Urinary kidney injury molecule-1 is related to pathologic involvement in IgA nephropathy with normotension, normal renal function and mild proteinuria.
Urinary kidney injury molecule-1 is related to pathologic involvement in IgA nephropathy with normotension, normal renal function and mild proteinuria.
复制标题
尿肾损伤分子-1与血压正常、肾功能正常和轻度蛋白尿的IgA肾病的病理受累有关。
DOI：
10.1186/1471-2369-15-107
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发表时间：
2014-07-07
期刊：
影响因子：
2.3
通讯作者：
Lin S
中科院分区：
文献类型：
--
作者：
Xu PC;Wei L;Shang WY;Tian SL;Gu DM;Yan TK;Lin S
对于一些没有任何临床危险因素的患者，免疫球蛋白A肾病(IgAN)可能进展为肾功能衰竭，临床上轻度的IgAN发现严重的病理损害并不罕见。因此，我们调查了尿肾损伤分子-1(Kim-1)是否与临床轻度IgAN的病理参与有关。对51例血压正常、肾功能正常、蛋白尿 、 为1.0g/24小时的IgA肾病患者进行了尿KIM-1/肌酐测定。分析尿KIM-1与病理特征的关系。51例患者中有18例尿Kim-1升高。尿KIM-1增高者肾小管萎缩/间质纤维化程度较尿KIM-1正常者明显加重(T0/T1/T2，13/5/0vs.33/0/0，P = 0.004)。尿KIM-1升高的患者肾小球中含有新月体的比例高于尿KIM-1正常的患者(50%比18%，P = 0.026)。尿KIM-1与总新月体比例(R = 0.303，p = 0.031)和纤维新月体比例(R = 0.456，p = 0.001)相关，与细胞性新月体和纤维细胞新月体比例无关。尿KIM-1升高组血管病变发生率(44.4%)明显高于尿KIM-1正常组(18.1%)，但差异无统计学意义(p = 0.057)。在短期随访期间，尿Kim-1升高的患者和无尿Kim-1升高的患者对治疗的反应没有差异。尿KIM-1是肾小管间质损伤的反映。对于临床轻度的IgA肾病患者，尿Kim-1升高与肾活检病理损害相对严重有关。
IgA nephropathy (IgAN) may progress to renal failure for some patients without any clinical risk factors and it is not unusual to find severe pathologic damage in clinically mild IgAN. We therefore investigated whether urinary kidney injury molecule-1 (KIM-1) was related to pathologic involvement in clinically mild IgAN. Urinary KIM-1/creatinine of 51 IgAN patients with normotension, normal renal function and proteinuria < 1.0 g/24 h were tested. Relationships between urinary KIM-1 and pathologic features were analyzed. Eighteen of the 51 patients had elevated urinary KIM-1. The tubular atrophy/interstitial fibrosis was more severe in patients with elevated urinary KIM-1 than that in patients with normal urinary KIM-1 (T0/T1/T2, 13/5/0 vs. 33/0/0, P = 0.004). Proportion of glomeruli containing cresecents was higher in patients with elevated urinary KIM-1 than that in patients with normal urinary KIM-1 (50% vs. 18%, P = 0.026). Urinary KIM-1 correlated with the proportion of total crescents (R = 0.303, p = 0.031) and fibrous crescents (R = 0.456, p = 0.001), but did not correlate with the proportion of cellular crescents or fibrocellular crescents. Although the proportion of vascular lesions was higher in patients with elevated urinary KIM-1 (44.4%) than that in patients with normal urinary KIM-1 (18.1%), the difference was not significant (p = 0.057). There was no difference of the response to treatment between patients with and without elevated urinary KIM-1 during a short-term follow-up. Urinary KIM-1 is a reflection of tubularinstitial injury. For patients with clinically mild IgAN, high urinary KIM-1 is related to relatively severe pathologic involvement on renal biopsy.