IgA肾病40例的中西医结合治疗体会

IgA肾病是指肾小球系膜区以IgA或IgA沉积为主的原发性肾小球疾病。IgA肾病是肾小球源性血尿最常见的病因。亚太地区和西欧地区该病分别占原发性肾小球疾病的20％-40％和10％～30％，10年内约10％-20％IgA肾病患者进入尿毒症，在欧洲和澳洲慢性透析和肾移植患者IgA肾病占7％-20％。目前认为IgA肾病是肾小球肾炎中最常见的一种类型，也是导致终末期肾衰最常见的原因之一。该病在我国发病率占肾小球疾病的26％-40％，男性多于女性，好发年龄在10-30岁，我科从2000～2004年开始肾脏病理活检，总结40例IgA肾病患者运用中西医辨证治疗IgA肾病，取得较好疗效，将其体会介绍如下。     

136例维持性血液透析患者临床分析

目的了解维持性血液透析（MHD）患者的病因构成、透析情况、生存率及死亡原因。方法回顾性分析1997年10月至2008年12月我院136例MHD患者的性别、年龄、原发病因、透析情况、付费方式、转归及死亡原因。结果病因中慢性肾小球肾炎占63．39％．梗阻性肾病10．2％,糖尿病肾病6．6％,高血压肾损害4．4％。死因构成：死亡65例。死亡患者中因经济原因放弃治疗33例,占总死亡率的50．77％,全身衰竭死亡10例．占总死亡率15．3％。除外放弃治疗及全身衰竭患者．22例死亡患者中,心力衰竭死亡13例占59．09％。结论在我院终末期肾脏疾病（ESRD）前四位病因为：慢性肾小球肾炎、梗阻性肾病、糖尿病肾病、高血压肾病。死亡原因主要是因经济原因放弃治疗或透析不充分至全身衰竭死亡,其次为心力衰竭。     

15例表现为恶性高血压的IgA肾病临床与病理分析

恶性高血压(MHT)常危及心、脑、肾等重要脏器,据统计,未获得有效治疗的MHT患者存活1年者不足25%,而存活5年以上者仅有1%[1].在MHT的病因中,15%为慢性肾小球肾炎[2],而在慢性肾小球肾炎中以IgA肾病占首位[3].现将我院近6年来,以MHT为主要表现的15例IgA肾病患者的临床资料进行回顾性分析,报道如下.     

目前西方对肾小球肾炎的认识

在临床实践中，肾小球疾病是一种常见病，也是导致终末期肾病（ＤＳＲＤ）最常见的病因。美国１９９１～１９９５年的统计资料表明，在接受治疗的ＥＲＳＤ患者中，原发病因为肾小球疾病者占５１％，其中糖尿病肾病（ＤＮ）占３７－９％，非糖尿病肾小球疾病占１３－５％。在我国，导致ＥＳＲＤ的病因也以肾小球疾病为主，占５４－４％，但其中ＤＮ仅占４－７％，肾小球肾炎却占４８－１％。某些常见的肾小球疾病并不发展至肾衰，但仍是导致患者发病和医疗费支出的重要因素［１，２］。肾小球肾炎（ＧＮ）的病变特征为：组织学上表现为肾小球…     

IgA肾病患者免疫抑制剂治疗

IgA肾病是我国乃至全世界大多数国家最常见的原发性肾小球肾炎。IgA肾病约占我国原发性肾小球肾炎的35%~55%~[1-3],其中约30%~50%的IgA肾病患者会进展至终末期肾脏病(end-stage renal disease,ESRD)~[1,4]。IgA肾病是一种复杂的多基因病,大多数原发性IgA肾病病因不详~[1],其主要病理表现为肾小球系膜区IgA免疫复合物沉积,其中最     

IgA肾病的治疗进展

IgA肾病是最常见的原发性肾小球肾炎，占肾活检的10％－50％，占终末期肾衰竭病因的10％－30％，由于其临床表现和病理改变不同，预后相差甚远。本文就其有关治疗方面的文献进展作一综述。     

单中心规律血液透析患者常见病因及其与年龄、超重关系的临床研究

目的探讨规律血液透析患者导致慢性肾衰竭的病因及其与年龄、超重的关系。方法选择符合入选标准的患者92例，调查导致慢性。肾衰竭的病因、年龄及体重指数，并进行回顾性分析。结果我中心血液透析患者以老年为主，常见病因是慢性。肾小球。肾炎，糖尿病。肾病，高血压肾病。糖尿病。肾病、高血压。肾病患者中60岁以上老年患者所占例数明显高于慢性肾小球肾炎组。糖尿病。肾病、高血压肾病患者中超重患者所占百分比明显高于慢性。肾小球。肾炎组。结论血液透析患者以老年为主，超重可能是加速慢性肾小球肾炎、糖尿病肾病、高血压肾病进展至慢性肾衰竭的主要原因之一。     

尿毒症合并脑血管意外23例临床分析

目的观察尿毒症合并脑血管意外的临床特点。方法对23例尿毒症合并脑血管意外患者进行回顾性分析。结果尿毒症合并脑血管意外患者存在多种危险因素,经治疗好转14例,死亡9例。其中脑出血患者好转3例,死亡6例,占66.7%（6/9）;脑梗死患者好转11例,死亡3例,占21.4%（3/14）。两者病死率比较差异有显著性（P〈0.05）。两组总病死率39.1%（9/23）。结论尿毒症合并脑血管意外病死率高,预防脑血管意外的各种综合因素,对减少脑血管意外的发生及延长生命十分重要。     

老年透析患者168例临床分析

目的 探讨老年透析患者肾衰的病因。方法 对168例老年透析患者的肾衰病因、贫血、高血压治疗状况、死亡原因等进行分析。结果 患者肾衰原因中原发性肾小球肾炎(30．95％)、高血压肾损害(29．76％)、糖尿病肾病(19．05％)患者共占79．76％，高血压患病率为87．50％，高血压控制率为30．61％，随血红蛋白水平升高患者心血管事件发生可能增大，患者死亡原因中以心血管事件为首位。结论 原发性肾小球肾炎、高血压肾损伤、糖尿病肾病为老年透析患者肾衰主要原因，高血压控制率较低。     

老年肾病综合征的临床表现和病理类型分析

目的：进一步了解老年肾病综合征的临床表现和病理特点。方法：对北京协和医院1980－1999年底住院老年肾病综合征病人进行临床表现和病理类型分析。结果：住院成人肾病综合征病人共513例,其中老年肾病综合征61例,占11．9％,原发病为原发性肾小球肾炎者49例,占80．3％,糖尿病肾病者7例,占11．5％。临床表现以浮肿、血尿为主,贫血的发生率为54．1％,慢性肾功能不全（CRF）为32．8％。肾活检发现,在非糖尿病肾病综合征病人用激素或激素加免疫抑制剂治疗的缓解率为47．85,有效率为30．4％,未缓解率为21．7％,一般激素或激素加免疫抑制剂效果较好,其临床表现与年轻人的肾病综合征相似,但合并贫血、急性肾功能不全（ARF）、CRF和感染的比例较高,最常见的病因是慢性肾小球肾炎,其病理类型以系膜增殖型肾小球肾炎最常见,其次是局灶增殖型肾小球肾炎,老年肾病综合征患者对激素或激素加免疫抑制剂治疗的反应尚可。     

2006—2007年广西血液净化中心新增尿毒症血透患者流行病学分析

目的探讨终末期肾病尿毒症血液透析患者的流行病学情况。方法对2006—2007年在广西血液净化中心首诊并进行维持性血液透析的终末期肾病尿毒症病人的流行病学进行分析。结果新终末期肾病血透患者为455例；男274例，女181例，平均年龄52．60岁。职业为农民占39．56％，机关干部37．72％。主要病因为慢性肾炎46．37％，糖尿病肾病18．46％，高血压肾病15．16％，梗阻性肾病9．89％；慢性肾炎与梗阻性肾病平均年龄显著小于糖尿病和高血压。开始透析时已存在多种并发症，同时合并4种并发症占12．09％，3种并发症占27．69％，2种并发症占47．25％。结论尿毒症的病因主要为慢性肾炎、糖尿病肾病、高血压肾病和梗阻性肾病。不同病因尿毒症有不同的流行病学特点，可能存在城乡差别。     

How Does Short-Term Low-Dose Simvastatin Influence Serum Prohepcidin Levels in Patients With End-Stage Renal Disease? A Pilot Study

Anemia is a common clinical problem in end-stage renal disease (ESRD). Despite adequate erythropoiesis-stimulating agent (ESA) supplementation, some ESRD patients still have suboptimal hemoglobin levels, and iron deficiency and inflammation are recognized as the two most common causes. Hepcidin, a newly discovered key regulator of iron homeostasis, is found to be accumulated in ESRD. As it controls iron uptake and release, better reflecting real-time iron demand and availability, hepcidin might become a target in the management of iron deficiency and ESA resistance in dialysis patients. For their pleiotropic functions apart from lipid-modulation, statins are also used as anti-inflammatory or immune-modulating agents. In this study, we applied simvastatin for the purpose of influencing serum prohepcidin level in a group of maintenance hemodialysis patients. Thirty-three ESRD patients undergoing hemodialysis were enrolled and assigned to experimental and hemodialysis control groups according to their lipid profile. Nineteen healthy adults were chosen as a normal control group. The subjects in the experimental group took 20 mg simvastatin orally per night for eight weeks, and those in the hemodialysis control group took no statins or any other lipid-modulating drugs. Before and after the experiment, the serum prohepcidin concentrations, plasma IL-6, and serum C-reactive protein (CRP), ferritin, hemoglobin, albumin, total cholesterol, glycerinate, and LDL and HDL cholesterol levels were determined. Of the 33 hemodialysis patients, the serum prohepcidin concentration was (175.8 ± 52.9) ng/mL, significantly higher than that in the normal control group (149.5 ± 24.2) ng/mL (P = 0.048). In the experimental group, the serum prohepcidin level was (156.7 ± 51.9) ng/mL before treatment, and (190.6 ± 49.6) ng/mL after eight weeks (P = 0.127). In the hemodialysis control group, the serum prohepcidin level was (190.6 ± 49.6) ng/mL at the beginning, and (193.5 ± 36.0) ng/mL after eight weeks (P = 0.728). In the experimental group, after taking simvastatin for eight weeks the serum total cholesterol and triglyceride levels had lowered by 18.6% (P = 0.004) and 55.1% (P = 0.007), respectively. The plasma IL-6, serum CRP, ferritin, hemoglobin, albumin, and LDL and HDL cholesterol levels in both the hemodialysis group remained unchanged. According to our preliminary study, eight weeks of 20 mg simvastatin did not significantly change the serum prohepcidin, high-sensitive CRP, or IL-6 concentrations in the group of maintenance hemodialysis patients.     

Heroin nephropathy: A clinicopathologic and epidemiologic study

The existence of a nephropathy secondary to intravenous narcotic use remains a matter of debate. To determine whether heroin use and renal disease are associated, a clinicopathologic and epidemiologic study was undertaken in the Buffalo Standard Metropolitan Statistical Area (Buffalo-SMSA).Over the past 10 years, 23 addicts presented with the nephrotic syndrome and/or renal insufficiency. All patients were black men 18 to 45 years of age. Kidney biopsies performed on 21 patients uniformly showed sclerosing glomerulonephritis. End stage renal disease (ESRD) developed in 15 of these patients.In the epidemiologic evaluation which spanned four and a half years, heroin use was highly correlated with both sclerosing glomerulonephritis and ESRD. A history of intravenous heroin use was found in 26 per cent of the new cases of sclerosing glomerulonephritis and in 13 per cent of the new cases of ESRD in patients aged 18 to 45 years (p < 0.000001).This investigation confirms the existence of heroin-associated sclerosing glomerulonephritis in black men. Heroin use appears to be a major risk factor for ESRD in the Buffalo-SMSA.     

Drug-induced interstitial nephritis. Coexistence with glomerular disease

Drug-induced interstitial nephritis is being recognized with increasing frequency. Pharmacologic agents responsible for inducing this entity include antibiotics, diuretics, and nonsteroidal anti-inflammatory drugs. We recently examined five patients with glomerular disease and drug-induced interstitial nephritis. In three patients prior biopsy specimens documented their glomerular disease (membranous nephropathy, crescentic glomerulonephritis, and presumptive lipoid nephrosis). A second biopsy specimen showed acute interstitial nephritis and the glomerular lesion. Two additional patients had single biopsy specimens demonstrating acute interstitial nephritis and either membranous nephropathy or crescentic glomerulonephritis. Our cases emphasize the need for recognizing this complex pattern of renal disease and the difficulties encountered in rendering a proper diagnosis.     

Renal Behçet's disease: a cumulative analysis

OBJECTIVE: To analyze cumulated data about renal involvement in Beh?et's disease (BD) and to report on 6 patients with BD and renal problems. METHODS: We found reports of 159 patients (including our patients) with BD and specific renal disease (amyloidosis 69, glomerulonephritis [GN] 51, renal vascular disease 35, and interstitial nephritis 4) in our survey. RESULTS: The frequency of renal problems among BD patients has been reported to vary between 0% to 55%. Male gender is a risk factor for all types of renal BD. Nephrotic syndrome was present in 83% of patients with amyloidosis, and renal failure was common at the time of diagnosis. The mean interval between the initial manifestation of BD and diagnosis of amyloidosis was shorter in men than in women (P =.02). AA-type amyloid fibrils were shown in all cases studied. Vascular involvement was common in the patients with amyloidosis (60%). The renal findings in GN show a wide spectrum, from asymptomatic hematuria and/or proteinuria to rapidly progressive GN. Several types of glomerular lesions ranging from minor glomerular changes to crescentic glomerulonephritis are observed in BD. The common types of glomerular lesions among the reported cases are crescentic GN, proliferative GN, and immunoglobulin A (IgA) nephritis. Aneurysms may be located throughout the renal artery, from the orifice of the main artery to intrarenal microaneurysms. Another type of renal disease (amyloidosis or GN) and other major vascular involvement were present in all cases with renal vein thrombosis. Hypertension is common among patients with renal artery aneurysm or stenosis. Microscopic vascular disease was described in 4 patients. CONCLUSIONS: Based on data in the literature, we suggest that renal involvement in BD is more frequent than has been recognized, although it is most often mild in nature. Amyloidosis is one of the prognostic factors affecting survival. Patients with vascular involvement carry high risk for amyloidosis, and administration of colchicine to these patients may be beneficial. More evidence is needed to accept interstitial nephritis as a manifestation of BD. In spite of some difficulties, hemodialysis and renal transplantation are safe treatment options in BD-related uremia.     

Membranous nephropathy and crescentic glomerulonephritis

The most frequent causes of glomerular diseases whose main clinical syndrome are nephrotic syndrome and acute renal failure may have several causes: acute tubular necrosis, thrombosis of renal veins, acute tubulointerstitial nephritis. Infrequently, the association between primary glomerular disease (membranous nephropathy and others) and crescentic glomerulonephritis can cause this clinical picture. We describe a young woman without systemic disease with nephrotic syndrome and acute renal failure secondary to membranous nephropathy and superimposed crescentic glomerulonephritis. She received steroids and cyclophosphamide with stabilization of renal function after two months of follow-up.     

Effect of Renal Function Impairment on the Mortality of Cirrhotic Patients With Hepatic Encephalopathy: A Population-Based 3-Year Follow-Up Study

Kidney is an important organ to clear neurotoxic substance in circulation. However, it is still unknown about the effect of renal function impairment (RFI) on the mortality of cirrhotic patients with hepatic encephalopathy (HE). We used the Taiwan National Health Insurance Database to identify 4932 cirrhotic patients with HE, hospitalized between January 1, 2007 and December 31, 2007. The enrolled patients were followed up individually for 3 years to identify their 3-year mortalities. There were 411 (8.3%) patients with RFI and 4521 (91.7%) patients without RFI. The adjusted hazard ratio (HR) of RFI for 3-year mortality was 2.03 (95% CI, 1.82–2.27). In RFI group, there were 157 (38.2%) patients with acute renal failure (ARF), 61 (14.8%) with hepatorenal syndrome (HRS), 93 (22.6%) with chronic kidney disease (CKD), and 100 (24.3%) with end-stage renal disease (ESRD). Compared with the non-RFI group, the adjusted HR of ARF for 3-year mortality was 2.57 (95% CI, 2.17–3.06), CKD 1.93 (95% CI, 1.55–2.40), ESRD 1.26 (95% CI, 1.01–1.57), and HRS 3.58 (95% CI, 2.78–4.63). Among ESRD patients, there were 99 patients receiving hemodialysis regularly. Compared with the CKD group, the adjusted HR of ESRD with hemodialysis for 3-year mortality was 0.664 (95% CI, 0.466–0.945). RFI increased the 3-year mortality of cirrhotic patients with HE, especially ARF and HRS. HE patients with ESRD receiving hemodialysis had better 3-year survival rate than those with CKD.     

Prognostic factors in lupus nephritis: diagnostic and therapeutic delay increases the risk of terminal renal failure

OBJECTIVE: To evaluate the prognostic significance of clinical and renal biopsy findings in an unselected cohort of patients with systemic lupus erythematosus (SLE) and nephritis. METHODS: Ninety-one patients with lupus nephritis were included in the study. Renal biopsies were classified according to the WHO criteria and examined for the presence of active and chronic histological changes. Predictors of endstage renal disease (ESRD) were identified by univariate and multivariate analyses. RESULTS: The median followup time was 6.1 years (0.1-30.0 yrs). In all cases, immunosuppressive treatment was initiated or intensified within one month following renal biopsy. The cumulative incidence of ESRD after 1, 5, and 10 years was 3.5%, 15%, and 17%, respectively. A variety of clinical and biopsy findings including several histological markers of chronic renal damage were identified as univariate predictors of ESRD. In multivariate regression analyses, duration of nephritis symptoms > 6 months prior to biopsy, s-creatinine > 140 micromol/l, diffuse proliferative glomerulonephritis, and tubular atrophy emerged as the strongest combination of independent risk factors (relative hazard ratios: 9.3, 5.6, 8.9, and 3.1, respectively). CONCLUSION: Our results confirm the negative prognostic impact of hypercreatininemia, class IV histopathology, and tubular atrophy in lupus nephritis. Our data show that delay between onset of nephritis and renal biopsy constitutes an important risk factor of ESRD. Patients with SLE should have kidney biopsy as soon as clinical signs of nephritis are evident in order to accelerate treatment decisions and minimize risk of inflammation-induced irreversible kidney damage.     

Does treating obesity stabilize chronic kidney disease?

Background

Much epidemiological evidence suggests that hydrocarbon exposure may induce glomerulonephritis and worsen its course in many patients. The mechanisms are unknown, however, no specific microscopic pattern has been identified, and it has also been argued that hydrocarbon exposure causes tubular damage mainly. Studying experimental animals may best answer these questions, and as no systematic review of glomerulonephritis produced experimentally by hydrocarbon exposure has been performed previously, I found it relevant to search for and analyse such studies.

Methods

Animal experiments having mimicked human glomerulonephritis by hydrocarbon exposure were sought on Medline and Toxnet

Results

Twenty-six experiments using thirteen different hydrocarbons were identified. Several human subtypes were observed including IgA nephritis, mesangial, proliferative and extracapillary glomerulonephritis, focal and focal-segmental sclerosis, minimal change nephropathy, anti-GBM and anti-TBM nephritis, and glomerulonephritis associated with peiarteritis nodosa. Glomerular proteinuria was seen in 10/12 experiments that included urine analyses, and renal failure in 5/8 experiments that included measurements of glomerular function. All experiments resulted in various degrees of tubular damage as well. In most studies, where the animals were examined at different times during or after the exposure, the renal microscopic and functional changes were seen immediately, whereas deposits of complement and immunoglobulins appeared late in the course, if at all.

Conclusion

These experiments are in accord with epidemiological evidence that hydrocarbon exposure may cause glomerulonephritis and worsen renal function. Probable mechanisms include an induction of autologous antibodies and a disturbance of normal immunological functions. Also, tubular damage may increase postglomerular resistance, resulting in a glomerular deposition of macromolecules. In most models a causal role of glomerular immune complex formation was unlikely, but may rather have been a secondary phenomenon. As most glomerulonephritis subgroups were seen and as some of the hydrocarbons produced more than one subgroup, the microscopic findings in a patient cannot be used as a clue to the causation of his disease. By the same reason, the lack of a specific histological pattern in patients with glomerulonephritis assumed to have been caused by hydrocarbon exposure is not contradictive.     

Changes in the incidence of end-stage renal disease due to lupus nephritis, 1982-1995

BACKGROUND: The availability of more effective treatments for severe lupus nephritis may have influenced the rate at which end-stage renal disease (ESRD) develops in these patients. OBJECTIVE: To examine changes in the incidence of ESRD due to lupus nephritis from 1982 to 1995. METHODS: All patients with incident ESRD included in the US Renal Data System from 1982 to 1995 were studied. The US Renal Data System includes information on all patients who receive Medicare-reimbursed renal replacement therapy, who constitute approximately 94% of all patients with ESRD in the United States. The incidence of ESRD due to lupus nephritis in each year, standardized to the age-sex-ethnicity composition of the US general population in 1990, was computed in this serial cross-sectional study. RESULTS: The standardized incidence rate of ESRD due to lupus nephritis increased steadily from 1.16 cases per million person-years in 1982 to 3.08 cases per million person-years in 1995. The rate of increase was comparable to that of ESRD due to all other primary renal diseases. CONCLUSION: The incidence of ESRD due to lupus nephritis increased steadily over the 14-year study period, despite the introduction of efficacious new treatment regimens for lupus nephritis during this time.