拟诊高血压肾硬化患者的临床病理分析

该文探讨拟诊高血压肾硬化（HN）患者的临床特征及影响预后的因素，以期提高临床对该病诊断及治疗的认识。方法：回顾性分析最初拟诊HN且有肾活检诊断的患者63例的临床资料。根据肾脏病理学结果分为原发性肾炎（PN）组、良性肾小动脉硬化症（BN）组及恶性肾小动脉硬化症（MN）组，比较各组间临床参数及组织学特征。对确诊HN的患者分析影响其预后的临床及病理因素。结果：临床拟诊为HN的患者63例经肾组织活检病理诊断，37例（58．7％）为BN；12例（19．0％）为MN；14例（22．2％）为PN，HN诊断符合率为77．79，6。BN组患者男性较多，年龄较大，高血压家族史比例及高血压病程明显高于PN组，而PN组尿蛋白定量高于BN及MN组。MN组左心室心肌重量指数（LVMI）高于PN组。BN组视网膜病变主要为0～Ⅱ级，占78％，而MN组则主要为Ⅲ～Ⅳ级。PN组球性硬化肾小球比率及小管慢性化指数（cI）积分均高于MN及BN组。MN及BN组肌内膜细胞增殖、小动脉玻璃样变等血管病变均较PN组明显，其中BN组改变最为显著。多因素回归分析提示收缩压（SBP）、尿蛋白定量、尿酸（UA）、总胆固醇（TC）是影响肾脏病进展的危险因素，优势比分别为2．563、2．467、2．323、2．357。结论：临床拟诊HN的患者不能排除PN。部分HN与PN患者临床表现相似。单纯依据病史及实验室检查难以区分。肾组织病理检查是确诊的最佳手段。SBP、尿蛋白、TO、UA等因素可加速HN的病变进展。     

拟诊高血压肾硬化患者的临床病理分析

该文探讨拟诊高血压肾硬化(HN)患者的临床特征及影响预后的因素,以期提高临床对该病诊断及治疗的认识。方法:回顾性分析最初拟诊HN且有肾活检诊断的患者63例的临床资料。根据肾脏病理学结果分为原发性肾炎(PN)组、良性肾小动脉硬化症(BN)组及恶性肾小动脉硬化症(MN)组,比较各组间临床参数及组织学特征。对确诊HN的患者分析影响其预后的临床及病理因素。结果:临床拟诊为HN的患者63例经肾组织活检病理诊断,37例(58.7%)为BN;12例(19.0%)为MN;14例(22.2%)为PN,HN诊断符合率为77.7%。BN组患者男性较多,年龄较大,高血压家族史比例及高血…     

高血压肾损害的临床病理特点及预后

目的:探讨行肾活检的高血压肾损害(HN)患者的临床、病理特点及长期预后,比较良性肾动脉硬化(BN)及恶性肾动脉硬化(MN)组患者的临床病理特征。方法:选取2003年1月至2012年12月在南京军区南京总医院肾脏科经临床及肾活检明确诊断的HN患者179例,回顾性分析其临床病理特点,探讨影响肾脏预后的危险因素。结果:HN患者平均年龄(43.8±11.2)岁,本组患者以男性为主(82%),肾活检时中位高血压病程5.0年,最高收缩压及舒张压分别为(196.5±35.9)mm Hg和(127.8±25.6)mm Hg,中位血清肌酐(SCr)144.1μmol/L,中位估算的肾小球滤过率(e GFR)47.1 ml/(min·1.73m2),中位蛋白尿0.8 g/24h。BN和MN的比例分别为54.7%及45.3%。MN组患者与BN组患者相比,高血压病程短、平均血压水平高,SCr及尿酸高、蛋白尿多,贫血较严重,靶器官损害(眼底、心脏)发生率高,且终末期肾脏病(ESRD)的发生率高。本组HN患者肾活检后随访时间0.3~10.8年,中位时间为2.9年,33例(18.4%)患者进入ESRD,5年和10年累积肾存活率分别为82.6%、38.4%。肾活检时e GFR下降、蛋白尿水平上升、动脉的恶性病变、肾小球硬化比例高是HN患者进展至ESRD的独立危险因素。结论:HN患者肾活检时e GFR、蛋白尿量,动脉恶性病变、肾小球硬化比例等对肾脏预后具有独立预测价值;MN和BN组患者临床、病理表现及预后明显差异。     

肾小球疾病患者肾间质泡沫细胞的分布及其临床意义

目的：观察肾小球疾病患者肾间质泡沫细胞的分布特点,分析其与临床表现及肾组织病理改变之间的联系.方法：选取经临床病理明确诊断的Alport综合征（AS）125例,特发性膜性肾病（IMN）192例,IgA肾病（IgAN）388例,局灶节段性肾小球硬化（FSGS）137例.观察肾组织泡沫细胞的分布,并对肾间质有无泡沫细胞患者的临床和病理进行比较.结果：（1）AS、IMN、IgAN、FSGS四种疾病肾组织中均存在肾间质泡沫细胞,发生率分别为64.8%、21.4%、12.4%、36.5%,其中以AS中最为多见.（2）肾间质泡沫细胞组肾小球节段硬化的发生率及硬化比例均显著高于无泡沫细胞的对照组,AS、IgAN患者泡沫细胞组间质纤维化程度重于对照组.（3）AS、IgAN患者肾间质泡沫细胞组尿蛋白、血脂水平显著高于对照组（P＜0.01）.FSGS患者肾间质泡沫细胞组三酰甘油水平显著高于对照组,但两组间尿蛋白水平未见差异.结论：肾间质泡沫细胞在AS、IMN、IgAN、FSGS患者中均可以发现,但以AS患者最多见.肾间质泡沫细胞的形成与尿蛋白、血脂的水平有关.肾间质泡沫细胞的存在可能与肾组织慢性化病变形成有关.     

1217例肾活检患者临床与病理资料分析

目的 了解行肾穿刺活检患者的流行病学特点及病理类型与临床表现间的关系.方法 回顾性分析1217例行肾活检者的性别、年龄、病理类型及临床表现等相关资料.结果 1217例患者行肾活检时的平均年龄为（30.86±13.41）岁,男性612例（50.3％）,女性605例（49.7％）.男性占本组原发性肾小球疾病（PGN）的52.2％,继发性肾小球疾病（SGN）的39.0％.肾脏病患者的高发年龄段为20 ～39岁（50.9％）.本组患者最常见的临床表现为肾病综合征（NS）610例（50.1％）,其余分别为尿检异常型（Uab）453例（37.2％）,反复发作性肉眼血尿型（rGH）89例（7.3％）,慢性肾衰竭（CRF）31例（2.5％）,急性肾损伤（AKI） 12例（1.0％）,高血压型（HT）11例（0.9％）,急性肾炎综合征（ANS）8例（0.7％）,孤立性肉眼血尿型（iGH）3例（0.2％）.原发性肾小球疾病以系膜增生性肾炎（MsPGN）,继发性肾小球疾以狼疮性肾炎（LN）为主要病理类型.本组患者中各临床分型均以系膜增生性肾炎为主要病理类型,除系膜增生性肾炎外,肾病综合征以MN,Uab以IgAN为主要病理类型.结论 原发性肾小球疾病是徐州地区最常见的肾脏疾病,男性、青壮年是高发人群,系膜增生性肾炎是最常见病理类型,肾病综合征是最常见的临床表现.     

IgA肾病预后不良因素与肾血管病变相关性分析

目的：探讨IgA肾病（IgAN）肾血管病变的危险因素。方法选择宁夏人民医院肾脏内科2010年10月至2013年7月经肾活检确诊的原发性IgAN患者100例,并将其分为肾血管病变组和无肾血管病变组,进行对照研究,比较肾血管病变与各项临床指标、病理改变之间的关系。结果100例IgAN患者中有肾血管病变者70例（70%）,无肾血管病变者30例（30%）。单因素分析结果表明,肾血管病变组24h尿蛋白、血尿酸、血肌酐均高于无肾血管病变组（P＜0.05）,血清白蛋白低于无肾血管病变组（P＜0.05）;病理学检查显示肾小球硬化、肾间质纤维化、新月体形成、炎性细胞浸润、肾小管萎缩严重病理表现发生率,肾血管病变组明显高于无肾血管病变组（P＜0.05）。多因素非条件logistic回归分析结果表明,高血压（OR＝7.728,95%CI 1.708～34.964）、24h尿蛋白定量（OR＝20.022,95%CI 3.869～103.623）、肾小球硬化（OR＝12.093,95%CI 2.431～60.149）、肾间质纤维化（OR＝8.511,95%CI 1.332～54.396）是IgAN肾血管病变加重的危险因素。结论 IgAN预后不良因素为高血压、24h尿蛋白定量、肾小球硬化、肾间质纤维化,上述指标与IgAN肾血管病变密切相关,进一步证实了肾血管病变可作为判断预后的一项重要病理指标。     

成人原发性肾小球肾炎远期预后的观察(附1 071例患者的长期随访)

目的前瞻性观察各种病理类型原发性肾小球肾炎患者的远期预后,了解影响肾小球肾炎预后的各种因素.方法1980年1月～1996年月12月间,在本院经肾活检确诊并常年定期随访的原发性肾炎患者共1071例,其中IgA肾病(IgAN)471例(44.3%)、系膜增生性肾炎(MsPGN)268例(25.0%)、IgM肾病(IgMN)80例(7.30%)、膜增生性肾小球肾炎(MPGN)68例(6.30%)、膜性肾病(MN)76例(7.10%)、局灶节段性肾小球硬化(FSGS)52例(4.80%)、毛细血管内增生性肾小球肾炎(EGN)36例(3.40%)及微小病变性肾小球肾炎(MCD)20例(1.80%).以血Cr＞800μmol/L确定为终末期肾衰(ESRF),并运用Kaplan-Meier方法计算每组患者的肾存活率.结果在平均随访39.9(13～192)个月后,共有240例(22.5%)患者发生程度不等的肾功能损害,其中ESRF的发生率为3.40%.就其病理类型分析,除MCD外,各类肾炎均有肾功能损害的发生,其中以FSGS(65.8%)及MPGN(41.2%)组的发生率最高,IgMN(25.3%)及EGN(2.70%)的预后相对较好,而IgAN(27.6%)、MN(19.7%)及MsPGN(12.7%)介于两者之间.进一步用Kaplan-Meier方法计算各组患者的肾存活率,发现各组间的肾存活率及病变进展速度均有明显的差别.病情预后的恶劣程度依次为MPGN、FSGS、IgAN、MsPGN;而MN、MCD及IgMN尚未有ESRF的现象发生.除病理类型外,疾病早期合并高血压,持续性大量蛋白尿亦对预后有重要影响.结论肾小球肾炎的预后主要取决于肾脏病理损害的性质,以微小病变、单纯性肾小球系膜或膜病变为病理改变特征的肾炎,病程进展相对较为缓慢,MPGN及FSGS的病情进展最为迅速.同一病理损害类型肾小球肾炎的预后则与起病年龄,就诊时肾功能状态,病理损害程度,高血压出现的早晚以及蛋白尿水平等因素有密切的关系.     

80例肾脏疾病患者肾活检病理资料分析

目的分析肾脏疾病病理类型,探讨其流行病学分布特征。方法统计分析2006年9月至2013年6月经皮肾活检的80例肾脏疾病患者的病理类型及其流行病学分布特征。结果临床分型:80例行肾穿刺活检的患者中,原发性肾小球疾病59例(占73.7%);继发性肾小球疾病12例(占15%);肾小管-间质疾病4例(占5%);遗传性肾病3例(占3.7%);慢性肾功能不全2例(占2.5%)。病理分型:80例行肾穿刺活检的患者中,微小病变肾病(MCD)5例(占6%);系膜增生性肾炎(MsPGN)3例(占3.7%);膜增生性肾炎8例(占10%);膜性肾病(MN)12例(占15%);局灶阶段性肾小球硬化(FsGs)5例(占6%);IgA肾病(IgAN)32例(占41%);狼疮性肾炎(LN)12例(占15%);紫癜性肾炎2例(占2.5%);乙型肝炎病毒性肝炎相关性肾炎2例(占2.5%);糖尿病肾脏病5例(占6%);硬化性肾小球肾炎2例(占2.5%);高血压肾动脉硬化2例(占2.5%)。结论通过肾活检和临床分析,不仅能明确肾脏疾病的病理类型,为临床选择最佳的治疗方案,而且能对疾病的预后作出比较正确的判断。     

肾小管周毛细血管损伤与原发高血压恶性肾硬化患者临床及长期预后的关系

正该文探讨原发性高血压恶性肾硬化(malignant nephrosclerosis,MN)患者的临床病理特点、肾小管周毛细血管(peritubular capillary,PTC)损伤情况及肾脏长期预后的影响因素。方法:纳入2003年1月1日至2012年3月30日在北京协和医院经肾脏病理诊断的MN患者52例,获取临床病理资料并进行随访,对肾活检标本进行CD34染色,对照组为良性肾硬化(benign nephrosclerosis,BN;17例)和肾小球轻微病变患者(glomerular minimal lesions,GML;19例),     

原发性局灶节段性肾小球硬化的临床病理及预后

目的:分析114例原发性局灶节段性肾小球硬化(FSGS)患者的临床、病理、免疫病理特点及预后.方法:回顾性分析1985～1996年12年间,114例原发性FSGS患者的临床表现,病理,免疫病理特点,以及其中45例长期随访结果. 结果:1985～1996年12年间,原发性FSGS占同期肾活检的2.62%,平均发病年龄28.54±12.34岁.临床表现为蛋白尿者占93.0%(肾病综合征范围蛋白尿占21.9%),血尿51.8%(肉眼血尿14.9%,镜下血尿36.8%),高血压43.8%.肾活检时已发生肾功能不全者占47.4%,随访中22.2%发展至尿毒症,激素治疗有效率小于10%.肾功能不全者与肾功能正常者相比,前者高血压更为常见(P＜0.05),小管间质病变重[尿渗量明显降低(P＜0.05),尿溶菌酶升高(P＜0.001)].肾小球全球硬化的比率显著升高(P＜0.001),节段性硬化病变更为明显,并伴有更为显著的小管间质损伤,大量炎细胞浸润. 结论:①原发性FSGS好发于中青年,病程隐匿,进展较快;②临床上蛋白尿最为常见,其次是血尿,高血压和肾功能不全.高血压,肾小球全球/节段性硬化及肾小管间质病变,肾组织细胞浸润的程度与预后相关;③对激素治疗反应差,临床治疗应着重控制高血压,保护肾功能.     

Hypertensive nephrosclerosis as a relevant cause of chronic renal failure

It is currently unclear whether hypertensive nephrosclerosis (HN), usually diagnosed solely on clinical grounds, is a relevant cause of end-stage renal disease. We biopsied 81 hypertensive outpatients (blood pressure >/=160/95 mm Hg) with moderate renal insufficiency, who were referred to our service from 1988 to 1998. Patients with known causes of hypertension, systemic disorders, rheumatic disease, or nephrotic syndrome were excluded. In 65% of patients, HN was the sole histological abnormality associated with renal dysfunction. Benign nephrosclerosis (BN), defined as isolated arteriolar hyalinosis and/or intimal fibrosis, was found in 18 HN patients (22%), whereas malignant nephrosclerosis (MN), denoted mainly by myointimal cell proliferation, appeared in 35 HN patients (43%). Previously undiagnosed primary nephritis (PN) was found in 13 patients (16%), whereas focal and segmental glomerulosclerosis, which might be either primary or secondary to hypertension, appeared in 15 patients (19%). These findings suggest that HN, in both its BN and MN forms, can be a definite cause of chronic renal insufficiency and that a substantial fraction of patients with renal insufficiency and clinical diagnosis of HN may actually have PN.     

Proteinuria in benign nephrosclerosis

Benign nephrosclerosis seldom is associated with significant proteinuria or reduced renal function. This study demonstrated that, despite the finding of benign nephrosclerosis on a renal biopsy specimen, concomitant proteinuria is predictive of a poor prognosis. Twelve patients, ranging in age from 24 to 59 years, with hypertension, proteinuria (greater than 1 g/d), and findings of benign nephrosclerosis on renal biopsy specimens were studied retrospectively. In three of these patients, the hypertension and proteinuria were diagnosed during pregnancy. Follow-up was possible in 11 patients. Nine patients became nephrotic in the course of their disease. Two patients had endstage renal disease and required maintenance dialysis treatment. Seven patients had decreased renal function as shown by the increase in serum creatinine levels. Thus, the combination of hypertension, proteinuria (greater than 1 g/d), and benign nephrosclerosis may be indicative of a progressive condition with a high percentage of patients having renal failure.     

Oliguric acute renal failure in malignant hypertension

Four cases of oliguric acute renal failure due to malignant nephrosclerosis are described. Four similar cases were found in a review of the English language literature. The main features in these patients were severe hypertension with diastolic pressures of 130 mm Hg or above, advanced hypertensive retinopathy and oliguria accompanied by rapidly progressive azotemia. Characteristically the patients demonstrated marked weight loss, left ventricular hypertrophy and microangiopathic hemolytic anemia. Kidney size was either normal or slightly reduced, and many had red blood cells and red cell casts in the urine sediment. The diagnosis of malignant nephrosclerosis was not suspected initially in any of the patients but was clearly established by renal biopsy. No restoration of renal function occurred despite vigorous antihypertensive therapy and maintenance dialysis.     

Anti-RNA polymerase III antibody-associated scleroderma renal crisis in a patient with limited cutaneous systemic sclerosis: A case report

A 69-year-old Japanese man was presented with hypertensive crisis. Renal histology revealed malignant nephrosclerosis, including an onion skin pattern with fibrinoid necrosis of the small arteries from arterioles up to interlobular arteries. Immunological investigation clarified positive anti-RNA polymerase (RNAP) III antibody, and limited cutaneous systemic sclerosis (Lc SSc) was diagnosed by skin biopsy as the underlying disease causing scleroderma renal crisis (SRC). Angiotensin covering enzyme (ACE) inhibitor therapy and calcium antagonist were effective for his renal condition. Although an association between SRC and anti-RNAP III antibody has already been reported in patients with diffuse cutaneous SSc (Dc SSc), this case indicates that SRC with hypetensive emergency with malignant nephrosclerosis can also be diagnosed on patients with Lc SSc patients by the examination of anti-RNAP III antibody.     

Improved clinical outcome of lupus nephritis during the past decade: importance of early diagnosis and treatment

OBJECTIVE: To evaluate the differences in the outcome of lupus nephritis diagnosed either in the 1980s or the 1990s in Heidelberg, Germany. METHODS: Fifteen patients with biopsy confirmed lupus nephritis (LN) were followed up between 1980 and 1989 and 41 patients were followed up between 1990 and 2000. Their status at diagnosis and their treatment schedules and outcome were analysed. 68% had WHO IV nephritis. RESULTS: In the decade from 1990 to 2000 there was significantly less proteinuria (46 v 17 g/l, p=0.008), significantly lower rates of renal failure (40% v 17%, p=0.02), and fewer histological signs of chronicity (33% v 10%, p=0.01) at the time of diagnosis of LN than in the decade from 1980 to 1989. The mean (SD) time from the first appearance of proteinuria until kidney biopsy was significantly shorter in the later decade (15.4 (15.6) v 3.9 (4.7) months). Although treatment schedules were not significantly different, the outcome of the disease was significantly better in the patients who were diagnosed with LN between 1990 and 2000 (p=0.045). Whereas 6/15 (40%) patients between 1980 and 1989 had terminal renal failure after a mean time of 94 months, in the group of 1990-2000 no patient developed terminal renal failure (median observation time 24 months). In both groups one patient died from infection. A high chronicity index in histology and the presence of arterial hypertension or renal failure, or both, at the time of diagnosis were significant risk factors for the development of terminal renal failure in the course of the disease. CONCLUSIONS: The outcome of patients with newly diagnosed LN was significantly better between 1990 and 2000 than between 1980 and 1989. Kidney damage and chronic histological changes at time of diagnosis were significantly less common between 1990 and 2000, which is attributable to earlier diagnosis and treatment in the later decade.     

Lupus podocytopathy superimposed on diabetic glomerulosclerosis: A case report

Rationale:Lupus podocytopathy (LP) is an entity that is increasingly being reported in the literature on systemic lupus erythematosus (SLE). LP is characterized by nephrotic syndrome in SLE patients with diffuse glomerular podocyte foot process effacement and no immune complex deposits along the capillary loops. Histologically, LP typically mimics minimal change disease or primary focal segmental glomerulosclerosis (FSGS) on a background of ISN/RPS class I or II lupus nephritis. In situations where there are coexistent glomerular diseases, however, LP may be easily masked by background lesions and overlapping clinical symptoms.Patient concerns:We report the case of a 24-year-old woman with type I diabetes, hypertension, psoriasis/rash, and intermittent arthritis who presented with abrupt onset of severe nephrotic proteinuria and renal insufficiency. Renal biopsy revealed nodular glomerulosclerosis and FSGS. Immune deposits were not identified by immunofluorescence or electron microscopy. Ultrastructurally, there was diffuse glomerular basement membrane thickening and over 90% podocyte foot process effacement. With no prior established diagnosis of SLE, the patient was initially diagnosed with diabetic nephropathy with coexistent FSGS, and the patient was started on angiotensin-converting enzyme inhibitors (ACEI) and diuretics. However, nephrotic proteinuria persisted and renal function deteriorated. The patient concurrently developed hemolytic anemia with pancytopenia.Diagnoses:Subsequent to the biopsy, serologic results showed positive autoantibodies against double strand DNA (dsDNA), Smith antigen, ribonucleoprotein (RNP), and Histone. A renal biopsy was repeated, revealing essentially similar findings to those of the previous biopsy. Integrating serology and clinical presentation, SLE was favored. The pathology findings were re-evaluated and considered to be most consistent with LP and coexistent diabetic nephropathy, with superimposed FSGS either as a component of LP or as a lesion secondary to diabetes or hypertension.Interventions:The patient was started on high-dose prednisone at 60 mg/day, with subsequent addition of mycophenolate mofetil and ACEI, while prednisone was gradually tapered.Outcomes:The patient''s proteinuria, serum creatinine, complete blood counts, skin rash, and arthritis were all significantly improved.Conclusion:The diagnosis of LP when confounded by other glomerular diseases that may cause nephrotic syndrome can be challenging. Sufficient awareness of this condition is necessary for the appropriate diagnosis and treatment.     

Idiopathic focal segmental glomerulosclerosis: a favourable prognosis in untreated patients?

BACKGROUND: Patients with focal segmental glomerulosclerosis (FSGS) are considered to have a poor prognosis and spontaneous remissions are seldom reported. However, FSGS is not a single disease entity. Our aim was to describe the clinical course in initially untreated patients with recently diagnosed idiopathic FSGS. METHODS: This was a retrospective study of patients with a diagnosis of FSGS by histology, who fulfilled the following criteria: proteinuria >3.5 g/day, normal renal function, duration of proteinuria or hypertension of less than one year, normal-sized kidneys, no underlying renal disease, and a negative family history. Renal biopsies were reviewed without knowledge of the clinical course. RESULTS: Twenty patients (13 male, 7 female) fulfilled the study criteria. Median age was 49.3 (range 21.8 to 73.0) years, serum creatinine 90 +/- 20 micromol/l, proteinuria 10.0 +/- 5.5 g/day and serum albumin 24 +/- 6 g/l. After a median follow-up of 9.4 (2.1-18.6) years, 13 patients (65%) were in remission of proteinuria. Renal function deterioration occurred in seven patients, and prompted treatment in four of them. The ten-year death-censored renal survival was 89%. Renal function deterioration and remission rate could be predicted by selectivity index, serum albumin at three months after renal biopsy and the percentage of glomeruli with segmental sclerosis. CONCLUSION: Focal glomerulosclerosis is not a single disease. Case definition using strict clinical criteria identifies a subgroup of patients with idiopathic FSGS who have a good prognosis. In the majority of these patients immunosuppressive therapy is not warranted.     

Clinical value of multiorgan damage in hypertensive crises: A prospective follow‐up study

Hypertensive crises are associated with high rates of target organ complications and poor outcomes. A recent shift from the definition of malignant hypertension to hypertension‐multiorgan damage (MOD) contributes to the diagnosis and management of hypertensive crises. Here, we prospectively included 166 adult (≥18 years old) patients with hypertensive crises (blood pressure >180/120 mm Hg). Target organs and causes of hypertension were assessed. Patients who were diagnosed with malignant hypertensive retinopathy, the absence of malignant hypertensive retinopathy but the presence of damage to at least 3 organs, and the absence of both retinopathy and MOD were classified as the malignant hypertension (n = 48), hypertension‐MOD (n = 42), and hypertension without MOD (n = 76) groups, respectively. Patients were followed to evaluate renal and cardiovascular prognoses. At baseline, patients with malignant hypertension had worse renal function, higher level of albuminuria, and more severe microvascular damage than those with hypertension‐MOD. Both had similar proportions of malignant arteriolar nephrosclerosis (83% vs 64%), left ventricular hypertrophy (90% vs 88%), abnormal repolarization (71% vs 60%), and left ventricular dysfunction (12% vs 21%). At the twenty months of follow‐up, both the malignant hypertension and hypertension‐MOD groups had similar blood pressure control rates and proteinuria. Both groups had worse renal outcomes than the hypertension without MOD group (P = .002). Patients with hypertension‐MOD (HR = 0.67, [95% CI: 0.30‐1.46], P = .31) had similar renal event‐free survival than patients with MHT after adjustments of age, sex, blood pressure, and proteinuria control. These results suggest that in hypertensive crises, both malignant hypertension and hypertension‐MOD have impact on adverse renal outcomes.     

Stent angioplasty of severe atherosclerotic ostial renal artery stenosis in patients with diabetes mellitus and nephrosclerosis.

Atherosclerotic renal artery stenosis (ARAS) may lead to deterioration of renal function or hypertension. The clinical outcome after stent angioplasty of ARAS on renal function and blood pressure control in patients with diabetes and nephrosclerosis is the subject of some controversy. We have analyzed the results of our single-center experience with stent angioplasty for severe (>/= 70%) ostial ARAS and present here the results of a subgroup analysis of those patients who had diabetes mellitus and nephrosclerosis. From 1996 to 2001, 241 patients underwent stent angioplasty for the treatment of ARAS at our center. Of these, 99 patients had diabetes mellitus (41%) and 176 patients (73%) had nephrosclerosis defined as intrarenal resistance index (RI) >/= 0.7 diagnosed by duplex ultrasound. All lesions (n = 355) were treated successfully. Mean blood pressure at baseline was comparable and significantly improved immediately after the intervention in all groups (nondiabetics: 102 +/- 12 to 93 +/- 10 mm Hg; diabetics: 102 +/- 14 to 93 +/- 11 mm Hg; RI < 0.7: 105 +/- 13 to 95 +/- 10 mm Hg; RI = 0.7-0.8: 100 +/- 12 to 92 +/- 10 mm Hg; RI > 0.8: 102 +/- 15 to 92 +/- 11 mm Hg; P < 0.0001 each). Baseline serum creatinine was not significantly lower in nondiabetics compared to diabetics (1.46 +/- 0.9 vs. 1.62 +/- 1.2 mg %; P < 0.05) and increased in patients with nephrosclerosis (RI < 0.7: 1.18 +/- 0.6 mg %; RI = 0.7-0.8: 1.57 +/- 1.1 mg %; RI > 0.8: 1.96 +/- 1.6 mg %). Except for patients without nephrosclerosis who had a normal baseline creatinine, serum creatinine decreased significantly in all subgroups during follow-up. Stent angioplasty of ARAS offers favorable acute and long-term clinical results for the preservation of the renal function and for blood pressure control in patients with diabetes mellitus and nephrosclerosis.     

以肾脏受累为主要表现的恶性高血压临床病理分析

目的了解以肾脏受累为主要表现的恶性高血压(MHPT)患者的临床与肾脏病理特征。方法回顾性分析我院肾内科11年来收治的27例(男21例,女6例,年龄19～51岁)MHPT患者的血压、眼底、尿和肾功能变化,对比分析原发性和肾实质性MHPT的临床与肾脏病理改变。结果27例MHPT患者中原发性、肾实质性和肾血管性分别为10例(37．0％)、10例(37．0％)和1例(3．7％),病因不明6例(22．3％)。急进性肾炎综合征和进行性肾功能损害是肾脏受累的主要表现。与肾实质性MHPT相比,原发性的MHPT尿蛋白量较少(P=0．001),多数病人有高血压家族史(7／10)。13例MHPT肾脏病理：原发性MHPT肾小动脉纤维素样坏死、内膜重度增生,呈现典型的洋葱皮样改变,肾小球为缺血性改变;肾实质性肾小动脉壁厚,细动脉玻璃样变,肾小球呈严重炎症病变。部分原发性MHPT经长期治疗肾功能可明显改善。结论以肾脏受累为主要表现的MHPT不少见,临床易误、漏诊;原发性与肾实质性MHPT的临床、肾脏病理改变及其预后均不同。