药物相关性间质性肾炎与IgA肾病肾间质炎症病变特点的比较

目的探讨人类药物相关性间质性肾炎(D-IN)和IgA肾病(IgAN)肾小管间质免疫炎症反应特点的异同。方法观察33例D-IN(急性23例,慢性10例)和32例IgAN患者肾活检组织中肾小管间质病变的特点,应用免疫组化法观察T淋巴细胞和单核/巨噬细胞浸润情况,α-平滑肌肌动蛋白(α-SMA)和骨桥蛋白(OPN)的表达,结合临床资料进行相关分析。结果两组患者CD3+的T淋巴细胞和CD68+的单核/巨噬细胞均为肾间质的主要浸润细胞。D-IN组急性病例以CD3+细胞为主(CD3+/CD68+为3.7±1.0),慢性病例以CD68+细胞为主(CD3+/CD68+为0.3±0.1,P0.05)。IgAN组两种细胞在数量上显著相关(r=0.839,P0.001),比例不随病变程度加重而变化。IgAN组,CD3+与CD68+细胞的浸润程度均与血肌酐、肾间质纤维化以及α-SMA阳性面积呈正相关(r=0.568,0.612;0.703,0.769;0.597,0.655,P均0.001)。D-IN组,CD3+/CD68+与肾间质纤维化和α-SMA阳性面积呈负相关(r=-0.587、-0.442,P0.05)。两组肾小管上皮OPN表达均明显增加并与CD68+细胞数量呈正相关(r=0.7604、0.8547,P0.001)。结论在IgAN中,T淋巴细胞和单核/巨噬细胞可能共同参与肾小管间质的慢性损伤过程;而在D-IN中,单核/巨噬细胞在肾功能恶化和病情慢性化过程中可能起主导作用。

Characteristics of interstitial inflammation in drug-induced tubulointerstitial nephritis and IgA nephropathy

Objective To compare the features of interstitial inflammation between tubulointerstitial nephritis (D-IN) and IgA nephropathy (IgAN). Methods Immunohistochemical SP method was applied to observe the inflammatory infiltration of CD3+ T lymphocytes, CD68+ monocytes/macrophages (Mo/Mac), and the expression ofα-SMA and osteopontin (OPN) in renal biopsy specimens of 33 cases of D-IN and 32 cases of IgAN. Results In D-IN, T lymphocytes were the major infiltrating cells in acute cases, while Mo/Mac were predominant in chronic cases. In IgAN, there was a close relationship between the numbers of infiltrating T lymphocytes and Mo/Mac (r = 0.839, P < 0.001). In IgAN, both T lymphocytes and Mo/Mac were associated with SCr, interstitial fibrosis and α-SMA expression (r = 0.568 and 0.612; 0.703 and 0.769; 0.597 and 0.655, P < 0.001). In D-IN, the ratio of T lymphocytes to Mo/Mac was associated with interstitial fibrosis (r = -0.587, P < 0.05). OPN was up-regulated in the tubules of both groups, which had positive correlation with Mo/Mac infiltrating (r = 0.7604 and 0.8547, P < 0.001). Conclusion In IgAN, both T lymphocytes and Mo/Mac are involved in chronic progression of the disease, while in D-IN, Mo/Mac might play the major role in the development of fibrosis.