双手双足痛风性关节炎合并巨大痛风结节钙化1例

患者,男,63岁,双手、双足肿痛10余年,反复发作,期间可自行缓解,近期加重6月余。查体：右手掌指关节及双足第1跖趾关节肿胀明显,扪之较硬,多处有结节,最大约2．5cm×3．2cm。右手掌背侧皮肤稍红,有压痛,中央有一破溃口,挤压有白色团粉状物流出。实验室检查：血沉38mm／h,血清尿酸518μmol／L,WBC 10．1×10^9/L,RBC 4．1×10^12／L,HGB 120g／L。X线检查：右手掌指关节、双足第1跖趾关节肿胀,密度增高,关节周围可见砂粒状、斑块状钙化;邻近关节面有小囊状破坏缺损,破坏区边缘锐利,部分呈穿凿状改变;     

肾病综合征并发双肾静脉血栓形成一例

患者女,29岁.1个月前,患者感左侧腰部胀痛,外院彩超发现盆腔积液,抗感染治疗好转;3周前无明显原因出现右侧腰部胀痛,伴双下肢水肿,外院查血常规、肾功能正常,尿蛋白+,彩超示双肾增大,左肾轻度积水,左肾输尿管上段扩张,经保肾降脂等治疗病情无缓解;2d前出现无尿,伴恶心、呕吐、腹泻;1h前,腰痛加剧,伴血尿2次,共约150 ml,入本院.     

痛风克汤对痛风性肾病的临床疗效观察

痛风性肾病是嘌呤代谢紊乱和/或尿酸排除障碍引起的长期高尿酸血症,导致尿酸盐沉积于肾脏所致。据不完全统计,发病5-10年后,可严重损害肾功能而致尿毒症给患者及家属造成严重身心影响。笔者从2000年3月-2005年9月观察了旷惠桃教授之经验方———痛风克汤对58例痛风性肾病患者的治疗效果,现报告如下。     

痛风饮治疗痛风性关节炎113例

痛风性关节炎是嘌呤代谢紊乱所引起的,临床表现以关节红肿、灼热、疼痛反复发作为主,日久关节变形,并伴有痛风石形成。随着人民生活水平的提高和饮食结构的改变,本病发病率逐年上升。我们2000年8月—2005年12月采用中药内服外敷治疗113例,取得满意疗效,现总结报告如下。1临床资料113例中男98例,女15例;年龄27~76岁,平均47.1岁。病程3d~15年,平均6.5年。病变侵犯第一跖趾关节者96例,踝关节者14例,掌指关节者3例。2治疗方法2.1中药内服痛风饮(自拟)组成:茜草20g,泽兰20g,赤芍30g,二花30g,元参30g,两头尖20g,金果榄12g,大黄6g,黄柏15g,山慈菇12…     

特发性肾静脉血栓形成一例

患者 女性,37岁,半个月前出现急性右腰腹疼痛,伴肉眼血尿,于当地医院诊断为泌尿系统结石,对症治疗后疼痛稍缓解,但血尿进行性加重,CT增强扫描提示右肾静脉、下腔静脉血栓形成,右肾肿大,右肾实质显影延迟.     

马蹄肾合并肾病综合征一例

正马蹄肾(horseshoe kidney,HSK)是最常见的先天性泌尿道融合畸形,其具有3个解剖特征即异位、旋转不良、血管变异~([1])。马蹄肾患者可发生一系列泌尿生殖并发症如输尿管肾盂连接处梗阻、泌尿系结石、泌尿系感染、肾脏良恶性肿瘤等~([1-3])。HSK合并肾病综合征(nephrotic symdrome,NS)在临床上比较罕见,现报一例年轻女性病例如下。     

指关节痛风结节30例临床分析

痛风（gout）是以嘌呤（purine）代谢障碍和血尿酸持续升高导致尿酸盐在组织沉积而引起一系列临床症状的多基因型疾病,发病率1%以上。随着人们生活水平的提高,其发病率有增加的趋势,痛风已逐渐成为临床的常见病、多发病[1]。该病好发于男性,大多发生于40岁以上。     

痛风性肩关节炎伴痛风石误诊一例并文献复习

痛风性关节炎是由于尿酸结晶沉积于关节腔或关节周围组织引起的炎症反应,累及肩关节少见。本文报告1例患者,男,49岁,主诉右肩疼痛9个月,加重伴活动受限2周。右肩外旋10°,背手达S5水平,MRI示右肩积液及关节内游离体。以右肩关节游离体、滑膜软骨瘤病可能收入院。关节镜探查见大量尿酸结晶沉积于滑膜、软骨及肩袖组织,行游离体取出及关节清理术。术后病理学检查提示滑膜炎性增生伴尿酸结晶沉积。通过文献回顾分析痛风性肩关节炎的临床特点、诊断及治疗方法。痛风性肩关节炎的临床表现主要为肩关节疼痛及活动受限。含钙盐沉积的痛风结石可以在X线和CT上显影;MRI可显示痛风结石,并能够评估关节内其他病变。痛风性肩关节炎临床表现不典型,影像学上无特异性征象,病理诊断是"金标准"。肩关节镜手术既能明确疾病诊断,又能完成治疗,是痛风性肩关节炎可靠的诊疗方法。     

先天性孤立肾并发肾病综合征一例

先天性孤立肾并发肾病综合征一例空军石家庄医院丁军广州南方医院张训患者女，４６岁，因蛋白尿，血尿一年余，浮肿、腹胀一月入院。查体：血压１４／９ｋＰａ，心肺无异常发现，腹部饱满，移动性浊音（＋），双下肢轻度指凹性浮肿。多次Ｂ超检查示左肾缺如，右肾８．８ｃ...     

Familial nephropathy with hyperuricemia and gout

Chronic interstitial nephropathy with disproportionate hyperuricemia (serum uric acid 10.5-14.8 mg/dl [625-880 mumol/l] at a GFR of 40 ml/min/1.73 m2) was observed in 2 girls and their mother who suffered from gout since the age of 20 years. Urinary excretion of uric acid was normal. Renal biopsies in the 3 patients showed focal tubulointerstitial nephropathy. Absolute values of GFR remained stable in the 2 pediatric patients over a period of 10 years, whereas the older patient required dialysis at the age of 34 years. We speculate that this family suffers from a primary interstitial nephropathy which is accompanied by a subtle defect in tubular excretion of urate. A few similar observations have been reported in literature which suggests that dominantly inherited interstitial nephropathy with hyperuricemia and gout represents a distinct entity.     

BK virus nephropathy in a patient with ABO-incompatible renal transplantation

Abstract:  A 43-year-old woman with end-stage renal disease originating from IgA nephropathy entered chronic haemodialysis therapy. She then received an ABO-incompatible living related renal transplantation. Initial immunosuppression consisted of azathioprine, methylprednisolone and tacrolimus. At 155 days after transplantation, the azathioprine was changed to mycophenolate mofetil for continuous graft dysfunction. Furthermore, a total of three courses of anti-rejection therapy was given. At 665 days after transplantation, diagnosis of BK-virus nephropathy was made by immunohistochemical analysis and viral DNA assay. Therefore the immunosuppression therapy was reduced for graft dysfunction. All five renal biopsy specimens were examined retrospectively in order to determine when the BK virus nephropathy had developed. The expressions of SV40 large T antigens were detected from the third (117 days) to the fifth (665 days) biopsies, with increasing numbers of SV40 large T antigen positive cells. In addition, many cells contained inclusion bodies which were already present in the urinary sediment for 3 months post-transplantation. Although it is difficult to make a diagnosis of early stage of BKVN, we have to consider with caution if urinary cells with inclusion body are seen. Awareness of BKVN at the earliest opportunity is important in order to avoid over-immunosuppression.     

Reflux nephropathy in a patient with crossed renal ectopia with fusion

Crossed renal ectopia with fusion is a rare congenital anomaly of the urinary tract. While vesicoureteral reflux has been noted frequently, reflux nephropathy has rarely been reported with this anomaly. I describe here a case of reflux nephropathy in a patient with crossed renal ectopia with fusion. A 14-year-old boy was referred to our hospital for further examination of proteinuria, detected by the school's annual urinary screening program. Laboratory study revealed proteinuria and renal insufficiency. Abdominal computed tomography and voiding cystography disclosed crossed renal ectopia with fusion and vesicoureteral reflux in each moiety. Renal biopsy of the orthotopic kidney showed diffuse interstitial fibrosis and mononuclear cell infiltration, periglomerular fibrosis, glomerular hypertrophy, and focal and global glomerulosclerosis, which were compatible with reflux nephropathy. A low-protein diet and an administration of angiotensin converting enzyme inhibitor decreased the urinary excretion of protein.     

A female patient with malarial nephropathy

Malaria remains one of the worlds major health problems, particularly in developing tropical countries. Imported malaria is reportedly increasing in Western countries. Acute renal failure (ARF) is the most common cause of death in severe malaria. We report the case of a 63-year-old female patient with a history of travel to a rural area in South Africa who was in coma and had a high fever on admission. Thirty percent of her erythrocytes were infected with Plasmodium falciparum. She had cerebral malaria, malarial nephropathy, anemia, hepatic dysfunction, and disseminated intravenous coagulation (DIC). Quinine and artesunate treatment decreased the number of parasites in the blood. To manage renal failure, hemodialysis was performed for 11 days. A relationship between ARF and hepatic dysfunction was suggested. This relationship is an indication of the clinical course of the disease. In this article, we discuss the mechanism underlying the development of malarial nephropathy and its management, particularly the usefulness of hemodialysis.     

Absence of HIV antigens in renal tissue from patients with HIV-associated nephropathy

HIV-associated nephropathy (HIV-N) is considered a distinctive disease, the pathogenesis of which is still undefined. Direct virus-induced renal cell damage has been postulated. The numerous cytolytic ultrastructural changes and a few studies by immunoperoxidase support this hypothesis, but there has been no demonstration of virus by electron-microscopy (EM) or by tissue culture. In seven out of 12 cases with histological characteristics of HIV nephropathy, with proteinuria (five cases) or with nephrotic syndrome (two cases), we tested renal tissue for HIV antigens: core p18 and p25; envelope gp45 and gp110, by means of immunoperoxidase avidin-biotin complex monoclonal antibodies (MoAbs). Light-microscopy (LM) showed in five patients a focal and segmental glomerular sclerosis, and in two a mesangial hyperplasia with vacuolisation of visceral epithelium and protein inclusions. Electron-microscopy, performed in five of seven patients, showed several protein inclusions in podocyte cytoplasm, tubuloreticular inclusions in endothelial cell cytoplasm in all cases, nuclear degranulation of tubular cells in four cases and nuclear bodies in two. HIV antigens by MoAbs on renal tissue were negative in all cases, in both glomeruli and tubules. These results do not confirm the presence of HIV proteins in renal tissue of patients with HIV nephropathy. A possible explanation, apart from no direct HIV in the disease, may be the low viral load in tissues, because of the early phases of renal damage in most cases.     

羟乙基淀粉代血浆致渗透性肾病重复肾活检一例

我们收治1例肾病综合征用羟乙基淀粉代血浆(HES)引起慢性肾功能衰竭,首次肾活检病理示渗透性肾病;6个月后重复肾活检病理示严重慢性肾小管间质病变,肾小球缺血性改变.报告如下.     

Polyoma virus-induced hemorrhagic cystitis in renal transplantation patient with polyoma virus nephropathy

We report a biopsy proven case of hemorrhagic cystitis in a cadaveric renal transplant patient with hematuria. Because more and more polyoma virus infection is being diagnosed in kidney transplant recipients, clinicians should be aware that gross hematuria in a recent transplant recipient may represent polyoma virus-induced hemorrhagic cystitis.     

羟乙基淀粉代血浆致渗透性肾病重复肾活检一例

我们收治1例肾病综合征用羟乙基淀粉代血浆(HES)引起慢性肾功能衰竭,首次肾活检病理示渗透性肾病;6个月后重复肾活检病理示严重慢性肾小管间质病变,肾小球缺血性改变.报告如下.