成人肾病综合征患者肾静脉血栓的诊断与防治

肾静脉血栓是肾静脉主干或分支的血栓。易患因素包括：①内皮受损：见于创伤、肿瘤、肾移植后排异、血管炎等。②血流淤滞：见于体液丢失（胃肠道失液、出血、脱水）、移植后血管扭曲、腹膜后疾患导致肾静脉受压迫等。③高凝状态：见于肾病综合征、败血症、口服避孕药物、内源性高凝疾患（蛋白S缺乏、蛋白C缺乏、抗磷脂综合征等）。本文将介绍成人肾病综合征患者肾静脉血栓的诊断与防治。     

丹参粉针合泼尼松治疗肾病综合征40例临床观察

原发性肾病综合征是肾内科的常见病,该病常存在高凝状态,如血脂增高、血黏度增高、凝血时间缩短、甚至静脉血栓形成等,均严重地影响该病的疗效及预后.从1998年1月～2004年12月,笔者对我院的76例原发性肾病综合征患者进行临床观察.     

肾静脉血栓形成后用链激酶挽救肾功能

有关纤维蛋白溶解疗法治疗肾静脉血栓形成的资料很少。一些报告认为肾静脉血栓形成后立即用肝素治疗可以恢复因血栓梗塞引起的肾功能障碍,虽然纤维蛋白溶解疗法在治疗肾静脉血栓形成中的价值尚不清楚,但是它在促进肺栓塞血栓迅速溶解方面优于肝素已被肯定。如果此优点能见于急性肾静脉血栓形成,那么这种疗法在恢复肾功能方面以时间短,肾静脉压升高后的病理后果最小而优于肝素。我们报告一例肾病综合征病人突然因急性肾静脉血栓形成引起肾     

肾病综合征患者血小板聚集性观察

肾病综合征患者血小板聚集性观察福州市第一医院林日渊福州市医学科学研究所李中途肾病综合征（ＮＳ）常处高凝状态，往往有血栓形成而使病情复杂化，高凝状态虽是多方面的，而血小板功能改变则是重要因素之一，本文对１５例ＮＳ患者血小板聚集变化进行了观察。一、病例与...     

黄芪对难治性肾病综合征凝血纤溶的影响

肾病综合征患者有凝血与纤溶障碍,临床表现为高凝状态,它也是难治性肾病的重要原因.     

黄芪改善肾病综合征患者血液高凝状态的临床观察

多种因素导致肾病综合征患者存在着血液高凝状态 ,其在血脂、血液流变学等方面有着明显的变化。黄芪是具广泛药理活性的中药。本文观察了黄芪对肾综患者血脂、血液流变学的影响 ,以改善肾综患者的血液高凝状态 ,提高临床疗效 ,旨在探讨其对肾综的治疗机制。资料与方法1　研究对象　 5 6例原发性肾综患者 ,均符合肾综的诊断标准[1] ,并排除了继发性肾小球疾病。其中 :男 34例 ,女 2 2例 ;年龄 15岁～ 5 8岁 ,平均 38.2岁。 5 6例肾综患者随机分成 2组 ,各组间年龄、性别、病程等均较匹配。2　治疗方法　对照组 (2 0例 )采用常规激素治疗 ;治…     

脉冲—喷射溶栓法治疗肾病综合征并发静脉血栓一例

脉冲—喷射溶栓法治疗肾病综合征并发静脉血栓一例李安谭昭杨爱华刘瑞林张兆权静脉血栓形成是肾病综合征（ＮＳ）的严重并发症。我们采用脉冲—喷射溶栓法成功地为一例ＮＳ并发静脉血栓患者溶栓，现报告如下。患者，男，１９岁，因发现尿有泡沫六周，颜面及下肢浮肿，腹胀...     

微小病变肾病合并急性肾损伤的研究进展

微小病变肾病(minimal change disease, MCD)是原发性肾病综合征中最常见的病理类型之一,尤其好发于儿童及青少年。肾病综合征患者容易合并一系列并发症,如感染、静脉血栓栓塞、急性肾损伤(acute kidney injury, AKI)等。近年来肾病综合征合并AKI的发病率明显上升,其中以MCD合并AKI最为常见。MCD合并AKI会致使患者病情加重,增加临床治疗难度,并与肾脏不良预后密切相关。MCD合并发生AKI的机制涉及多种不同途径,常见的包括有效循环血容量下降导致的肾小球滤过率下降,肾血管病变带来的肾单位缺血,以及蛋白尿对肾小管的直接毒性作用,等等。本文回顾近年来有关MCD合并AKI领域的临床和基础研究,对其发病率、病理生理学机制、早期的诊断指标和防治原则进行综述,旨在提高临床对MCD合并AKI的认识和诊疗水平。     

水蛭对儿童原发性肾病综合征高凝状态的影响

肾病综合征时由于血浆凝血因子和血小板的增多，抗凝血酶和纤溶酶原降低，加之低蛋白、高脂血症、糖皮质激素及强利尿剂的使用，从而导致血液浓缩、血液黏稠度增加，因而肾病综合征时常伴有高凝状态。我们以肝素为对照，观察水蛭对于肾病综合征患儿高凝状态的影响，现报告如下。     

Risk assessment and multidimensional nursing interventions for prevention of venous thromboembolism in patients with nephrotic syndrome

目的 探讨预防肾病综合征患者静脉血栓形成的有效方法.方法 将80例肾病综合征患者按照住院时间先后分为对照组和观察组各40例.对照组采用常规护理方法;观察组应用静脉血栓形成风险评估表对患者进行评估,按照血栓形成的风险程度,采取饮食、认知、行为干预等.比较两组患者血栓形成情况和相关知识掌握程度及满意度.结果 观察组无一例静脉血栓形成,对照组发生4例.观察组患者满意度及相关知识知晓率显著高于对照组(均P＜0.05).结论 对肾病综合征患者进行血栓风险评估能够为护理干预提供科学依据,有助于预防静脉血栓形成,保证患者安全.     

Budd-Chiari syndrome during nephrotic relapse in a patient with resistance to activated protein C clotting inhibitor

It has long been known that patients with nephrotic syndrome have a hypercoagulable state, which explains the association between nephrotic syndrome, renal vein thrombosis, and thromboembolism. However, the Budd-Chiari syndrome has never been reported in nephrotic patients. This is the first report of such an association that, most likely, depended on a primary resistance to activated protein C.     

Thrombose artérielle du membre inférieur sur un syndrome néphrotique

Thromboembolic complications are frequent in the nephrotic syndrome. Arterial localizations have been rarely reported. There is no consensus on their management; it depends on the location and hypercoagulable state. We report a case of acute lower limb ischemia occurring in children with a history of nephrotic syndrome, complicated by toes necrosis. The diagnosis was made by Doppler ultrasonography. Thrombectomy was performed and the patient received an anticoagulant treatment. Local cares have improved the local state, avoiding surgical necrosectomy.     

Prophylaxis with AT III for thromboembolism in nephrotic syndrome: why should it be done?

Children with nephrotic syndrome (NS) are at risk for sinovenous and arterial thrombosis, uncommon but serious complications of the nephrotic syndrome. Multiple factors are involved in the hypercoagulable state of patients with NS, for instance, enhanced platelet reactivity and deficiency of antithrombin III due to urinary loss of this protein. We report the case of a 7-year-old girl with relapse of nephrotic syndrome and with a clinical risk for thromboembolic complications, identified by very low AT III and albumin serum levels and high fibrinogen and cholesterol serum levels. However, having symptoms of hypovolemia, she was treated with albumin and diuretics, known risk factors for thrombotic incidents, although these drugs were both administered after prophylactic intravenous antithrombin. There are no randomized controlled clinical trials supporting prophylactic anticoagulation in the management of nephrotic syndrome. Arterial thromboses during nephrotic syndrome has been associated with thrombophilic states and the use of diuretics. It might be advisable to do laboratory monitoring for coagulation profiling and, in children at risk, prophylactic treatment with AT III before administering albumin infusion and diuretics.     

Platelet activation markers in patients with nephrotic syndrome. A comparative study of different platelet function tests

BACKGROUND/AIM: Enhanced platelet reactivity may play a significant role in the genesis of the hypercoagulable state of nephrotic syndrome. However, the role of platelet function testing in nephrosis is controversial, partly because the methods used to assess platelet function (platelet aggregation and immunoassays of plasma beta-thromboglobulin and platelet factor 4) have such marked methodological problems. In the present study, we evaluated several tests assessing platelet function in 18 adult patients with idiopathic nephrotic syndrome and normal renal function. METHODS: Platelet function was assessed by measurement of plasma beta-thromboglobulin (enzyme-linked immunosorbent assay, ELISA), plasma P-selectin (ELISA), circulating platelets exposing the activation-dependent antigens P-selectin (CD62P) and lysosomal GP53 (CD63) (flow cytometry), and by aggregation response to agonists such as ADP and collagen. Results were compared to those obtained in a group of 16 age- and gender-matched healthy subjects. RESULTS: Levels of plasma beta-thromboglobulin (p = 0.001), plasma P-selectin (p < 0.001), and CD62P/CD63-positive platelets (p < 0.001 for both) were increased in nephrotic patients as compared to healthy controls. Platelet hyperaggregability in vitro was found in 13/18 patients. The reproducibility of platelet activation markers, as assessed by blood sample collection a week later from all patients, was found to be higher for plasma P-selectin (Spearman correlation coefficient, R = 0.99) and circulating activated platelets (CD62P: R = 0.97; CD63: R = 0.96) than for plasma beta-thromboglobulin (R = 0.78). CONCLUSIONS: Pronounced platelet activation takes place in nephrotic syndrome and may contribute to the hypercoagulability of nephrosis. Whole blood flow cytometry assay of platelet activation and plasma P-selectin assay may represent useful tests to assess the hypercoagulable state in nephrotic patients.     

Complications of the nephrotic syndrome and their treatment

The nephrotic syndrome occurs in association with a diverse array of primary and secondary glomerular disorders. Despite the different etiologies, many of the clinical effects are similar. This review focuses on the pathogenesis and treatment of edema formation, hyperlipidemia, and the hypercoagulable state. Major abnormalities of the endocrine system and evidence of erythropoietin deficiency will be reviewed. Finally, non-specific treatments aimed at reducing proteinuria will also be discussed.     

A case of heterozygous protein C deficiency associated with nephrotic syndrome and deep femoral artery thrombosis

A 54-year-old male patient with heterozygous Protein C deficiency associated with the nephrotic syndrome and deep femoral artery thrombosis is described. He was admitted to the hospital because of nephrotic syndrome. A few days later, severe pain appeared in his left leg and a diagnosis of deep femoral artery thrombosis was made. Thrombectomy was performed immediately. His proteinuria disappeared in response to corticosteroid. He was found to have Protein C deficiency, antigen: 44%, activity 31%, which was also present in his father and son. Digital subtraction angiography (DSA) revealed the obstruction of left internal iliac and deep femoral arteries at their origins. Renal and hepatic biopsy revealed minor glomerular abnormalities, and chronic active hepatitis. The presence of heterozygous Protein C deficiency, nephrotic syndrome and chronic active hepatitis seem to cause marked decrease in serum Protein C level and deep femoral artery thrombosis. He is now under successful control with warfarin (1.7 mg/day) and bucolome (300 mg/day). It was reported that Protein C might have a suppressive effect on hypercoagulability in nephrotic syndrome. Therefore, Protein C deficiency may not counteract the hypercoagulable state and promote thrombus formation in the case. The present report is the first of a case of Protein C deficiency associated with nephrotic syndrome and arterial thrombosis.     

D二聚体与原发性肾病综合征临床及病理的相关分析

目的 对血清D二聚体（D-Dimer,简称D-D）与原发性肾病综合征（primary nephrotic syndrome,PNS）临床及病理资料相关性进行分析,探讨血清D-D在PNS中的临床意义.方法 符合肾病综合征的诊断标准及本研究排除标准的肾病综合征患者为PNS组,健康体检者为对照组,收集一般临床指标和患者的病理资料,进行病例对照研究与临床及病理资料分析.结果 （1）120例PNS患者血清D-D水平较60例正常人的血清D-D水平明显升高,差异有统计学意义（P＜0.05）.（2）临床资料显示120例PNS患者中,血清D-D水平与C-反应蛋白（CRP）、24 h尿蛋白之间存在正相关（r=0.429,P=0.000;r=0.481,P=0.000）,但与白蛋白（Alb）、血尿素氮（BUN）、血肌酐（SCr）、血清三酰甘油（TG）、血清总胆固醇（CHOL）之间无相关性（P＞0.05）.（3）微小病变型肾病、系膜增生性肾小球肾炎、系膜毛细血管性肾小球肾炎、膜性肾病及局灶性节段性肾小球硬化5种病理类型间血清D-D水平相比有统计学意义（P＜0.05）,其中微小病变型肾病和膜性肾病患者的血清D-D水平均较其他3种病理类型患者的血清D-D水平明显升高,有统计学意义（P＜0.05）,而微小病变型肾病和膜性肾病患者间及其余3种病理类型患者间的血清D-D水平相比无统计学意义（P＞0.05）.结论 PNS存在高凝状态,血清D-D水平可间接提示蛋白尿严重程度,并且可能间接预测PNS病理的类型.     

Cerebral venous thrombosis in minimal change nephrotic syndrome]

A 46-year old man presented with an eight-day history of edema and was found to be nephrotic, with a plasma albumin level of 1.1 g/dl and urine protein excretion of 13.3 g/24 hrs. The level of plasma creatinine was normal at 1.0 mg/dl. A finding of renal biopsy was consistent with minimal change glomerulopathy. On the 6th hospital day, he suddenly developed a severe headache and was noted to have bilateral papilledema. Lumbar puncture revealed an opening pressure of 250 mm of water. Magnetic resonance venography showed an irregular flow in the superior sagittal sinus and right transverse sinus, a finding consistent with thrombus. The diagnosis of cerebral venous thrombosis was made, and the patient was given both Warfarin 2 mg/day and prednisolone 60 mg/day. A complete recovery from nephrotic syndrome was achieved within eight weeks. Nephrotic syndrome causes a hypercoagulable state, leading to both venous and arterial thrombosis. The most common clinical features are renal vein thrombosis, femoral vein thrombosis, and pulmonary embolism, however, cerebral venous sinus thrombosis is rare in patients with nephrotic syndrome. It is important to be aware of this complication, since prompt treatment with anticoagulation and control of nephrotic syndrome can lead to a successful outcome.     

Treatment of renal vein thrombosis associated with nephrotic syndrome

Renal vein thrombosis is a rare entity in which true incidence is unknown. The disease occurs most frequently in patients with nephrotic syndrome, but it also can occur in the presence of other hypercoagulable state. Two cases of renal vein thrombosis with nephrotic syndrome which were treated by thrombectomy are reported here. One patient was successfully treated by renal vein and inferior vena cava thrombectomy before developing severe pulmonary embolism. The other was treated by renal vein thrombectomy by which fatal shock was able to be prevented. In those cases, immediate operation was indicated, primarily to prevent additional, possibly fatal, pulmonary embolism and also to improve perfusion of the kidney. In the hope of salvaging the kidney, thrombectomy may be the treatment of choice for acute renal vein thrombosis, complication of pulmonary embolism and inferior vena cava thrombosis, right renal vein thrombosis without collateral flow and acute renal vein thrombosis with shock.     

Bilateral renal infarctions and lower limbs artery thrombosis in a patient with nephrotic syndrome

Thromboembolism is a well-recognized complication in patients with nephrotic syndrome owing to their hypercoagulable status. Usually, the venous system is affected, whereas the very rare occurrence of arterial thrombosis is mainly restricted to pediatric patients. This complication often results in high rates of mortality and limb loss. We report the case of an adult female patient with histologically diagnosed minimal change disease and nephrotic syndrome associated with malignant thymoma, who eventually developed concurrent bilateral kidney and lower limb thrombosis. Conservative systemic anticoagulation was administered and she recovered ample kidney function. In addition, although she underwent an emergent thrombectomy of the left popliteal artery, an amputation was necessary. To the best of our knowledge, this is the first reported arterial thrombosis case involving bilateral kidney and lower limb simultaneously in nephrotic patients. Our experience indicates that arterial thrombosis is a serious complication in nephrotic patients, and early detection and aggressive management are crucial in these patients to improve their outcome.