心钠素,抗利尿激素在正常和缺氧新生儿水钠代谢中的作用

为了阐明心钠素（ＡＮＰ）和抗利激素（ＡＤＨ）在正常和缺氧新生儿生后早期体液平衡中的作用，测定了４４例正常新生儿和３６例缺氧新生儿生后第１、３、７天血浆心钠素（ＰＡＮＰ）、抗利尿激素（ＰＡＤＨ）以及血、尿各项指标。结果表明：正常新生儿第１天ＰＡＮＰ和ＰＡＤＨ都升高，两者之间存在着负相关关系；尿量、尿钠、尿渗透压和ＡＮＰ呈正相关；缺氧新生儿的ＰＡＮＰ和ＰＡＤＨ均较正常儿升高，其第３天的悄量、尿钠和尿渗     

颅脑损伤之若干并发症

颅脑损伤尤其是重型患者出现并发症在临床中较常见 ,并且同一病人可出现诸多并发症。本组在此略述若干种。1　低钠血症严重颅脑损伤引起的低钠血症可分为两大类 :丘脑下部—垂体系统受损 ,ＡＣＴＨ和ＡＤＨ分泌异常 ,尿中Ｎａ+ 排出增多 ,肾对水的重吸收增加 ,导致低血钠、低血渗而产生的一系列神经受损 ,临床表现为ＡＤＨ不适当分泌综合征 (ＳＩＡＤＨ)。继发于急慢性中枢神经系统损伤 ,肾保钠功能下降 ,血容量没有增加而引起的低钠血症为脑耗盐综合征 (ＣＳＷＳ)。常发生于脑外伤后[1 ] 。2　高钠血症常见的病因是 :大剂量使用脱水药 ,过…     

术后血管升压素异常分泌综合征的内分泌变化

动态监测２０例大手术创伤患儿术后血管升压素异常分泌综合征（ＳＩＡＤＨ）的发生情况。采用放射免疫法分别于术前、术后ｌｈ、８ｈ和４８ｈ测定血浆血管升压素（ＡＤＨ）、心房钠尿肽（ＡＮＰ）、肾素（ＰＲＡ）、血管紧张素ＩＩ（ＡＩＩ）和醛固酮（ＡＬＤ），以探讨术后ＳＩＡＤＨ的内分泌调节机制。结果：８例于术后发生ＳＩＡＤＨ，其术后１ｈ血浆ＡＤＨ、ＡＮＰ、ＰＲＡ、ＡＩＩ和ＡＬＤ均升高；术后８ｈＡＤＨ和ＡＮＰ继续升至峰值，ＰＲＡ、ＡＩＩ和ＡＬＤ则明显下降，低于术前水平。术后４８ｈ除ＡＬＤ外均逐渐恢复。１２例术后未发生ＳＩＡＤＨ者，上述激素水平无显著变化。提示术后８ｈ内应限制输入液量。     

术后血管升压素异常分泌综合征的内分泌变化

动态监测２０例大手术创伤患儿术后血管升压素异常分泌综合征（ＳＩＡＤＨ）的发生情况。采用放射免疫法分别于术前、术后１ｈ，８ｈ和４８ｈ测定血浆血管升压素（ＡＤＨ）、心房钠尿肽（ＡＮＰ）、肾素（ＰＲＡ）、血管紧张素ＩＩ（ＡＩＩ）和醛固酮（ＡＬＫ），以探讨术后ＳＩＡＤＨ的内分泌调节机制。结果：８例于术后发生ＳＩＡＤＨ，其术后１ｈ血浆ＡＤＨ、ＡＮＰ、ＰＲＡ、ＡＩＩ和ＡＬＤ均升高；术后８ｈＡＤＨ和ＡＮＰ继续升     

全身照射加足叶乙甙联合自体造血干细胞移植治疗非霍奇金淋巴瘤的疗效评价

目的评价全身照射（ＴＢＩ）加足叶乙甙（Ｖｐ１６）作为自体造血干细胞移植（ＡＨＳＣＴ）的预处理方案治疗非霍奇金淋巴瘤（ＮＨＬ）的疗效和安全性。方法２４例诱导治疗缓解的中高度恶性ＮＨＬ进行ＡＨＳＣＴ，其中２３例为首次缓解，１例为第３次缓解。自体骨髓移植（ＡＢＭＴ）１０例，自体外周血干细胞移植（ＡＰＢＳＣＴ）１４例，采用ＴＢＩ８００（７００～８５０）ｃＧｙ／Ｖｐ１６７５７（３２３～１１４０）ｍｇ／ｍ２作为预处理方案。结果中位随访２２．５（２～９２）个月，诱导治疗达完全缓解者ＡＨＳＣＴ后的１年无病生存率（ＤＦＳ）为８６７％（１３／１５），３年、５年、７年ＤＦＳ均为８００％（１２／１５），诱导治疗达部分缓解者移植后６６７％（４／６）获长期无病生存，ＡＨＳＣＴ前复发者无长期生存，全组无移植相关死亡。ＡＰＢＳＣＴ较ＡＢＭＴ可使造血功能快速重建。结论首程诱导治疗缓解的中高度恶性ＮＨＬ行ＡＨＳＣＴ可获得满意的临床疗效，ＴＢＩ／Ｖｐ１６是ＮＨＬ患者ＡＰＢＳＣＴ的一个安全有效的预处理方案。     

二硫化碳肾脏毒性研究

为探讨二硫化碳（ＣＳ_２）对大鼠的肾脏毒性，３个染毒组分别以５０，２５０，１２５０ｍｇ／ｍ￣３的浓度静式吸入ＣＳ_２，每天２ｈ，每周６天，连续８周，并与对照组比较。结果：１、各染毒组尿γ－ＧＴ、ＡＫＰ活性、尿β_２－ＭＧ含量，大、中剂量组尿ＬＤＨ活性、尿Ａｌｂ含量，以及大剂量组尿ＩｇＧ、总蛋白含量、血ＢＵＮ含量均较对照组显著增高；２、光镜检查发现肾小管上皮细胞浊肿、空泡变性、肾小球肿大；电镜下见基底膜紊乱、线粒体肿胀、嵴断裂等；３、肾皮质小管中ＡＫＰ、ＡＴＰａｓｅ、ＳＤＨ、ＡＮＡＥ酶活性下降，以ＡＫＰ，ＳＤＨ活性下降最为明显。     

高血压病患者血清脂蛋白,载脂蛋白与胰岛素的关系

通过检测４１例高血压病患者和２７例正常对照者血清脂质、脂蛋白、载脂蛋白、葡萄糖及胰岛素含量。结果表明：与正常对照者比较，高血压病患者血清甘油三酯、低密度脂蛋白胆固醇（ＬＤＬ－ＣＨ）、ＡｐｏＢ、Ｉ及Ｉ／Ｇ比值均显著增加，高密度脂蛋白胆固醇（ＨＤＬ－ＣＨ）、ＨＤＬ２－ＣＨ、ＡｐｏＡＩ及ＡｐｏＡｉ／ＡｐｏＢ比值均显著降低。相关性分析显示，高血压病Ｉ与ＴＧ和ＡｐｏＢ均呈正相关，与ＨＤＬ２－ＣＨ和ＡｐｏＡＩ     

脑梗塞患者红细胞变形性与其膜脂质及血脂的研究

采用激光衍射法检测３０例脑梗塞人和３０例同年龄正常人的红细胞变形指数（ＤＩ），发现在２００ｄｙｎ／ｃｍ＾２剪切力下，病人组ＤＩ值较正常对照组明显降低；同时还测定了两组红细胞膜脂质成分－－膜胆固醇、磷脂、二者比值及血浆脂质等成分，结果膜Ｃｈ、Ｃｈ／Ｐ１明显高于后才，血浆ＨＤＬ－Ｃ、ＡｐｏＡ－Ｉ明显降低，ＡｐｏＢ明显升高，而血总胆固醇（ＴＣ）无升同。相关分析发现，ＤＩ值与Ｃｈ／Ｐ１呈负相关。膜Ｃｈｄｇ     

无症状心肌缺血患者血脂及载脂蛋白的变化

测定１４８例无症状心肌缺血（ＳＭＩ）患者及３０名健康人血脂及载脂蛋白。结果表明：各型ＳＭＩ血脂及载脂蛋白均有异常，以Ⅱ和Ⅲ型更为显著。患者ＳＴ段下移程度与血清ＴＧ，ＴＣ，ＬＤＬ，ＡｐｏＢ１００，ＡｐｏＢ１００／ＡｐｏＡⅠ，Ｌｐ（ａ）呈正相关，与ＡｐｏＡＩ，ＨＤＬ－Ｃ，ＨＤＬ２－Ｃ，ＨＤＬ－Ｃ／ＴＣ呈负相关。提示血清ＴＧ，ＬＤＬ－Ｃ浓度以及ＡｐｏＢ１００／ＡｐｏＡⅠ值升高和ＨＤＬ２－Ｃ浓度降低是ＳＭＩ的独立危险因素     

免疫印迹法检测SLE病人血清抗Sm抗体阳性判断及检出率探讨

抗史密斯抗体是ＳＬＥ的标记抗是性用于诊断ＳＬＥ。免疫印迹法（ＩＢＴ）抗Ｓｍ的抗体，根据ＮＣ膜上三个印迹区带（２９ＫＤ／Ｂ、２８．５ＫＤ／Ｂ、１３．５ＫＤ／Ｄ） 以与否判断抗Ｓｍ抗体最性或生。对１２３例临床仍ＳＬＥ病人表同时测定ＡＮＡ－ＩＦ、抗ＥＮＡ－ＩＢＴ（包括抗Ｓｍ），结果ＡＮＡ阳性率９５．１２％，抗Ｓｍ＝ＣＩＥ阳性率４２．３％，抗Ｓｍ－ＩＢＴ以三区带同时显色判断阳性率３５．７７％，以一区带任一     

Are the increasing clinical demands for osmolality measurements and their associated electrolytes appropriate?

An audit of urine and plasma osmolalities and their associated urea and electrolytes over a 4 week period found that there were 124 plasma and 96 urine osmolality requests from 67 patients. In 21 patients (31.3 per cent), the osmolality results were useful in reaching a more precise diagnosis. In a further 11 cases, urine osmolality rather than plasma would have been appropriate. Seventy-one per cent originated from the Intensive Therapy Unit and were largely requested reflexly by the hospital computer order communication system. Plasma osmolal gaps could be calculated on 80 occasions (65 per cent). The formula 1.89 Na + 1.38 K + 1.03 urea + 1.08 glucose + 7.45 proved to be more accurate than the formula [Na+K] × 2 + urea + glucose (in mmol/L) with the latter showing a positive bias when compared to measured values. The osmolal gap was > 10 mOsm/Kg using the more complex formula on 23 occasions in 16 patients but only twice using the simpler calculation. These 16 patients usually had organ failure and were very ill. Urine sodium and potassium were measured on 72 occasions in 27 of these patients but urine chloride was never requested. Urine sodium < 20 mmol/L was found in 7 patients all of whom had relative or absolute hypovolaemia. Urine sodium was measured in 73 per cent of patients investigated for SIADH in general wards. Data was available to calculate the urine osmolal gap on 52 occasions. The value was >100 mmol/L in 10 cases and this may be used as an index of the renal ammonium response to acidosis. Much potential derived information from simple indices is unused. As a result of this study, there was an approximate halving of the subsequent request volume.     

The hyponatremic patient: a systematic approach to laboratory diagnosis

HYPONATREMIA (SERUM SODIUM LEVEL LESS THAN 134 MMOL/L) is a common electrolyte disturbance. Its high prevalence and potential neurologic sequelae make a logical and rigorous differential diagnosis mandatory before any therapeutic intervention. A history of concurrent illness and medication use as well as the assessment of extracellular volume status on physical examination may provide useful clues as to the pathogenesis of hyponatremia. Measurement of the effective serum tonicity (serum osmolality less serum urea level) is the first step in the laboratory evaluation. In patients with normal or elevated effective serum osmolality (280 mOsm/kg or greater), pseudohyponatremia should be excluded. In the hypo-osmolar state (serum osmolality less than 280 mOsm/kg), urine osmolality is used to determine whether water excretion is normal or impaired. A urine osmolality value of less than 100 mOsm/kg indicates complete and appropriate suppression of antidiuretic hormone secretion. A urine sodium level less than 20 mmol/L is indicative of hypovolemia, whereas a level greater than 40 mmol/L is suggestive of the syndrome of inappropriate antidiuretic hormone secretion. Levels of hormones (thyroid-stimulating hormone and cortisol) and arterial blood gases should be determined in difficult cases of hyponatremia.     

颅脑肿瘤手术后低钠血症89例临床分析

目的 探讨颅脑肿瘤手术后发生低钠血症的可能发生原因、临床分类以及治疗体会.方法 统计653例颅脑肿瘤术后病例,术前血钠监测均正常,术后第2日始,每日监测血电解质,所有病例记录24小时出入液量,每日监测5次中心静脉压(CVP),鞍区肿瘤手术患者监测尿比重,记录每小时尿量.在血钠＜125mmol/L后,监测尿钠、血浆渗透压、尿渗透压.结果 653例中术后出现血钠偏低者122例,其中诊断为低钠血症89例.结论 结合颅脑肿瘤手术后低血钠发生可能机制,我们将低钠血症分为中枢性低钠、非中枢性低钠两种.非中枢性低钠的治疗,首先补盐,其次去除原发诱因.针对低血钠综合征,首先明确抗利尿激素分泌异常综合征(SIADH)和脑性盐耗综合征(CSWS)的诊断,治疗首先按照CSWS治疗有一定意义,如果效果不佳,考虑SIADH及其他治疗手段.     

Demeclocycline in the treatment of the syndrome of inappropriate antidiuretic hormone release: with measurement of plasma ADH.

A patient with the syndrome of inappropriate antidiuretic hormone release (SIADH) following head injury and meningitis was studied during treatment with demeclocycline, a drug known to produce a reversible nephrogenic diabetes insipidus. No changes were observed during six days of demeclocycline 1200 mg/24 hr but urine output increased significantly, with the production of a dilute urine, when the dose was increased to 2400 mg/24 hr. The patient lost weight, and all biochemical features of the syndrome were rapidly corrected despite an unchanged fluid intake and despite the persistence of high plasma levels of ADH. The rise in serum sodium was accompanied by mild sodium retention, as measured by external balance and exchangeable sodium. A complication of treatment was the development of acute renal failure possibly induced by a nephrotoxic effect of high circulating levels of demeclocyline. On stopping demeclocyline renal function returned to normal and, after some delay, SIADH returned, and was still present 9 months after initial presentation. This confirms earlier reports of the efficacy of demeclocycline in SIADH; but the authors advise caution against increasing the dose above 1200 mg/24 hr.     

急性颈髓损伤后低钠血症15例报告及文献复习

目的 探讨急性颈髓损伤后低钠血症的病因、发病机制、诊断和治疗。方法 回顾性分析2000年～2004年收治的急性颈髓损伤后低钠血症患者15例的临床资料。结果 全组患者入院24～72h内血钠低于130mmol／L，其中5例低于120mmol／L。14例尿钠40～68mmol／L，1例尿钠为148mmol／L；尿渗透压420～980mmol／L。12例患者经适当的补盐和限制水摄入量治疗，低钠症状2～3周内改善；2例发热患者因发热不能严格限制水摄入，其中1例2个月后恢复，另1例失访；1例患者补盐限水后病情加重，调整治疗方案后恢复。结论 颈髓损伤越重，损伤后低钠血症发生率越高；颈髓损伤后低钠血症多由抗利尿激素分泌异常综合征引起；血钠浓度，血、尿渗透压等是诊断依据；适当补充钠盐和液体量是有效的治疗方法。     

表现为严重低钙血症、周期性麻痹的Gitelman 氏综合征

患者,女,63岁,因反复乏力,双下肢瘫痪,双手搐搦50 年,加重2 年入院。查体:P80/min,BP120/70mmHg,BMI23.0kg/m2,WHR0.84,焦虑,四肢肌力正常,膝反射、踝反射轻度减弱。无阳性家族史,无服用利尿剂及泻药史。实验室检查示低血钾(2.77～3.17mmol/L),低血镁(0.31～0.35mmol/L),低血钙(1.79～1.99mmol/L),和低尿钙(0.12～1.10mmol/24h)。血浆肾素活性升高,血浆醛固酮水平正常,PTH水平正常。尿钙及尿肌酐比低(5.17～23.57×10-3mg/mgCr),血气分析显示代谢性碱中毒。在该患者进行的速尿或双氢克尿噻的清除率试验中,使用速尿后其尿量及氯离子的清除率增加,远端肾小管氯离子的重吸收分数降低;而使用双氢克尿噻后以上变化均不明显,提示缺陷位于远曲小管而不是亨利氏襻的厚壁升之段。因此,Gitelman氏综合征(Gitelman'ssyndrome,GS)诊断明确。给予消炎痛50mg,tid治疗3d后,复查患者的血钾水平开始上升,但血镁及血钙水平无明显改善,加用氨苯蝶啶50mg,tid治疗,4d后发现血钾及血钙水平恢复正常,血镁从0.35mmol/L升到0.52mmol/L出院;院外随访18个月,复查血钾、血钙及血镁水平完全恢复正常。GS可伴有严重低钙血症、周期性麻痹,肾脏清除率试验在临床上可帮助诊断,消炎痛及氨苯蝶啶联合应用治疗有效。     

Failure of loop diuretics to improve the long term outcome of ischaemic damage in rat kidneys

The effects of furosemide administered at the onset of postischaemic renal failure were investigated in Sprague-Dawley rats one month after exposing the left kidney to 45 min of renal ischemia. In the experimental group, 13 mg furosemide was given intravenously both before and a few minutes after induction of the ischaemia and then, by an osmotic pump, in a daily dose of 2-3 mg for the following 7 days. The animals of the control group were treated similarly but with saline alone. After one month, the glomerular filtration rate (GFR) in the damaged left kidneys of the furosemide-treated rats was 0.5+/-0.08 ml/min, which was not significantly different from that in the untreated control rats, of 0.8+/-0.14 ml/min. As expected, the right intact kidneys responded with an increase in GFR to about 2 ml/min. Further effects that were similar in the damaged kidneys of the furosemide-treated and untreated animals were a decrease in potassium secretion and in the urine concentration ability; the urine osmolality in the diseased left kidneys was thus 1000-1500 mOsm/kg, as against over 2000 mOsm/kg in the right, intact kidneys. The function of the individual nephrons in terms of such variables as single nephron filtration rate, fractional fluid reabsorption and tubular and vascular hydrostatic pressures remained unaltered, however. Hence, the severe reduction in whole kidney GFR appeared to be due to a loss of nephrons rather than to an equal decrease in each individual nephron. It is also clear that furosemide did not improve the long-term outcome of acute postischaemic renal failure.     

促红细胞生成素对缺血再灌注损伤大鼠肾脏水通道蛋白2表达的影响

目的 观察促红细胞生成素(EPO)对缺血再灌注损伤(IR)大鼠肾脏水通道蛋白(AQP2)表达的影响,以探讨EPO对IR的保护作用.方法 制备大鼠肾IR模型,将Wistar大鼠随机分为假手术组、肾IR组及EPO治疗组,通过免疫组化、聚合酶链反应及Wostem印迹等方法 ,检测肾组织中AQP2及其mRNA的变化,同时检测肾功能及尿量、尿渗透压的改变和肾组织形态学变化.结果 EPO治疗组肾脏中AQP2及其mRNA的变化、肾功能[血肌酐(51±5)μmol/L]及尿量[(26.0±2.3)μl·min-1·kg-1]、尿渗透压[(1508±121)mOsm/kg H2O]和肾组织形态学变化与肾IR组[血肌酐(141±5)μmol/L、尿量(59.1±1.3)μl·min-1·kg-1,尿渗透压(235±99)mOsm/kg H2O]相比均有明显改善(均P<0.05).结论 EPO可以促进IR大鼠肾脏AQP2表达,EPO具有改善大鼠肾脏IR的作用,EPO促进AQP2表达这一机制可能参与了其改善大鼠肾脏IR作用.     

日间连续性肾替代治疗重症急性低钠血症

目的探讨日间连续性肾替代治疗（CRRT）重症急性低钠血症的有效性、安全性。方法对我院2005年1月～2010年12月的17例重症急性低钠血症住院患者使用金宝Prisma行连续性肾替代治疗（CVVH），每天治疗8h，连续3d，置换液使用前稀释，置换液流量4L／h，治疗前患者血清钠水平（112．5±4．0）mmol／L，第1天设定置换液钠浓度比血清钠水平高（10-14）mmol／L，第2、3天设定置换液治疗结束时钠浓度比实际血清钠水平高（9～12）mmol／L、（6～9）mmol／L。结果所有患者治疗时间3d，每天8h，均顺利完成，血清钠由治疗前（112．5±4．0）mmol／L上升到（140．2±2．8）mmol／L，血清渗透压逐渐恢复正常，神经精神症状明显好转，G1asgow评分由治疗前的（8．3±1．7）上升到（14．5±0．6）。结论CBP治疗急性严重低钠血症避免了传统方法使血清钠升得过快或过慢等缺点，能够按目标调整纠正血钠速度，本组研究表明CBP治疗急性严重低钠血症疗效确切，成功率高、安全，不失为急性重症低钠血症重要治疗手段。     

血清CysC联合RBP检测在诊断早期肾损伤中的应用价值

目的:探讨联合检测血清胱抑素C(CystatinC,CysC)和视黄醇结合蛋白(Retinol-Binding Protein,RBP)在早期诊断肾损伤的应用价值。方法:对照组选择50例,为健康体检无肾脏病史且尿蛋白定性为阴性者;试验组选择36例尿蛋白定性为弱阳性,肾穿刺活检确诊为早期肾损伤的患者。采用免疫透射比浊法分别测定血清CysC和RBP的浓度,并测定血清肌酐(Crea)及尿素(Urea)的浓度,并进行相关的统计学分析。结果:CysC的浓度对照组为(1.12±0.23)mg/L,试验组为(1.78±0.46)mg/L;RBP的浓度对照组为(47.19±14.34),试验组为(85.87±21.64);肌酐的浓度对照组为(60.8±16.17)μmol/L,试验组为(72.5±45.7)μmol/L。尿素的浓度对照组为(5.35±1.46)mmol/L,试验组为(6.21±2.39)mmol/L。结论:联合检测血清CysC和RBP对诊断早期肾损伤具有较高的临床应用价值。