肾小管间质性肾炎-眼葡萄膜炎综合征患儿的护理

总结1例肾小管间质性肾炎-眼葡萄膜炎综合征患儿的护理经验。提出制定科学的饮食计划,做好肾活检术护理、缓解眼部疼痛、应用糖皮质激素的用药护理,以及针对患儿及家属不同阶段的心理护理是该病护理的重点。     

中药和解法治疗肾小管间质性肾炎-葡萄膜炎综合征急性肾损伤1例并文献复习

<正>肾小管间质性肾炎-葡萄膜炎(tubulointerstitial nephritis and uveitis,TINU)综合征,是引起急性肾小管间质性肾炎的少见原因,常被误诊为药物性间质性肾炎。而急性肾小管间质炎是急性肾损伤(acute kidney injury,AKI)的最常见原因,在AKI肾活检病例中占15%～27%[1]。TINU综合征全身系统性症状多非特异性、肾脏症状和眼部症状常常非同期发作,造成一定     

老年肾小管间质性肾炎-眼色素膜炎综合征一例

患者,女,60岁,因发热半个月,肾功能不全1周于2009年4月12日入院.半个月前出现发热,达39.0℃,伴寒颤、咳嗽、恶心、乏力,于当地诊所治疗无效,并出现双眼视物模糊、疼痛、流泪及结膜充血,以左眼显著.1周前当地查BUN 9.59 mmol/L,Scr 395 μmol/L,24 h尿蛋白量0.42 g.1 d前复查BUN 29.1 mmol/L,Scr 589 μmol/L,后入我院.查体:T 38.6℃,BP 130/85 mm Hg,双眼结膜充血,心肺腹部检查无异常,双下肢无水肿.     

老年肾小管间质性肾炎-眼色素膜炎综合征一例

患者,女,60岁,因发热半个月,肾功能不全1周于2009年4月12日入院.半个月前出现发热,达39.0℃,伴寒颤、咳嗽、恶心、乏力,于当地诊所治疗无效,并出现双眼视物模糊、疼痛、流泪及结膜充血,以左眼显著.1周前当地查BUN 9.59 mmol/L,Scr 395 μmol/L,24 h尿蛋白量0.42 g.1 d前复查BUN 29.1 mmol/L,Scr 589 μmol/L,后入我院.查体:T 38.6℃,BP 130/85 mm Hg,双眼结膜充血,心肺腹部检查无异常,双下肢无水肿.     

老年肾小管间质性肾炎-眼色素膜炎综合征一例

患者,女,60岁,因发热半个月,肾功能不全1周于2009年4月12日入院.半个月前出现发热,达39.0℃,伴寒颤、咳嗽、恶心、乏力,于当地诊所治疗无效,并出现双眼视物模糊、疼痛、流泪及结膜充血,以左眼显著.1周前当地查BUN 9.59 mmol/L,Scr 395 μmol/L,24 h尿蛋白量0.42 g.1 d前复查BUN 29.1 mmol/L,Scr 589 μmol/L,后入我院.查体:T 38.6℃,BP 130/85 mm Hg,双眼结膜充血,心肺腹部检查无异常,双下肢无水肿.     

小管间质性肾炎-眼葡萄膜炎综合征一例

小管间质性肾炎.眼葡萄膜炎综合征(tubulointerstitial nephritis and uveitis syndrome,TINU)临床较为少见,迄今全球相关报道仅约200多例,现报道1例.     

小管间质性肾炎-眼葡萄膜炎综合征一例

患者,女性,43岁。入院前6周出现眼红,流泪和视物有黑影,伴发热。眼科检查示双眼结膜混合充血,双角膜见粉尘状角膜后沉着物,前房见细胞,房水闪光Tyn( ),晶体前见色素沉着,瞳孔圆,光敏,虹膜无后粘连,双眼底乳头界清,血管无迂曲,右眼黄斑中心凹反光可见,左眼中心凹反光无,右眼于8:30处见马蹄形裂孔,无网膜。诊断为“眼葡萄膜炎”,予以地塞米松和洁霉素静滴3d,甲基泼尼松龙20mg球旁注射,0.5%地塞米松、阿托品和碘必殊眼药水及右眼网膜裂孔激光治疗后,眼部症状明显好转。但体温仍38.0～38.8℃,伴有腰酸、乏力、纳差,偶有尿频、尿急,经抗感染无效…     

迟发眼葡萄膜炎的肾小管间质肾炎1例

<正>病例刘某,女,49岁,以"乏力,恶心呕吐3月余"于2016年10月12日收住入院。3月前因便秘自服"番泻叶煎剂"后出现腹泻,伴乏力、恶心呕吐、食欲减退; 2月前于当地卫生院静滴"奥美拉唑"、"氨苄青霉素"4 d,口服"安乃静"1片,上述症状无改善; 10 d前症状加重,胃镜检查提示"食管炎、慢性萎缩性胃炎";血常规检查:HGB 103 g/L,肾功能检查:Scr 174μmol/L,UA 129μmol/L,e GFR 29. 16 ml·min-1·1. 73 m-2。入院表现:疲倦乏力,恶心呕吐,上腹部不适,尿量正常,无夜尿增多。自发病以来体重下降8 kg。否认肾脏疾病史,无高血压、糖尿病史,无食物、药物过敏史,无关节痛、皮疹、脱发及口腔溃     

中国肾小管间质肾炎-葡萄膜炎综合征的疾病特征及研究现况

正肾小管间质肾炎-葡萄膜炎(tubulointerstitial nephritis and uveitis,TINU)综合征是一类以急性肾小管间质肾炎(acute tubulointerstitial nephritis,ATIN)伴发眼部葡萄膜炎为主要特征的疾病。1975年首次发现至今,全球已先后报道300余例TINU综合征病例~([1])。由于TINU综合征发病     

中药致急性肾小管间质性肾炎临床病理特点分析

目的分析中药致药物相关性急性肾小管间质性肾炎(drug-induced acute tubulointerstitial nephritis,D-ATIN)的临床病理特点以及预后情况。方法回顾性分析2002年1月至2013年1月北京大学第一医院肾内科经临床病理确诊的119例D-ATIN患者临床及随访资料,入选11例单纯应用中药致D-ATIN患者为中药组,并选择同期的10例β内酰胺类抗生素致D-ATIN的患者为抗生素组,进行临床病理特征及预后分析。结果中药组患者以女性(10/11)为主。与β内酰胺类致D-ATIN组患者相比,中药组患者过敏反应少见,用药时间及患者开始用药至临床发病的时间较长。2组患者全身炎症反应以及肾功能损害程度(血肌酐水平)无统计学差异,但中药致D-ATIN患者尿N-乙酰-D葡萄糖酐转化酶(N-acetyl-β-D-glucosaminidase,NAG)以及微量白蛋白水平(micro-albumi,mAlb)均显著低于抗生素组患者[NAG:18(12.5,19.5)比28(14,72.5),P=0.05;mAlb:62.4(47,85.6)比107(76.4,172.5),P=0.031]。2组患者肾脏病理急性评分没有明显差异;中药组患者慢性病变评分(包括肾小管萎缩和肾间质纤维化)明显高于抗生素组[1.0(0,1.0)比0(0,0),P=0.033]。随访1个月和1年时中药致D-ATIN患者的估计肾小球滤过率均小于内酰胺类抗生素致D-ATIN患者[1个月时:(40.1±19.6)ml·min·(1.73 m~2)~(-1)比(50.8±15.8)ml·min·(1.73 m~2)~(-1),P=0.207);1年时:(64.9±21.7)ml·min·(1.73 m~2)~(-1)比(73.1±24.5)ml·min·(1.73 m~2)~(-1),P=0.448)],但无统计学差异。结论中药致D-ATIN的患者起病隐袭,容易延误诊断。临床医生应提高警惕,减少不必要用药并加强对用药人群的肾损害监测。     

Biopsy-proven vancomycin-associated interstitial nephritis and acute tubular necrosis

Fewer than ten biopsy-proven case reports exist on vancomycin-associated interstitial nephritis (VAIN) and vancomycin-associated acute tubular necrosis (VAATN). Among these, several are confounded by the use of other potentially offending drugs. We report a case of isolated VAIN/VAATN in a patient on no other potentially nephrotoxic agents other than vancomycin. The patient received intravenous vancomycin for coagulase-negative staphylococcus bacteremia. Her baseline serum creatinine of 0.9 mg/dL increased to 9.6 mg/dL after 1 week of therapy during which vancomycin levels peaked at 141 μg/mL. Renal biopsy revealed acute interstitial nephritis with lymphocytic and eosinophilic infiltrate and acute tubular necrosis. Upon discontinuation of vancomycin and administration of prednisone complete renal recovery ensued over a period of 4 weeks.     

Non-steroidal anti-inflammatory drugs-associated acute interstitial nephritis with granular tubular basement membrane deposits

Acute tubulo-interstitial nephritis (ATIN) is an important cause of acute renal failure resulting from a variety of insults, including immune complex-mediated tubulo-interstitial injury, but drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) are a far more frequent cause. Overall, as an entity, ATIN remains under-diagnosed, as symptoms resolve spontaneously if the medication is stopped. We report on a 14-year-old boy who developed acute renal failure 2 weeks after aortic valve surgery. He was put on aspirin following surgery and took ibuprofen for fever for nearly a week prior to presentation. He then presented to the emergency department feeling quite ill and was found to have a blood urea nitrogen (BUN) concentration of of 147 mg/dl, creatinine of 15.3 mg/dl and serum potassium of 8.7 mEq/l. Dialysis was immediately initiated. A kidney biopsy showed inflammatory infiltrate consistent with ATIN. However, in the tubular basement membrane (TBM), very intense granular deposits of polyclonal IgG and C3 were noted. He needed dialysis for 2 weeks and was treated successfully with steroids for 6 months. His renal recovery and disappearance of proteinuria took a year. In conclusion, this is a first report of NSAIDs-associated ATIN, showing deposits of granular immune complex present only in the TBM and not in the glomeruli.     

A syndrome of acute interstitial nephritis and anterior uveitis

A syndrome of acute interstitial nephritis (AIN) and anterior uveitis is described in two children and the literature is reviewed. These disorders appear to improve, in uncontrolled studies, with systemic and topical ophthalmic corticosteroid treatment. Although the renal and ocular prognoses appear good, it is important to recotnize that patients with AIN are at risk for uveitis and if present, consultation with an ophthalmologist is recommended.     

群蜂蜇伤致急性肾小管坏死伴间质性肾炎一例

单蜂蜇伤人后多仅产生轻度的过敏反应,但群蜂蜇伤可导致多脏器功能障碍.其中急性肾损伤主要表现为急性肾小管坏死(ATN),罕见急性间质性肾炎(AIN),两者合并发生,国外仅1例报道[1].     

Possible mechanisms explaining the tendency towards interstitial fibrosis in aristolochic acid-induced acute tubular necrosis.

BACKGROUND: We explored possible mechanisms responsible for the inability of plerosis and the tendency towards fibrosis in aristolochic acid-induced acute tubular necrosis (AA-ATN). METHODS: Renal biopsy tissues from eight AA-ATN cases were examined. Tubulointerstitial injury was semiquantitatively assessed. Immunohistochemical steptavidin-peroxide (SP) methods were used to determine the expressions of proliferating cell nuclear antigen (PCNA), epidermal growth factor (EGF), alpha-smooth muscle actin (alpha-SMA), transforming growth factor-beta(1) (TGF-beta(1)), connecting tissue growth factor (CTGF), fibronectin (FN), collagen III (Col-III), collagen IV (Col-IV), factor VIII-related antigen (VIII-Ag) and vascular endothelial growth factor (VEGF). Ultramicrostructure of endothelial cells and basement membrane of peritubular capillaries (PTC) and glomerular capillaries was detected by electron microscopy. These data were compared with that of 9 cases of antibiotic-induced ATN (a-ATN) and 10 cases of minor mesangioproliferative non-IgA glomerulonephritis, which served as a control group. RESULTS: In AA-ATN, almost no renal tubular epithelial cells (RTEC) were PCNA-positive (0.01 +/- 0.02%), and EGF expression was considerably decreased (9.55 +/- 7.22%). This was in contrast with the highly active tubular proliferation (PCNA-positive RTEC 47.25 +/- 19.33%, P < 0.05) and increased EGF expression in a-ATN (64.38 +/- 19.22%, P < 0.05). The expression of alpha-SMA in the tubulointerstitium, the number of interstitial TGF-beta(1)-positive cells and the CTGF-positive interstitial area were all increased in both a-ATN and AA-ATN, with no obvious differences between the two groups. With respect to extracellular matrix (ECM) deposition, FN, Col-III and Col-IV were detected only in the interstitium of AA-ATN. PTC lumina were decreased in size and misshapen in the AA-ATN group. Also in AA-ATN, the luminal wall was partially disrupted, endothelial cells were swollen and vacuoles and granules were found in the cell plasma. Parts of the endothelial cells were detached from the tubular basement membrane. CONCLUSION: The strong ability for RTEC repair after acute injury was severely diminished in AA-ATN, and this effect may be partly due to reduced EGF expression. Anti-fibrosis mechanisms may also be impaired in AA-ATN, since both a-ATN and AA-ATN had increased expression of TGF-beta(1) and CTGF, whereas only the latter group showed ECM deposition. Injury and loss of PTC occurred in AA-ATN, and this may contribute to tubulointerstitial damage, the inability of plerosis and the tendency towards fibrosis in this disease.