Development of hyperthyroidism in a patient with idiopathic nephrotic syndrome

We present a 13-year-old boy who developed hyperthyroidism during the clinical course of idiopathic nephrotic syndrome treated with glucocorticoid. He had a second relapse of minimal change nephrotic syndrome, and complete remission of nephrotic syndrome was achieved immediately with oral glucocorticoid. However, when the steroid dosage was reduced, signs of hyperthyroidism such as systolic hypertension and tachycardia were observed. Laboratory findings revealed thyroid-stimulating hormone (TSH) below 0.05 μU/ml, free tri-iodothyronine of 16.1 pg/ml, free thyroxine of 5.6 ng/dl, and anti-TSH receptor antibody of 90%. Thus, a diagnosis of hyperthyroidism was made and treatment with thiamazol was started. Massive proteinuria may decrease the activity of hyperthyroidism due to urinary loss of thyroid hormones. A decrease in glucocorticoid dosage may also be involved in the development of hyperthyroidism due to a reduced immunosuppressive effect. Received: 11 July 2001 / Revised: 22 October 2001 / Accepted: 27 November 2001     

Management of steroid-sensitive nephrotic syndrome in children with type 1 diabetes

Four children with steroid-sensitive nephrotic syndrome (SSNS) coexisting with type 1 diabetes are presented. This number is higher than expected according to the estimated prevalence rates for each disease separately. In three, diabetes preceded nephrotic syndrome (NS), and in one it developed almost simultaneously. None of the patients had hypertension or retinopathy. Two had a renal biopsy: in one it was compatible with minimal change histology (MCH), and the other had MCH and early diabetic nephropathy changes. In addition to the two presented here, in 11 of 12 previously reported cases with biopsy proven SSNS coexisting with type 1 diabetes, the biopsy showed MCH. In none was treatment influenced by biopsy results. However, our experience suggests that daily steroid taper allows easier glycaemic control than alternate day steroids. We conclude that the indications for a renal biopsy in nephrotic children with and without insulin-dependent diabetes mellitus (IDDM) should be similar. Received: 27 July 2001 / Revised: 15 January 2002 / Accepted: 15 January 2002     

Asymptomatic intracardiac thrombus in steroid-sensitive nephrotic syndrome

Arterial and venous thrombotic events can lead to severe complications in the nephrotic syndrome, but may remain clinically silent in a substantial proportion of patients. Intracardiac thrombi associated with multiorgan thrombosis have been described in autopsy cases of the earlier literature, but have never been documented in vivo. We here report an asymptomatic intracardiac thrombus in a child with frequently relapsing steroid-sensitive nephrotic syndrome and a ventricular septal defect. Received: 7 May 2001 / Revised: 19 November 2001 / Accepted: 24 November 2001     

Premature acute myocardial infarction in a child with nephrotic syndrome

We report a case of acute myocardial infarction in a nephrotic child. A 7-year-old boy with a 4-year history of steroid-unresponsive nephrotic syndrome due to mesangial proliferation disease presented with acute vomiting and chest pain. An electrocardiogram showed ST elevation and pathological Q waves in leads consistent with anterior and septal myocardial infarction. Subsequent cardiac catheterization showed no evidence of atherosclerotic coronary artery disease, and thrombotic occlusion of the anterior descending coronary artery was the likely cause of the event. Myocardial scintigraphy showed extensive myocardial damage. The child had no long history of extreme hypercholesterolemia or hypertriglyceridemia. The case suggests that children with long-lasting nephrotic syndrome may be at increased risk for ischemic cardiovascular events, due to hyperlipidemia as well as a hypercoagulability state. The literature is reviewed regarding the relationship between nephrotic syndrome and the incidence of ischemic heart disease. Received: 2 May 2001 / Revised: 31 October 2001 / Accepted: 18 November 2001     

60例慢性肾脏疾病患者血液流变学改变的研究

目的通过对60例慢性肾脏疾病患者血液流变学检测结果的分析,探讨其临床应用价值.方法应用国产XBH-31型旋转式粘度计和XH-10型血栓形成仪,对正常对照组、慢性肾小球肾炎、肾病综合征、慢性肾功能衰竭患者血液流变学指标进行检测并对结果进行分析.结果慢性肾小球肾炎、肾病综合征患者全血粘度、血浆粘度、血栓湿重及血栓干重高予正常对照组,具有统计学意义（P＜0.01）;慢性肾功能衰竭患者各项检测指标明显低于正常对照组,具有统计学意义（P＜0.05）.结论慢性肾小球肾炎、肾病综合征发展过程中伴有血液流变学改变,血液凝固性增加,治疗中应注意采用抗凝疗法;慢性肾脏疾病发展到慢性肾功能衰竭时血液凝固性降低,治疗过程中应注意防治出血并发症.     

11例肾病综合征并发肺栓塞临床病理分析

目的探讨肾病综合征并发肺栓塞的临床病理特征以及相关危险因素。方法对2001年～2004年期间收治的11例肾病综合征并发肺栓塞患者进行回顾性分析。结果肾病综合征并发肺栓塞通常起病隐匿,临床症状不典型;大量或长期应用激素和利尿剂,低蛋白血症,高脂血症,以及特殊的病理类型等均可能是导致肺动脉栓塞的危险因素。结论肾病综合征并发肺栓塞容易漏诊和误诊,重视肾病综合征并发肺栓塞的危险因素,对早期诊断和改善预后非常重要。     

尿RBP、β2-MG、NAG对原发性肾病综合征患儿激素治疗敏感性的预测意义

目的通过测定原发性肾病综合征患儿尿视黄醇结合蛋白（RBP）、β2-微量球蛋白（β2-MG）和N-乙酰-β-D氨基葡萄糖苷酶（NAG）,了解肾病综合征患儿肾小管功能与激素治疗效果之间的关系.方法测定60例小儿原发性肾病综合征患儿治疗前和激素治疗8周后尿RBP、β2-MG和NAG含量,根据治疗后尿蛋白水平将患儿分为完全效应、部分效应和无效应3组,比较各组间治疗前、后肾小管功能指标变化.结果治疗前3组患者尿RBP、NAG、β2-MG和蛋白质含量间差别均无显著性意义（P＞0.05）.治疗后3组患儿RBP、β2-MG、NAG的含量间差别均有显著性意义（P＜0.05）;部分效应组与无效应组RBP、β2-MG、NAG含量间差别有显著性意义（P＜0.05）;完全效应组与无效应组RBP、β2-MG和NAG含量间差别亦有显著性意义（P＜0.05）.结论尿RBP可预测原发性肾病综合征患儿激素治疗的敏感度,且效果优于β2-MG和NAG.     

六味地黄丸对糖皮质激素治疗肾病综合征增效减毒作用的临床研究

目的探讨六味地黄丸对糖皮质激素治疗肾病综合征增效减毒作用.方法采用随机分组对照法,将符合标准的92例患者分为试验组和对照组,两组均给予泼尼松,并予必要的对症处理.同时试验组48例,加服六味地黄丸.结果试验组总体疗效、Ⅰ型者疗效均显著优于对照组（P＜0.05）;尿蛋白定量、血浆白蛋白、TG、TC等指标两组均改善显著（P＜0.05、0.01）,但均以试验组为优（P＜0.05）;其复发率亦以试验组为低（P＜0.05）.试验组出现的阴虚火旺证候积分值及副作用的发生率均较对照组为低（P＜0.05、0.01）.结论六味地黄丸能显著提高激素治疗肾病综合征的疗效、减少肾病综合征的复发,并能对抗激素的副作用,值得临床推广应用.     

重组生长激素改善肾病综合征患者低蛋白血症的研究

目的观察基因重组生长激素(recombinanthumangrowthhormone,rhGH)对肾病综合征(nephro-ticsyndrom,NS)患者血清总蛋白、白蛋白、胰岛素样生长因子-1(insulin-likegrowthfactor-1,IGF-1)和胰岛素样生长因子结合蛋白-3(insulin-likegrowthfactorbindingprotein-3,IGFBP-3)的作用。方法原发性NS患者100例,随机分为2组,治疗组50例,在常规治疗的基础上加用rhGH治疗;对照组50例用常规治疗。以放射免疫法测血清IGF-1及IGFBP-3水平,S-丽春红测24h尿蛋白定量,全自动生化仪检测血清蛋白。结果①rhGH治疗2周后血清IGF-1、IGFBP-3和血清蛋白与对照组相比显著上升;②rhGH治疗组与NS对照组相比尿蛋白排出差异无统计学意义。结论短期小剂量使用外源性rhGH能在不增加尿蛋白排出的情况下提高NS患者血清蛋白水平,且安全可靠。     

Glomerulosclerosis in Adriamycin-induced nephrosis is accelerated by a lipid-rich diet

The present study was performed to determine quantitatively the effect of hypercholesterolemia induced by a lipid-rich diet on glomerulosclerosis in an animal model of nephrotic syndrome (NS) induced by Adriamycin (ADR). Twenty NS Wistar rats administered ADR with a single intravenous dose of 5 mg/kg body weight were divided into standard and lipid-rich chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as controls. Quantitative analyses of renal histological changes were performed with determination of blood and urine biochemical parameters. It was found that serum cholesterol was markedly higher in rats with lipid-rich chow in both NS and non-NS rats. Urinary protein was significantly higher in rats on the lipid-rich diet in the NS group. The mesangial matrix and cell indices were significantly increased in rats with the lipid-rich diet and the most obvious changes were found in the NS group. Lipid deposits and foam cells were observed in mesangial areas, and some glomeruli had progressed to form focal and segmental glomerulosclerosis in the NS group. Findings indicated that diet-induced hyperlipidemia can lead to proliferation of mesangial cells and accumulation of mesangial matrices, and further aggravate glomerulosclerosis in Adriamycin-induced nephrosis. Received: 1 March 2000 / Revised: 11 July 2000 / Accepted: 14 July 2000