-5% NaCl solutions) because of the danger of the development of serious CNS complications (intracranial bleeding, etc.). It is recommended to adjust the plasmatic concentration of sodium up to 120 mmol/l during the first four hours and a subsequent correction should not be higher than 2 mmol per an hour. Treatment of the basic illness is very important. We present 2 case histories: a 74-year old female patient and a 69-year old female patient both with the hyponatremia caused by taking of carbamazepine. We want to inform and warn about not only a well known side effect during long-term treatment but about hyponatremia that arose within 48 hours after the start of taking medicine as well.     

Close association of urinary excretion of aquaporin-2 with appropriate and inappropriate arginine vasopressin-dependent antidiuresis in hyponatremia in elderly subjects

The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) participates in the involvement of arginine vasopressin (AVP) in hyponatremia less than 130 mmol/L in 33 elderly subjects (> or =65 yr old) during the last 5-yr period. Subjects were separated into euvolemic hyponatremia groups: 13 with hypopituitarism, 8 with syndrome of inappropriate secretion of antidiuretic hormone (SIADH), 8 with mineralocorticoid-responsive hyponatremia of the elderly, and 4 with miscellaneous diseases. Approximately 40% of those with hyponatremia was derived from hypopituitarism, but severe hyponatremia was found in the patients with SIADH and mineralocorticoid-responsive hyponatremia of the elderly. Plasma AVP levels remained relatively high despite hypoosmolality and were tightly linked with exaggerated urinary excretion of AQP-2 and antidiuresis in the 3 groups of patients, except for one miscellaneous one. An acute water load test verified the impairment in water excretion, because the percent excretion of the water load was less than 42% and the minimal urinary osmolality was not sufficiently diluted. Also, plasma AVP and urinary excretion of AQP-2 were not reduced after the water load. The inappropriate secretion of AVP was evident in the patients with SIADH and hypopituitarism, and hydrocortisone replacement normalized urinary excretion of AQP-2 and renal water excretion in those with hypopituitarism. In contrast, the appropriate antidiuresis seemed to compensate loss of body fluid in the patients with mineralocorticoid-responsive hyponatremia of the elderly, who lost circulatory blood volume by 7.3% (mean). Fludrocortisone acetate increased renal sodium handling and body fluid, resulting in the reduction in AVP release and urinary excretion of AQP-2 in mineralocorticoid-responsive hyponatremia of the elderly. These findings indicate that urinary excretion of AQP-2 may be a more sensitive measure of AVP effect on renal collecting duct cells than are plasma AVP levels, and that increased urinary excretion of AQP-2 shows exaggerated AVP-induced antidiuresis in hyponatremic subjects in the elderly. In addition, mineralocorticoid-responsive hyponatremia of the elderly has to be carefully differentiated from SIADH in elderly subjects.     

Severe hyponatremia associated with the combined use of thiazide diuretics and selective serotonin reuptake inhibitors

Thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs) are among the most commonly prescribed medications. Each medication has been associated with the development of severe hyponatremia. The mechanisms involved in the development of hyponatremia differ for each medication. Thiazide diuretics induce hyponatremia by impairment of urinary dilution, renal loss of sodium and potassium, stimulation of antidiuretic hormone (ADH), and perhaps from a dipsogenic effect. SSRIs cause hyponatremia through the syndrome of inappropriate ADH release. Two cases of severe hyponatremia in patients taking both a thiazide diuretic and an SSRI highlight the possibility of a synergistic effect in impairment of renal free water clearance when both medications are given. These two cases serve as a cautionary example and should prompt careful monitoring of patients prescribed both an SSRI and a thiazide diuretic (especially in elderly women, who seem to be at increased risk for this complication).     

Hyponatremia in cirrhosis: clinical features and management

The presence of dilutional hyponatremia has a poor prognosis for survival in patients with cirrhosis and ascites. Effective and safe treatments are needed to improve prognosis in patients with cirrhosis and dilutional hyponatremia. The initial approach to management includes fluid restriction, low sodium diet, and minimizing the use of diuretics. In addition, the use of hypertonic saline should be avoided in patients with cirrhosis and dilutional hyponatremia. Furthermore, patients should be placed on the top of the list for liver transplantation if they are appropriate candidates. Although V2 arginine vasopressin receptor antagonists that selectively enhance solute-free water excretion in patients with cirrhosis seem very promising, two points must be considered in relation to the available data. First, although the results of phase-2 studies are encouraging, the efficacy and safety of these compounds should be further evaluated. Second, the clinical utility of these agents in cirrhosis has only been assessed in short-term studies. The long-term effects of these drugs remain unknown. Future research with these compounds should not only focus on the effects on serum sodium, but also on treatment and prevention of recurrence of ascites. In addition, the possible beneficial effects of these drugs in the prevention of hepatic encephalopathy would be worth studying.     

Thiazide diuretics and calcium metabolism

Thiazide diuretics reduce urinary excretion of calcium by about 40% in patients with intact parathyroid glands (normal parathyroid function or primary hyperparathyroidism). Despite equivalent sodium losses, thiazide diuretics do not lower calcium excretion in patients with hypoparathyroidism. Thiazide diuretics diminish hydroxyproline excretion by about 22%, and they do not affect 3′5′-cyclic AMP excretion in subjects with intact parathyroid glands. These findings, together with additional data in the literature, suggest that thiazides may potentiate the renal action of parathyroid hormone, resulting in retention of calcium and partial suppression of parathyroid hormone secretion.     

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome

Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin-1 and aquaporin-2 in patients with cirrhosis at different stages of the disease. Twenty-four-hour urine was collected from 11 healthy volunteers, 13 patients with compensated cirrhosis (without ascites), and 20 patients with decompensated cirrhosis (11 with ascites without renal failure and 9 with hepatorenal syndrome). Aquaporin-1 and aquaporin-2 excretion was analyzed by immunoblotting. Urinary aquaporin-2 excretion was reduced in patients with cirrhosis compared to healthy subjects. A progressive decrease in urinary aquaporin-2 excretion was observed as the severity of cirrhosis increased, from compensated cirrhosis to cirrhosis with ascites and hepatorenal syndrome. Patients with hyponatremia had lower urinary aquaporin-2 excretion than patients without hyponatremia. Vasopressin plasma level did not correlate with aquaporin-2 excretion. There were no differences between healthy subjects and patients with cirrhosis with or without ascites in urinary excretion of aquaporin-1, but urinary aquaporin-1 excretion of those with hepatorenal syndrome was extremely low. In conclusion, patients with cirrhosis appear to exhibit a decreased abundance of renal aquaporin-2 and therefore lower water permeability in the collecting tubules. This may represent an adaptive renal response to sodium retention, with expansion of extracellular fluid volume and dilutional hyponatremia observed in those who have cirrhosis with ascites. Finally, aquaporin-1 does not appear to play a role in the progressive dysregulation of extracellular fluid volume in cirrhosis.     

Value of fractional uric acid excretion in differential diagnosis of hyponatremic patients on diuretics

BACKGROUND: The syndrome of inappropriate antidiuresis (SIAD) is the most frequent cause of hyponatremia. Its diagnosis requires decreased serum osmolality, inappropriately diluted urine (e.g. >100 mOsm/kg), clinical euvolemia, and a urinary sodium (Na) excretion (U-Na) more than 30 mmol/liter. However, in hyponatremic patients taking diuretics, this definition is unreliable due to the natriuretic effect of diuretics. Here, we examined the diagnostic potential of alternative laboratory measurements to diagnose SIAD, regardless of the use of diuretics. METHODS: A total of 86 consecutive hyponatremic patients (serum Na <130 mmol/liter) was classified based on their history, clinical evaluation, osmolality, and saline response to isotonic saline into a SIAD and a non-SIAD group. U-Na, serum urate concentration, and fractional excretion (FE) of Na, urea, and uric acid (UA) were measured in all subjects. The accuracy to diagnose SIAD was assessed using receiver operating characteristic analysis. RESULTS: A total of 31 patients (36%) had a diagnosis of SIAD, and 55 (64%) were classified as non-SIAD. There were 57 patients (68%) who were on diuretics (15 in the SIAD group, 42 in the non-SIAD group). In the absence of diuretic therapy, SIAD was accurately diagnosed using U-Na (area under the receiver operating characteristic curve 0.96; 0.92-1.02). However, in patients on diuretics, the diagnosis was unreliable (area under the curve 0.85; 0.73-0.97). There, FE-UA performed best compared with all other markers tested (area under the curve 0.96; 0.92-1.12), resulting in a positive predictive value of 100% if a cutoff value of 12% was used. CONCLUSION: FE-UA allows the diagnosis of SIAD with excellent specificity. Combining the information on U-Na and FE-UA leads to a very high diagnostic accuracy in hyponatremic patients with and without diuretic treatment.     

Refractory ascites and dilutional hyponatremia: current management and new aquaretics

Ascites is the most common complication of cirrhosis and is associated with 50% mortality at 2 years if patients do not receive orthotopic liver transplantation. Recently the International Ascites Club defined ascites into three groups: In grade I ascites fluid is detected only by ultrasound; in grade II, ascites is moderate with symmetrical distention of the abdomen; and in Grade 3 ascites is large or tense with marked abdominal distention. About 10% of patients with ascites are refractory to treatment with diuretics. In refractory ascites, patients do not respond to highest doses of diuretics (spironolactone 400 mg/day and furosemide 160 mg/ day) or develop side effects (hyperkalemia, hyponatremia, hepatic encephalopathy, or renal failure) that prohibit their use. Patients may be treated either by repeated large volume paracentesis plus albumin or transjugular intrahepatic portosystemic shunts (TIPS). Dilutional hyponatremia in cirrhotic patients is defined as serum sodium < or = 130 mEq/L in the presence of an expanded extracellular fluid volume, as indicated by the presence of ascites and/or edema. This complication of cirrhotic patients with ascites has recently gained attention given that several reports indicate that when serum sodium concentration is combined with the Model for End-Stage liver disease (MELD) it improves the prognostic accuracy of MELD score in patients awaiting orthotopic liver transplant (OLT). The first step in the management of dilutional hyponatremia is fluid restriction and discontinuation of diuretics. Water restriction at 1,000 mL/day helps prevent the progressive decrease in serum sodium concentration but usually does not correct hyponatremia in most cases. Actually are developing drugs that are active orally and act by selectively antagonizing the specific receptors (V2 receptor) of arginine vasopressin. These agents act in the distal collecting ducts of the kidneys, by increasing solute free water excretion and, thus, improving serum sodium concentration in hyponatremic patients.     

The effect of sodium and potassium loading on urinary kallikrein-like activity in young patients with borderline hypertension

We studied the effects of a potassium supplement on urinary kallikrein excretion in a setting of high sodium intake after sodium deprivation with diuretics in young patients with borderline hypertension. Eleven patients, who took the potassium supplementation during the high sodium diet period, showed lower increments in mean blood pressure with salt loading than 12 patients without the potassium supplementation. In the non-potassium-supplemented patients, urinary kallikrein was increased significantly when plasma renin activity (PRA), plasma aldosterone concentration (PAC), and urinary aldosterone were increased during the diuretic treatment. It was decreased significantly when the other hormones were decreased during the sodium load. During the high sodium diet period, PRA, PAC and urinary aldosterone were greater in the potassium-supplemented patients than in the non-potassium-supplemented ones, but urinary kallikrein excretion was not higher when potassium was supplemented. Thus, the present results did not support the theory that the kallikrein-kinin system may be involved in the natriuretic and antihypertensive effects of potassium. In addition, these finding suggest that some kallikrein-modulating factor(s) may counteract the increased urinary kallikrein excretion with the augmented renin-angiotensin-aldosterone system during salt loading with potassium supplementation.