肾病综合征患者心钠素与糖皮质激素的相互关系

糖皮质激素（ＧＣ）应用于肾病综合征（ＰＮＳ）已有近４０年历史。因人类心钠素（ＡＮＦ）基因的第二个内含子存在有ＧＣ特异性结合位点，故认为ＧＣ可能是参予ＡＮＦ调控的体液因素之一。我们研究通过动态观察ＰＮＳ患者使用ＧＣ的过程中，血浆心钠素（ＰＡＮＦ）、皮质醇（ＰＣＴＳ）、促肾上腺皮质激素（ＰＡＣＴＨ）的水平变化，探讨ＧＣ发挥效应可能的分子生物学机理。一、材料与方法１．病历选择：随机选择１９９５年９月～１９９６年３月在我科住院的ＰＮＳ的３６例（按１９９２年黄山第三届全国肾脏病学术会议标准），男２０例，女…     

氯胺酮,安氟醚麻醉对子宫切除术患者血浆心钠素,肾素,血管紧…

本文研究了氯胺酮、安氟醚麻醉对子宫肌瘤切除术患者血浆心钠素（ＡＮＰ）、肾素（ＰＲＡ）、血管紧张素（ＡⅡ）和醛固酮（ＡＬ）水平的影响。通过１５例子宫肌瘤切除术患者的临床观察，结果表明，子宫肌瘤手术患者氯胺酮、安氟醚麻醉后１０ｍｉｎ、３０ｍｉｎ、１ｈ和术毕ＡＮＰ显著高于麻醉前；ＰＲＡ与麻醉前比较有升高趋势；ＡⅡ在麻醉后３０ｍｉｎ至术毕低于麻醉前；血浆ＡＬ自麻醉后１０ｍｉｎ开始升高，至麻醉后１ｈ和术毕非     

肺心病患者血浆心钠素,醛固酮测定的临床意义

用放射免疫法测定了４０例肺心病患者血浆心钠素，醛固酮含量。结果发现：肺心病急性发作期、缓解血浆心钠素显著高于对照组（Ｐ＜０．０１），急性发作期显著高于缓解期；肺心病急性发作期、缓解期血浆醛固酮显著低于对照组。     

氯胺酮、安氟醚麻醉对子宫切除术患者血浆心钠素、肾素、血管紧张素和醛固酮的影响

本文研究了氯胺酮、安氟醚麻醉对子宫肌瘤切除术患者血浆心钠素(ANP)、肾素(PRA)、血管紧张素(AⅡ)和醛固酮(AL)水平的影响。通过15例子宫肌瘤切除术患者的临床观察,结果表明,子宫肌瘤手术患者氯胺酮、安氟醚麻醉后10min、30min、1h和术毕ANP显著高于麻醉前(P<0.05);PRA与麻醉前比较有升高趋势;AⅡ在麻醉后30min至术毕显著低于麻醉前(P<0.05);血浆AL自麻醉后10min开始升高,至麻醉后1h和术毕非常显著升高(P<0.01)。本文还讨论了它们之间的相互关系。     

应用ROC曲线评价醛固酮肾素比值对原发性醛固酮增多症诊断的临床意义

目的应用接受者操作特性曲线（ROC曲线）选择术前诊断原发醛固酮增多症（原醛症）的醛固酮肾素比值（ARR）的最佳切点,并探讨醛固酮肾素比值在诊断原醛症方面的临床意义。方法从2004年1月到2007年6月在同济医院行手术治疗的肾上腺肿瘤病例133例分为总原醛症组、醛固酮瘤组、肾上腺增生组和非原醛组,用ROC工作曲线选择醛固酮肾素比值的最佳切点。结果总原醛症组和醛固酮瘤组的醛固酮肾素比值的最佳切点为40,而肾上腺增生组的最佳切点为20,醛固酮肾素比值与肾素活性（r=-0.615,P〈0.01）和血管紧张素Ⅱ（r=-0.527,P〈0.01）有负相关性。结论运用醛固酮肾素比值来诊断原醛有很大价值,但还存在不足。     

肾病综合征并发低血容量休克患儿的护理

目的探讨小儿肾病综合征伴发低血容量休克的护理观察方法 ,总结护理经验,以不断提高护理水平。方法对49例患儿予以治疗原发病及抗休克治疗的同时,进行水肿、呕吐、腹泻、感染、生命体征、生化指标的观察和护理,实施针对性健康教育。结果 49例患儿住院9～56(20.2±10.9)d,血压从0/0～90/56mmHg恢复到140/88～90/60mmHg,休克均纠正,原发病好转出院。结论对小儿肾病综合征患儿,加强临床表现、生命体征及生化指标变化的观察,可及早发现和纠正休克,有利于提高疗效。     

Inferior vena cava indices determine volume load in minimal lesion nephrotic syndrome

The pathogenesis of edema in nephrotic syndrome has not been entirely understood. We investigated the value of the echographic parameters [inferior vena cava index (IVCI), inferior vena cava collapsibility index (IVCCI), and left atrium diameter (LAD)] to determine the volume load in children with minimal lesion nephrotic syndrome (MLNS). Twelve children with MLNS (seven boys, five girls) were included in this study. The patients were classified into three different stages (stage A: edematous; stage B: 50% decrease in weight gain; stage C: edema free) following measurement of their ideal weights. The ideal weight of patients in stage A was increased 13 +/- 7%. Serum total protein, albumin and urine sodium levels were found to be low in these patients. Plasma renin activity (PRA) and serum aldosterone levels in stage A were significantly different from those of the control group (P<0.05). PRA and serum aldosterone levels were not different from those of the control group in stage B (P>0.05). However, the increase in PRA was significant in stage C. Although a significant weight decrease was found in stages B and C, it had no effect on IVCI, LAD, and cardiothoracic index. We consider IVCI, IVCCI, and LAD measurements by echocardiography (ECHO) to be easy and reliable clinical methods for assessing the intravascular volume load in patients with MLNS.     

Biological activity of endogenous atrial natriuretic peptide during cardiopulmonary bypass

To evaluate the effect of cardiopulmonary bypass (CPB) on atrial natriuretic peptide (ANP) biological activity in patients undergoing cardiac operations, we conducted a prospective study. Ten patients undergoing mitral valve surgery were enrolled. Plasma levels of ANP and cyclic guanosine monophosphate (cGMP), hemodynamic variables, and renal function parameters were assessed perioperatively. The molar ratio of cGMP to ANP (as a marker for ANP biological activity) decreased significantly (p < 0.05) during CPB despite similar plasma ANP levels. The ratio correlated inversely with the duration of CPB (r = -0.85, p = 0.002). The ratio also correlated with fractional sodium excretion (r = 0.65, p = 0.04) and correlated inversely with pulmonary vascular resistance (r = -0.79, p = 0.009) and atrial filling pressure (r = -0.84, p= 0.003) postoperatively. CPB decreased the molar ratio of cGMP to ANP, which may represent ANP biological activity, such as vasodilation and natriuresis. The phenomenon may contribute to water-sodium retention and pulmonary hypertension after cardiac surgery.     

Atrial natriuretic peptide, sodium retention, and proteinuria in nephrotic syndrome

BACKGROUND.: Oedema formation in the nephrotic syndrome is primarily dueto tubular sodium retention. The pathogenetic role of alphaatrial natriuretic peptide (ANP), a hormonal promoter of natriuresisis unknown. METHODS.: In 31 patients (aged 35±11 years) with nephrotic syndromeand histopathological evidence of primary glomerulonephritis,we investigated plasma ANP concentration and its influence onrenal haemodynamics, natriuresis, and proteinuria (total protein,albumin, IgG excretion). Patients with a compensated treatedform of nephrotic syndrome due to primary glomerulonephritiswere included in the study. Serum creatinine levels were 1.4mg/dl. Diuretic medication was discontinued at least 24 h beforethe investigation was started. Patients were randomly assignedto ANP infusion (0.005 µg/kg*min; group II, n=15) or receivedplacebo (group III, n=16). Ten healthy subjects (group I) servedas normal controls. RESULTS.: In normal subjects (group I), ANP caused an increase in natriuresisfrom 14.5±4.2mmol/h to 26.4±11.1 mmol/h (P<0.01).In patients with nephrotic syndrome (group II), baseline sodiumexcretion of 10.5±6.0 mmol/h was increased to 19.6±14.8mmol/h with ANP infusion (P<0.01). No changes were seen inthe placebo group III. The absolute increase in ANP inducednatriuresis was not significantly different between group Iand II. However, plasma ANP levels were significantly higherin patients with nephrotic syndrome (166±87 pg/ml vs.74±21 pg/ml, P<0.05) and also reached higher levelsafter ANP infusion (P<0.01). Therefore, natriuresis was significantlyreduced when circulating ANP levels were taken into account(P<0.05). ANP administration resulted in an increase of totalprotein excretion in patients with the nephrotic syndrome (groupII, from 219±277 mg/h to 264±268 mg/h). Albuminelimination rose from 128±151 mg/h to 167±170mg/h (P<0.05) and IgG excretion from 4.91±6.67mg/hto 9.27±10.78mg/h (P<0.05). Healthy subjects alsoshowed a small but significant increase in albuminuria (48±38%,P<0.05). Low-dose ANP infusion did not, however, induce anysignificant alteration in GFR, ERPF and blood pressure. CONCLUSION.: ANP plasma concentrations in the steady state are elevated inpatients with the nephrotic syndrome. The natriuretic effectof ANP is reduced when referring to circulating ANP plasma levels.Elevated ANP levels enhance urinary protein excretion in thenephrotic syndrome. This is not due to modulation of GFR orFF, but is most probably attributable to increased glomerularpermeability.     

颈髓损伤后血浆心房肽动态变化与低血钠

目的:观察颈髓损伤(CSCI)患者血浆心房肽(ANP)的动态变化,探讨其与低血钠的关系。方法:采用放免分析法对15例CSCI并低血钠患者血浆心房肽水平进行测定,并与23例CSCI不伴低血钠患者及12例正常同龄组进行对照比较。同时检测血清钠和部分患者的24h尿钠及尿量。并将低血钠患者分为吸氧组和非吸氧组,观察吸氧对血浆ANP和血清钠恢复的影响。结果:⑴CSCI伴低血钠者血浆ANP水平较不伴低血钠者及正常对照组显著升高(P<0.01)。⑵CSCI急性期血浆ANP水平与CSCI程度(Frankel分级)密切相关,CSCI越重,ANP水平越高(P<0.05);ANP水平越高,血钠越低,二者呈显著负相关。⑶吸氧可加速血浆ANP的下降和血清钠的恢复。结论:⑴CSCI后低血钠患者血浆心房肽明显异常,且与CSCI的严重程度(Frankel分级)成正相关。血浆心房肽水平升高可能是导致CSCI后低血钠的一个重要因素;⑵纠正低氧血症可降低ANP水平,从而纠正CSCI后顽固性低血钠。     

Atrial natriuretic peptide and N-terminal atrial natriuretic peptide in plasma reflect right ventricular volumes following coronary artery surgery

Background: Atrial natriuretic peptide (ANP) and the more stable N-terminal fragment (N-ANP) of prohormone are peptides, released in equimolar amounts from cardiac myocytes in response to atrial stretch or ventricular overload and myocardial ischaemia. Protection of the right ventricular (RV) myocardium during ischaemia in cardiac surgery is difficult, especially in patients with severe right coronary artery (RCA) disease. This prospective study was designed to ascertain a possible relationship between changes in plasma ANP/N-ANP concentration and RV function in RCA-diseased patients.
Methods: Plasma ANP and N-ANP concentrations and RV function, measured by fast-response thermodilution, were determined serially in 15 patients with total RCA stenosis and in another 15 with no significant RCA disease (controls) before, during and after coronary artery surgery.
Results: The RV ejection fraction was lower and the RV end-systolic volume index higher in the RCA-diseased patients than in the controls ( P < 0.05) on the second postoperative day, and both ANP and N-ANP were higher in the RCA patients ( P < 0.05) from 6 h after cardiopulmonary bypass till the second postoperative day. At the same time the changes in N-ANP concentrations from the levels before induction of anaesthesia correlated with RV ejection fraction and RV volume indexes, but not with heart rate or parameters indirectly reflecting left-sided loading. Right atrial pressure did not differ between the groups nor did it increase significantly during the study.
Conclusions: The relationships found between N-ANP and RV volume indexes and RV ejection fraction suggest ventricular expression of ANP: ANP release may be stimulated by RV distension, the more so the poorer the RV function.     

Plasma renin activity in haemolytic uraemic syndrome

Plasma renin activity (PRA) was measured in 50 consecutive patients (aged 4 months to 12 years) admitted during the acute phase of the haemolytic uraemic syndrome (HUS). Blood samples were taken as soon as the diagnosis was made and prior to any diuretic, anti-hypertensive or dialysis treatment. Prodromal diarrhoea was present in all but 3 patients, 17 were anuric and 12 were oliguric. PRA ranged from 0.3 to 24.2 ng/ml per hour and was low compared with values in normal infants and children: in 13 HUS patients PRA was above the median and in 37 it was below the median. PRA was significantly, independently and inversely related to age. There was no correlation, however, with blood pressure, urine output, volume status and serum levels of sodium, potassium and creatinine. Moreover, no relationship was found between PRA and the course of the disease. Our findings do not support the idea that renin activation plays a role in the pathophysiology of the haemolytic uraemic syndrome.     

心肺复苏期血浆内皮素、心钠素、降钙素基因相关肽含量的变化

目的研究血浆内皮素(ET)、心钠素(ANP)、降钙素基因相关肽(CGRP)在心脏骤停缺血-再灌注损伤前后含量变化规律及意义。方法健康家兔40只,随机均分为A、B两组。制作家兔心脏骤停缺血-再灌注模型,观察心肺复苏期各时相血浆ET、ANP、CGRP、BP及ECG变化。结果动物在心脏骤停及复苏即刻血浆ET含量未见明显变化,心肺复苏后5min开始升高,而同期血浆ANP、CGRP水平降低(P<0.05),复苏后0.5h血浆ET明显升高(P<0.01),复苏后1、2h血浆ET、ANP、CGRP均较复苏前显著升高(P<0.05)。结论在心脏骤停缺血-再灌注损伤过程中ET、ANP、CGRP水平变化及相关关系可能是一种调节机制并在病理生理过程中起重要作用。     

Normal renal sensitivity to atrial natriuretic peptide in Gordon's syndrome

To test the hypothesis that renal sensitivity to atrial natriuretic peptide (ANP) is impaired in Gordon's syndrome (hypertension and hyperkalaemia with normal glomerular filtration rate) we infused -hANP into two patients with this syndrome (a sister and a brother, 19 and 18 years of age). For comparison, 11 healthy volunteers were also examined. The infusion of -hANP increased urinary volume and excretion of sodium similarly in the patients and controls. The excretion of potassium did not change in either the patients or the controls. The infusion of -hANP had no effect on the serum potassium levels or the plasma CO₂ content in the patients. The present results do not confirm the hypothesis of lack of sensitivity to ANP as a pathophysiological concept in Gordon's syndrome.     

Intra- and extrarenal factors of oedema formation in the nephrotic syndrome

The role of intra- and extrarenal factors in oedema formation in children with nephrotic syndrome is reviewed. Oedema reflects an abnormal accumulation of fluid within the interstitial tissue. At the capillary level oedema develops when increased lymph flow is no longer effective for the removal of interstitial fluid and the maintenance of intravascular volume. Alterations of intrarenal haemodynamics and tubular sodium reabsorption contribute to sodium retention. Recent studies suggest that during oedema formation reduced effective circulatory volume triggers changes in various hormonal systems, such as renin-angiotensin-aldosterone, noradrenaline, dopamine, vasopressin, prostaglandins and natriuretic factors, which contribute to sodium and water retention. It appears that the release of atrial natriuretic peptide following central volume expansion is responsible for the increased urine flow and natriuresis after intravenous administration of albumin.     

Salt-losing nephropathy associated with inappropriate secretion of atrial natriuretic peptide – a new clinical syndrome

A state of normokalemic renal sodium wasting associated with an apparently inappropriate secretion of atrial natriuretic peptide (ANP) has not been previously recognized. We here report an 11-year-old boy who presented with a chronic “salt-losing” nephropathy manifested by normonatremic or mildly hyponatremic extracellular fluid volume depletion, hypodipsia, absence of salt appetite, normokalemic metabolic alkalosis, hyper-reninemic hyperaldosteronism, hypertrophy of the juxtaglomerular apparatus, and highly conserved capacities for concentrating diluting the urine. Plasma ANP values were paradoxically elevated (between 10 and 47 fmol/ml), despite the coexistence of intravascular volume depletion and increased plasma levels of renin and aldosterone. Although the patient had some clinical similarities to Bartter’s syndrome, fractional sodium chloride (NaCl) reabsorption during hypotonic saline diuresis was normal and no clinical amelioration was observed while on indomethacin therapy. Neither a tumor nor cardiac or cerebral abnormalities, which could be responsible for the increased ANP secretion, were detected. These clinical, biochemical, and histological features have not been previously described together and may represent a new clinical syndrome. The pathophysiology of this entity remains unknown, but an attractive, although unproven, hypothesis is that the renal defect in NaCl reabsorption in this patient could be related to an inappropriate and unregulated secretion of ANP. Received December 30, 1996; received in revised form and accepted March 20, 1997