本文選題：干燥綜合征 + 腎損害　； 參考：《山西醫(yī)科大學(xué)》2014年碩士論文

【摘要】：目的對(duì)原發(fā)性干燥綜合征(pSS)伴腎損害患者及無(wú)腎損害患者的臨床資料進(jìn)行回顧性對(duì)比分析,進(jìn)一步研究pSS腎損害的臨床特點(diǎn)、免疫學(xué)特點(diǎn)及病理學(xué)特點(diǎn)和預(yù)后,提高對(duì)本病的認(rèn)識(shí),改善預(yù)后。 方法收集387例住院pSS患者臨慶資料,并分為兩組,其中合并腎臟損害組的患者198例,189例不合并腎臟損害組的患者為一組。回顧性分析對(duì)比兩組之間臨床表現(xiàn)、血液檢查、尿液檢查及免疫學(xué)特點(diǎn)的差別。分析72例伴腎損害患者的病理特點(diǎn)。 結(jié)果387例住院pSS患者,其中男42例,女345例,男女之比為1：8.2。198例伴腎損害患者中,其中男30例,女168例,男女之比為1：5.58。兩組間臨床表現(xiàn)比較：兩組間口干、眼干、關(guān)節(jié)痛、發(fā)熱、口腔潰瘍發(fā)生率差異無(wú)統(tǒng)計(jì)學(xué)意義；兩組間血清免疫球蛋白IgA、IgM、自身抗體(抗ANA、抗ds-DNA、抗SSA、抗SSB)及補(bǔ)體C3、C4的水平差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)；腎臟損害組血清類風(fēng)濕因子及免疫球蛋白IgG水平明顯增高,差異有統(tǒng)計(jì)學(xué)意義(P0.05)；腎損害組中,以Ⅰ型腎小管酸中毒(RTA)為表現(xiàn)的患者為102例,其中表現(xiàn)為低鉀血癥者為54例,周期性低鉀性麻痹12例,合并骨質(zhì)疏松6例；以腎小球病變?yōu)橹鞯陌槟I損害患者共69例,其中36例表現(xiàn)為腎病綜合征,33例為慢性腎小球腎炎;81例腎功能不全(40.9%),其中CKD1期27例,CKD2期18例,CKD3期9例,CKD4期15例,CKD5期12例；72例行腎穿刺患者中,69例為慢性間質(zhì)性腎炎(interstitial nephritis,IN);3例為輕微病變型腎小球腎炎,36例為IN合并系膜增生性腎小球腎炎；9例為增生硬化性腎小球腎炎；局9例為灶節(jié)段性腎小球硬化；6例為膜性腎病。72例行腎穿病理患者中33例IgM沉積、21例有IgG沉積、21例IgA沉積、、18例C4沉積、15例C1q沉積、12例C3沉積。隨訪66例腎活檢患者8-30月(中位時(shí)間18月)。至隨訪末,除一例死于腦血管意外外,其余患者全部存活,腎功能正�；蚝棉D(zhuǎn)。 結(jié)論1.間質(zhì)性腎炎為pSS患者主要的病理表現(xiàn),但同時(shí)合并腎小球腎炎患者也并不少見(jiàn)； 2.RF及IgG升高分別是pSS腎損害的獨(dú)立危險(xiǎn)因素； 3.腎病理檢查有助于pSS合并腎損害患者個(gè)體化治療,改善預(yù)后
[Abstract]:Objective to compare and analyze the clinical data of primary Sjogren's syndrome (PSS) with and without renal damage, and to study the clinical, immunological and pathological features and prognosis of PSS. To improve the understanding of the disease and improve the prognosis. Methods 387 inpatients with PSS were divided into two groups: 198 patients with renal damage and 189 patients with no renal damage. The clinical manifestations, blood examination, urine examination and immunological characteristics were retrospectively analyzed and compared between the two groups. The pathological features of 72 patients with renal damage were analyzed. Results there were 387 hospitalized patients with PSS, including 42 males and 345 females. The ratio of male to female was 1: 8.2.198, of which 30 were male and 168 female, the ratio of male to female was 1: 5.58. Comparison of clinical manifestations between the two groups: there was no significant difference in the incidence of xerostomia, ocular trunk, arthralgia, fever and oral ulcer between the two groups. There was no significant difference between the two groups in the levels of serum immunoglobulin IgA, autoantibodies (anti-ANA, anti-ds-DNA, anti-SSA, anti-SSBs) and complement C _ 3N _ 4 (P 0.05), but the levels of rheumatoid factor and immunoglobulin IgG in renal injury group were significantly higher than those in control group (P 0.05). In the renal injury group, 102 patients with type I renal tubular acidosis were found, including 54 patients with hypokalemia, 12 patients with periodic hypokalemic paralysis and 6 patients with osteoporosis. There were 69 cases of glomerular lesion with renal damage, of which 36 cases were characterized by nephrotic syndrome and 33 cases were chronic glomerulonephritis and 81 cases were chronic glomerulonephritis. Among them, 27 cases were CKD1 stage, 18 cases were CKD3 stage, 9 cases were CKD4 stage 15 cases were CKD5 stage 12 cases. In 72 cases of renal puncture, 69 cases were chronic interstitial glomerulonephritis and 3 cases were mild lesion glomerulonephritis. 36 cases were IN complicated with Mesangial proliferative glomerulonephritis. 9 cases were proliferative sclerosing glomerulonephritis. Among the 9 cases of focal segmental glomerulosclerosis, 6 cases were membranous nephropathy. 72 cases were treated with renal puncture pathology. Among them, 33 cases had IgM deposition 21 cases had IgG deposition 21 cases had IgA deposition, 18 cases had C4 deposition, 15 cases C 1q deposition and 12 cases C 3 deposition. A total of 66 patients with renal biopsy were followed up for 8-30 months (median 18 months). At the end of follow-up, all but one died of cerebrovascular accident, and the renal function was normal or improved. Conclusion 1. Interstitial glomerulonephritis is the main pathological manifestation of PSS, but it is not uncommon in the patients with glomerulonephritis. 2. The increase of RF and IgG are independent risk factors of PSS renal damage. 3. Renal pathological examination is helpful to individual treatment of PSS patients with renal damage and to improve prognosis.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R593.2;R692

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 唐福林;原發(fā)性干燥綜合征的發(fā)病機(jī)制[J];中華風(fēng)濕病學(xué)雜志;2000年01期

2 張卓莉,王燕,董怡;原發(fā)性干燥綜合征并發(fā)腎小管酸中毒的預(yù)后與治療[J];中華風(fēng)濕病學(xué)雜志;2001年02期

3 任紅,陳楠,陳曉農(nóng),潘曉霞,張文,郝翠蘭;干燥綜合征合并腎臟損害147例臨床病理及隨訪情況[J];中華風(fēng)濕病學(xué)雜志;2005年06期

4 吳媛媛;陳松華;謝迎東;郭思岑;張麗;張瑜;;干燥綜合征腎損害的超聲表現(xiàn)[J];臨床軍醫(yī)雜志;2011年05期

5 張磊;王淑清;王景宇;冬冬;;干燥綜合征致腎小管酸中毒腎臟影像學(xué)改變一例[J];臨床放射學(xué)雜志;2008年03期

6 程小云;劉怡欣;劉鋼;;原發(fā)性干燥綜合征腎臟損害38例臨床分析[J];四川醫(yī)學(xué);2008年12期

7 張波,劉志紅,曾彩虹,陳惠萍,周虹,黎磊石;原發(fā)性干燥綜合征腎損害的臨床病理分析[J];腎臟病與透析腎移植雜志;2002年06期

8 劉正釗;胡偉新;章海濤;鮑浩;劉志紅;;原發(fā)性干燥綜合征腎損害的臨床病理特征及預(yù)后[J];腎臟病與透析腎移植雜志;2010年03期

9 李萍,王偉剛;原發(fā)性干燥綜合征的腎損害[J];中國(guó)社區(qū)醫(yī)師;2004年14期

10 王潔,葉任高;38例原發(fā)性干燥綜合征并腎臟損害的病理與臨床分析[J];醫(yī)師進(jìn)修雜志;2003年05期

，

本文編號(hào)：2045662