Increased urinary excretion of monocyte chemoattractant protein-1 in proteinuric renal diseases
Increased urinary excretion of monocyte chemoattractant protein-1 in proteinuric renal diseases
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DOI：
10.1081/jdi-120021156
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发表时间：
2003-01-01
期刊：
影响因子：
3
通讯作者：
Ito, S
中科院分区：
文献类型：
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作者：
Morii, T;Fujita, H;Ito, S
单核细胞趋化蛋白-1(MCP-1)是一种趋化因子，主要由肾小管上皮细胞产生，参与肾间质炎症和纤维化。最近，我们发现在2型糖尿病患者中，尿单核细胞趋化蛋白-1的排泄量与蛋白尿(蛋白尿)的程度成正比，并与尿N-乙酰氨基葡萄糖苷酶(NAG)水平呈正相关。根据这些发现，我们认为大量蛋白尿本身可能通过增加肾小管MCP-1的表达而加重糖尿病肾病的肾小管损害，加速疾病进展。在本研究中，我们检测了IgA肾病伴大量白蛋白尿患者(IgAN组，n=6)的尿单核细胞趋化蛋白-1(MCP-1)水平，并与2型糖尿病伴明显糖尿病肾病(DN组，n=23)和无糖尿病肾病(Non-糖尿病肾病，n=27)患者的尿MCP-1水平进行了比较。尿单核细胞趋化蛋白-1排泄量在非糖尿病肾病组为157.2(52.8%~378.5)，糖尿病肾病组为346.1(147.0~1276.7)，免疫球蛋白肾病组为274.4(162.2~994.5)ng/g肌酐(中位数)。与非糖尿病肾病组相比，糖尿病肾病组和IgAN组尿MCP-1和NAG排泄量明显升高。因此，我们认为MCP-1在蛋白尿状态下肾小管上皮细胞表达增强，与肾脏疾病的类型无关，并且MCP-1表达增加可能是蛋白尿状态下肾小管损伤的原因之一。
Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that is produced mainly by tubular epithelial cells in kidney and contributes to renal interstitial inflammation and fibrosis. More recently, we have demonstrated that urinary MCP-1 excretion is increased in proportion to the degree of albuminuria (proteinuria) and positively correlated with urinary N-acetylglucosaminidase (NAG) levels in type 2 diabetic patients. Based on these findings, we have suggested that heavy proteinuria, itself, probably aggravates renal tubular damage and accelerates the disease progression in diabetic nephropathy by increasing the MCP-1 expression in renal tubuli. In the present study, to evaluate whether urinary MCP-1 excretion is increased in the proteinuric states not only in diabetic nephropathy but also in other renal diseases, we examined urinary MCP-1 levels in IgA nephropathy patients with macroalbuminuria (IgAN group; n = 6), and compared the results with the data obtained from type 2 diabetic patients with overt diabetic nephropathy (DN group; n = 23) and those without diabetic nephropathy (non-DN group; n = 27). Urinary MCP-1 excretion levels in non-DN, DN, IgAN groups were 157.2 (52.8-378.5), 346.1 (147.0-1276.7), and 274.4 (162.2-994.5) ng/g creatinine, median (range), respectively. Expectedly, urinary MCP-1 and NAG excretion levels in DN and IgAN groups were significantly elevated as compared with non-DN group. Therefore, we suggest that MCP-1 expression in renal tubuli is enhanced in proteinuric states, irrespective of the types of renal disease, and that increased MCP-1 expression probably contributes to renal tubular damage in proteinuric states.