正常人与原发性肾小球肾炎及狼疮性肾炎患者血尿IL-18水平比较

目的:探讨IL-18在原发性肾小球肾炎(PGN)及狼疮性肾炎(LN)发生、发展中的作用,以及寻找有助于两类疾病的鉴别诊断和对肾组织炎症活动程度进行评估的指标。方法:应用酶联免疫吸附检测(enzyme-linkedimmunosorbent assay,ELISA)法测定16例正常人、21例原发性肾小球肾炎(PGN)患者和18例LN患者血浆和尿液IL-18水平的变化。结果:LN患者血浆及尿液IL-18水平显著高于正常对照组(P均<0.001)和PGN组(P均<0.05),而且WHOⅣ型LN患者血浆及尿IL-18水平均明显高于非Ⅳ型LN患者(P<0.05);PGN患者尿液IL-18水平也高于正常人(P<0.05),但血浆IL-18水平与正常人比较无统计学差异(P>0.05);LN患者血浆IL-18水平与SLEDAI呈正相关(P<0.01),而尿IL-18水平与狼疮性肾炎RHSAI是密切正相关(P<0.001),但尿IL-18水平与血浆IL-18水平相关性没有统计学意义(P>0.05)。结论:IL-18参与LN的全身免疫病理过程,但可能仅参与PGN肾组织局部炎症过程;血浆IL-18检测可能有助于区分LN和PGN,尿IL-18的检测可望作为一项估计LN肾组织病变活动程度的有用指标。     

Erythrocyte Sodium and Sodium Flux in Relation to Hypertension in Chronic Renal Failure

Erythrocyte sodium and sodium fluxes in plasma and in physiologicalbuffer solution were studied in normotensive and hypertensiveuraemic patients and normal subjects. Erythrocyte sodium wasreduced in the uraemic patients due primarily to low sodiuminflux, further supported by low passive membrane permeability.These differences were much more marked in normotensive patients.There was no evidence for sodium pump inhibition in the erythrocytes.The low erythrocyte sodium influx in the uraemic patients appearedto be due to a plasma factor which could be reversed in youngcells but not in old. However, erythrocyte sodium flux in bothplasma and physiological buffer was lower in normotensive thanin hypertensive uraemic patients. Therefore, a membrane changeto compensate for the effects of the plasma factor on sodiuminflux may be related to the development of hypertension inthe uraemic patients.     

原发性肾小球肾炎患者Th1/Th2细胞因子失平衡状况的研究

目的：探讨原发性肾小球肾炎（PGN）Th1／Th2细胞因子失衡情况，以及不同病理类型、不同病程对Th1／Th2失平衡的影响。方法：采用酶联免疫吸附（ELISA）法测定16例正常人及38例PGN患者血浆IL-18及IL-13水平，同时应用免疫组织化学检测6例正常肾组织和38例PGN患者肾组织IL-18及IL-13的表达量。结果：无论在肾组织抑或外周血，PGN患者IL-18水平及IL-13水平均较正常对照组显著上升（P均〈0．001），但肾组织抑或外周血IL-18／IL-13比率与正常对照组比较无统计学差异（P〉0．05）；在肾组织局部，除膜增生性肾小球肾炎（MPGN）患者IL一18／IL-13显著高于正常对照组（P均〈0．001）外，其他病理类型PGN患者IL-18／IL-13比率与正常人比较无统计学差异（P〉0．05），各病理类型PGN患者血浆IL-18／IL-13比率与正常对照组比较也无统计学差异；虽然外周血及肾组织IL-18及IL-13水平与血清肌酐（Ser）水平具有密切正相关关系，但IL-18／IL-13比率与Ser水平无相关关系（P〉0．05）。结论：除极个别病理类型外，PGN患者免疫紊乱状态似乎不能简单的按Th1优势／Th2优势进行二分法分类，其免疫紊乱状态远较此复杂，试图通过简单的调节Th1／Th2平衡来治疗PGN似乎仍缺乏坚实的理论及实验基础。     

Renal Oncocytoma Associated with Necrotizing Glomerulonephritis

A case of renal oncocytoma associated with focal segmental necrotizing glomerulonephritis is described. The patient showed haematuria, mild proteinuria and arterial hypertension; the diagnosis was made after right nephrectomy performed because of the presence of a renal mass. A severe re-activation of the glomerulonephritis was observed 15 months after the nephrectomy and a steroid and immunosuppressive therapy was started. Our case is the first reported in which the removal of renal oncocytoma is not followed by the disappearance of renal symptoms, as currently reported in literature, suggesting that the two diseases are not always related.     

肾脂肪囊注射甲基泼尼松龙及川芎嗪治疗原发性系膜增殖性肾炎疗效观察

目的:观察肾脂肪囊注射甲基泼尼松龙及川芎嗪注射液治疗原发性系膜增殖性肾小球肾炎的疗效.方法:选择经肾活检病理证实的原发性非IgA系膜增殖性肾炎30例.治疗分3组,即:A组12例,每侧肾囊内注射甲基泼尼松龙40 mg,每周2次;B组8例,同A组治疗基础上,向每侧肾脂肪囊注射川芎嗪40 mg,每周1次;C组10例,口服泼尼松1 mg·kg-1·d-1.治疗6周.观察治疗前后24 h尿蛋白(UP)、血白蛋白(Alb)、24 h尿内皮素排泌量(UEt-1),血压,血糖,水肿变化及糖皮质激素副作用.结果:20例(A、B组)肾囊注射治疗后尿蛋白明显减少或转阴,血浆白蛋白升高.而A组与B组比较无明显差别,治疗后UEt-1下降,且未发现明显糖皮质激素的副作用.A组、B组疗效优于C组.结论:肾脂肪囊注射甲基泼尼松龙是治疗原发性系膜增殖性肾炎的有效方法,且可降低全身用药的副作用.     

HBV-GN肾小管间质损害的发生影响因素及临床意义

目的:探讨乙肝相关性肾炎(HBV-GN)中肾小管间质损害(TIL)的发生情况、影响因素及临床意义。方法:单因素及多因素分析227例HBV-GN患者TIL发生的影响因素,比较不同程度TIL患者的临床病理资料。结果:肾小管间质损害轻度者占59.5%,中度者占17.6%,重度者占4.8%,无肾小管间质损害者仅占18.1%。不同病理类型HBV-GN患者其TIL发生率各不相同,年龄>14岁、高血压、尿蛋白≥0.3g/d、血肌酐≥132.6μmol/L、球囊黏连、新月体形成、系膜增殖程度和肾小球硬化率是TIL发生的危险因素,其中高血压、系膜增殖程度和肾小球硬化率是TIL发生的独立影响因素;随着肾小管间质损害的发生或加重,尿蛋白≥0.3g/d、高血压、高尿酸血症、肾功能异常和上述4种肾小球病理改变的发生率亦增高。结论:肾小管间质损害在HBV-GN患者的十分常见,高血压、系膜增殖程度和肾小球硬化率是TIL的独立危险因素,TIL发生或加重对其肾小球病理改变也有明显影响,是影响HBV-GN预后的不良因素之一。     

慢性肾炎致慢性肾衰竭患者心衰发生相关危险因素分析

目的：了解慢性肾炎致慢性肾衰竭患者血压、血红蛋白、血清白蛋白、血脂、血肌酐、电解质及尿素氮、胱抑素C、同型半胱氨酸及高敏C反应蛋白等指标与心力衰竭发生之间的关系,分析并探讨相关危险因素。方法：回顾性分析我院343例慢性肾炎致慢性肾衰竭患者心衰发生及其同期血压等指标变化情况,了解其规律及相互关系。结果：（1）343例患者有77例合并发生心衰（22．4％）,其中19岁～39岁占20．5％,40岁～59岁占22．8％,〉60岁占33．3％;合并发生心衰多为CKD5期患者（97．4％）。（2）血压、血红蛋白、CO2CP、血肌酐、高敏C反应蛋白在有无心衰发生组存在统计学差异（P〈0．01）,其中血压、血肌酐、光抑素C、高敏C反应蛋白等与心衰发生呈负相关（P〈0．05）,而年龄、钙磷、血清白蛋白及血脂、尿素氮、同型半胱氨酸组间无统计学差异。结论：慢性肾炎致慢性肾衰竭患者心力衰竭发生率很高,其发生可能与高血压、贫血、酸中毒、血肌酐及微炎症状态等因素有关。     

Hypertension in adults with idiopathic glomerulonephritis and normal serum creatinine. A report from the MRC Glomerulonephritis Registry

The Medical Research Council's Glomerulonephritis Registry wasused to determine the prevalence and clinical characteristicsof hypertension occurring in patients with idiopathic glomerulonephritis(GN) and normal serum creatinine (males <120µmol/l,females <100µmol/l). The hypertension prevalence ratewas 23.0% in 1221 such patients, increased significantly withage, and within each age group was greater in males than infemales. These patterns closely mirror those seen for hypertensionin the United Kingdom general population. However, the hypertension prevalence rates in the GN patientssignificantly exceeded those seen in the corresponding age/sexbands in the general UK population and varied considerably betweenGN subtypes; thus hypertension in patients with GN and ‘nearnormal’ renal function is not solely due to essentialhypertension. Logistic regression analysis demonstrated thatin addition to increasing age, the presence of hypertensionwas significantly associated with increased serum creatinine,even in these patients with serum creatinines within the normalrange. One possible explanation for these findings may be that peoplewith an inherited tendency to essential hypertension may alsobe more prone to hypertension if they develop GN. Our data suggeststhat this early hypertension is closely associated with mildimpairment of GFR, occurring within the accepted normal rangefor serum creatinine.     

Acute Post-Bacterial Glomerulonephritis in Renal Transplant Patients: Description of Three Cases and Review of the Literature

Only a few cases of acute post-infectious glomerulonephritis have been described in renal transplant patients. We report here three cases of acute post-bacterial glomerulonephritis in renal transplants. In contrast to the classic cases of post-streptococcal glomerulonephritis the type of infection was heterogeneous: respectively, Escherichia coli bacteremia, a skin abscess, and cholangitis. The clinical presentation was characterized by a deterioration of graft function in two of our three patients. Acute renal dysfunction recovered in both patients, but in the long term the outcome was severe; two of the three patients lost their graft function. It is difficult to ascertain whether progression was due to chronic allograft nephropathy, to glomerulonephritis, or both. It may be concluded that acute post-infectious glomerulonephritis is a possible, although rare, complication in renal transplant recipients. It has an unusual presentation and may have a poor outcome in the long term. The role of therapy, if any, is still undefined.     

Fibrillary Glomerulonephritis Presenting as Rapidly Progressive Renal Failure in a Young Female: A Case Report

Fibrillary Glomerulonephritis (FGN) is a rare clinical entity presenting in majority of patients with nephrotic range proteinuria, microscopic hematuria, impaired renal function and hypertension. The mean age of presentation is reported to be beyond 50 years with 50 patients developing end stage renal disease within a few years. A 28-year-old female presented to us with non-nephrotic range proteinuria, rapidly progressive renal failure (RPRF), microscopic hematuria and mild hypertension. The patient had undergone a renal biopsy at a peripheral center, which was reported as membranoproliferative glomerulonephritis (MPGN) and was being treated with steroids without any benefit. The patient on re-biopsy at our center was diagnosed as FGN on electron microscopy (EM). The patient responded to intravenous pulse methylprednislone and oral cyclophosphamide and is off dialysis for 10 months now. This case highlights the varied clinical and histological presentations of FGN which makes the disease difficult to diagnose more so, in a country like ours where EM is available in only a few centers. An accurate diagnosis aided by high index of clinical suspicion and EM can help in the initiation of appropriate therapy, thereby improving the outcome in this disease which otherwise has a poor prognosis.     

Urotensin-II Immunoreactivity in Children with Chronic Glomerulonephritis

Background. Human urotensin-II (hU-II) is one of the most potent vasoconstrictors in mammals. To our knowledge, there is no study about the role of U-II in childhood glomerulonephritis.We first determined the expression of h U‐II in kidneys of children with chronic glomerular diseases. Methods. Normal human kidneys were obtained from postmortem biopsies and compared with the kidney biopsy specimens of 24 children with membranoproliferative glomerulonephritis (MPGN) and 6 children with membranous GN. Kidney needle biopsies in 10% neutral buffered-formalin prior to routine processing through to embedded blocking sections were cut, and immunohistochemical reactions were performed on parafin-embedded tissue by an avidin-biotin peroxidase complex method. The antibodies used in the present study were hU-II. The positivities were revealed as weak (+), moderate (++), and severe (+++), according to the color intensity. Results. In kidneys of children with MPGN, differently fom the normal kidneys, more dense U-II immunoreactivity was seen in the glomerular basement membrane (GBM), glomerular mesangium, Bowman capsule, and tubules. Interestingly, we also observed U-II immunoreactivity in crescents. In children with MGN, U-II was mostly seen in GBM and Bowman capsule. Conclusion. Our findings suggest that U-II may have a possible autocrine/paracrine function in the kidneys, and may be an important target molecule in studying renal pathophsiology.     

Factors Determining the Prevalence of Hypertension After Renal Transplantation

The prevalence of hypertension was studied in renal transplantrecipients followed for at least 1 year. Twenty-eight patientswith a transplant renal artery stenosis, all with hypertension,were excluded from further study. Hypertension was present at1 year after transplantation in 48.3% of 329 cadaveric renalgraft recipients, treated with azathioprine. These hypertensivepatients had experienced more rejection episodes. The prevalenceof hypertension was higher in patients with (n=237) than inthose without (n=92) host kidneys in situ (57.8% and 23.9% respectively,P<0.001). In patients with host kidney, the prevalence ofhypertension was higher in patients with glomerulonephritis(n=108) than in those in whom interstitial nephritis (n=63)was the original renal disease (71.3% and 42.8 respectively,P<0.001). In 41 patients initially treated with cyclosporinand in 42 recipients of a kidney from a living donor, the prevalenceof hypertension was not clearly lower than in the azathioprine-treatedpatients. In 30 patients without host-kidneys who did not experienceacute rejections, only three had hypertension. In all threepatients a specific cause for the hypertension was found. Inhypertensive patients, blood pressure decreased gradually inthe years following transplantation. In conclusion, besidestransplant renal artery stenosis, the main determinants of theprevalence of hypertension after renal transplantation are hostkidneys original renal disease, and rejection.     

双肺移植治疗终末期原发性肺动脉高压

双肺移植治疗原发性肺动脉高压１例。男病人，３０岁。多年来有气短等症状，晕厥４次，反复咯血４年，近期大咯血３次。肺动脉压２０．３／７．３（１３．７）ｋＰａ，全肺阻力３５４．９７８ｋＰａ·ｓ／Ｌ，有中至重度三尖瓣关闭不全。１９９８年１月２０日在体外循环（心脏不停跳）支持下手术。术毕肺动脉压基本正常，三尖瓣关闭不全及反流消失。术后给予三联免疫抑制剂。围手术期有明显的血液动力学紊乱，无明确的急性排斥发生，最主要的并发症是左主支气管吻合口、右上叶及中间干支气管狭窄，目前仍间断行球囊扩张治疗。病人已生存８个多月，状态稳定，在扩张狭窄的支气管后可出院外自由活动     

Transformation from Tubulointerstitial Nephritis to Crescentic Glomerulonephritis: An Unusual Presentation of ANCA-Associated Renal Vasculitis

A 44-year-old man with acute renal failure and antineutrophil cytoplasmic antibodies (ANCA) positivity was described. The first renal biopsy specimen showed tubulointerstitial nephritis (TIN) with normal glomeruli. However, delayed recovery of renal function with low-dose steroid treatment for TIN prompted a second renal biopsy 1 month later; and the specimen demonstrated a dramatically different morphology, with necrotizing and crescentic glomerulonephritis. Improvement in renal function occurred, together with reduction of ANCA titers, following intensive immunosuppressive therapy. This case illustrates an unusual presentation of TIN in ANCA-associated renal vasculitis. The possible pathogenetic mechanism are discussed.     

Effects of Heparin-Induced Aldosterone Deficiency on Renal Function in Patients with Chronic Glomerulonephritis

The effects of heparin-induced aldosterone deficiency on renalsodium and potassium transport and renal function were studiedin 65 patients with chronic glomerulonephritis and initial hyperaldosteronism.Heparin-induced aldosterone deficiency resulted in increaseddiuresis, in natriuresis due to decreased sodium reabsorptionin the distal nephron, in a fall in serum sodium and an increasein serum potassium concentration. A transient reduction in potassiumexcretion occurred during the 2–4 days of heparin treatment.In patients with chronic glomerulonephritis and a compromisedrenin–angiotensin–aldosterone system, heparin maycause drug-induced selective hypoaldosteronism. The suppressiveeffect of heparin on aldosterone production was partially compensatedfor by increasing plasma renin activity. Heparin-induced aldosteronedeficiency did not change glomerular filtration rate in patientswithout renal failure. In those with chronic sclerosing glomerulonephritisand a glomerular filtration rate less than 35 ml/min, heparincaused a further decrease in renal function.     

Impact of Immunosuppressive Medication on the Risk of Renal Allograft Failure due to Recurrent Glomerulonephritis

Recurrent glomerulonephritis is a major problem in kidney transplantation but the role of immunosuppression in preventing this complication is not known. We used data from the United States Renal Data System to examine the effect of immunosuppressive medication on allograft failure due to recurrent glomerulonephritis for 41 272 patients undergoing kidney transplantation from 1990 to 2003. Ten-year incidence of graft loss due to recurrent glomerulonephritis was 2.6% (95% confidence interval [CI]: 2.3–2.8%). After adjusting for important covariates, the use of cyclosporine, tacrolimus, azathioprine, mycophenolate mofetil, sirolimus or prednisone was not associated with graft failure due to recurrent glomerulonephritis. There was no difference between cyclosporine and tacrolimus or between azathioprine and mycophenolate mofetil in the risk of graft failure due to recurrent glomerulonephritis. However, any change in immunosuppression during follow-up was independently associated with graft loss due to recurrence (adjusted hazard ratio 1.30, 95% CI: 1.06–1.58, p = 0.01). In patients with a pretransplant diagnosis of glomerulonephritis, the risk of graft loss due to recurrence was not associated with any specific immunosuppressive medication. The selection of immunosuppression for kidney transplant recipients should not be made with the goal of reducing graft failure due to recurrent glomerulonephritis.     

Oxidative Stress in Children with Acute Glomerulonephritis

Background. Oxidative stress has not been adequately investigated in acute glomerulonephritis (AGN); therefore, we aimed to evaluate the oxidative stress (OS) status in children with AGN both at acute and remission stages. Patients and methods. Seventeen children (mean ± SEM, age 9.0 ± 0.5 years) with AGN and 17 healthy controls were included. In addition to routine laboratory investigations, two blood samples were obtained from patients, at admission and after 6–10 weeks, to measure erythrocyte superoxide dismutase (SOD) activity and plasma malondialdehyde (MDA) level. Results. Significantly elevated MDA levels (5.11 ± 0.28 vs. 3.15 ± 0.25 nmol/mL; p < 0.001) were found in acute stage of AGN compared with the controls; however there was no significant difference in SOD activities (3732 ± 193 vs. 4035 ± 142 U/gHb; p > 0.05) between acute stage-AGN and control subjects. Significantly elevated SOD activities (3985 ± 195 U/gHb, p?=?0.034) and decreased MDA levels (4.01 ± 0.38 nmol/mL, p?=?0.001) were found at remission stage when compared with the acute stage. MDA levels and SOD activities of remission phase were similar to those of controls (p > 0.05). A significantly positive correlation was found between MDA levels and SOD activities in remission period (r?=?0.654, p?=?0.004). Patients with and without impaired renal functions had similar MDA levels and SOD activities (p > 0.05). No significant correlation was found between glomerular filtration rates (GFR) and MDA levels (p > 0.05) and between GFR and SOD (p > 0.05) activities in acute stage-AGN. Conclusions. Oxidative stress may play important role in the pathogenesis of AGN and not be correlated with renal functions. Further research is needed to determine magnitude of OS and indications for antioxidants in other glomerulopathies.     

Plasma atrial natriuretic peptide and endothelin levels in acute poststreptococcal glomerulonephritis

Plasma levels of atrial natriuretic peptide (ANP) and of endothelin (ET) were significantly elevated (87.7±13.9 pg/ml and 79.7±10.8pg/ml, respectively) during the acute phase of acute poststreptococcal glomerulonephritis (APSGN). Plasma renin levels were normal, fractional excretion of sodium (FE_Na) was 0.5±0.1% and creatinine clearance (C _Cr) averaged 82.2±18.3 ml/min per 1.73 m². In the recovery phase of the disease (n=12), levels of ANP (23.6±6.7 pg/ml) and ET (43.1±2.4 pg/ml) fell and were not significantly different from those measured in 11 control subjects. FE_Na increased to 1.3±0.1% andC _Cr to 113.5±12.1 ml/min per 1.73 m² (all values mean ± standard error). ANP did not correlate with PRA, blood pressure,C _Cr or FE_Na. There was an inverse relationship between the ET level and FE_Na in the acute phase of the disease (r=0.489,P<0.05), but no significant correlation between ET and blood pressure, PRA,C _Cr or ANP was found. We suggest that, despite the sodium retention, the increased ANP level in APSGN indicates unresponsiveness of the kidneys to ANP; the increased ET levels may contribute to this.