Serum and Urine Interferon Gamma-Induced Protein 10 (IP-10) Levels in Lupus Nephritis.
Serum and Urine Interferon Gamma-Induced Protein 10 (IP-10) Levels in Lupus Nephritis.
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DOI：
10.3390/jcm11113199
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发表时间：
2022-06-03
影响因子：
3.9
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中科院分区：
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背景：狼疮性肾炎（LN）是系统性红斑狼疮（SLE）的一种常见且严重的并发症。非侵入性诊断是有限的，目前的治疗有不足的反应率。趋化因子干扰素-γ诱导蛋白10 （IP-10）的表达受干扰素-γ信号和NF-κB的调控，其分子活性和尿浓度升高与LN有关，但其作为诊断标志物的用途及其与人口统计学、临床或病理特征的关联尚不明确。方法：38例LN患者和11例伴有活动性疾病的非LN肾小球疾病（GD）患者。18名LN患者在研究期间的一次随访中获得缓解。取血清和尿液，测定IP-10水平。结果：活动性LN患者的血清和尿液IP-10水平明显高于正常人（血清平均179.7 pg/mL vs. 7.2 pg/mL, p < 0.0001；尿平均28.7 pg/mg vs. 1.6 pg/mg, p = 0.0019）和其他肾小球疾病患者（血清平均179.7 pg/mL vs. 84.9 pg/mL, p = 0.0176；尿平均28.7 pg/mg vs. 0.18 pg/mg, p = 0.0011）。增生性LN （PLN）患者的尿IP-10水平显著高于膜性LN （MLN）患者（平均32.8 pg/mg vs. 7.6 pg/mg, p = 0.0155）。MLN患者的尿IP-10水平也高于原发性膜性肾病（MN）患者（平均7.6 pg/mg vs. 0.2 pg/mg, p = 0.0193）。重要的是，血清IP-10水平在活动性LN和LN缓解期间保持升高，但72%的患者从活动性LN到缓解期尿液IP-10水平下降。最后，非裔美国LN患者在活动性LN（平均227.8 pg/mL vs. 103.4 pg/mL, p = 0.0309）和LN缓解期（平均254.6 pg/mL vs. 89.2 pg/mL, p = 0.0399）的血清IP-10水平显著高于美国白人LN患者（而非尿IP-10水平）。结论：我们的研究结果表明，血清和尿液IP-10测量为监测LN活动、LN分类之间的区分以及LN与其他形式的肾小球疾病之间的区分提供了有希望的测试。我们还得出结论，进一步评估高危人群（即非裔美国人）血清和尿液中IP-10水平升高可能有助于确定为什么许多这些患者预后较差，对标准治疗无反应。
Background: Lupus nephritis (LN) is a prevalent and severe complication of systemic lupus erythematosus (SLE). Non-invasive diagnostics are limited, and current therapies have inadequate response rates. Expression of the chemokine Interferon-γ-induced protein 10 (IP-10) is regulated by Interferon-γ signaling and NF-κB, and its molecular activity and enhanced urine concentrations are implicated in LN, but its utility as a diagnostic marker and association with demographic, clinical, or pathologic features is not defined. Methods: 38 LN patients and 11 patients with non-LN glomerular diseases (GD) with active disease were included. Eighteen of the LN patients had achieved remission at one follow-up during the study time. Serum and urine were obtained from these samples, and the IP-10 levels were measured. Results: Serum and urine IP-10 levels are significantly enhanced in LN patients with active disease as compared with normal individuals (serum average 179.7 pg/mL vs. 7.2 pg/mL, p < 0.0001; urine average 28.7 pg/mg vs. 1.6 pg/mg, p = 0.0019) and patients with other forms of glomerular disease (serum average 179.7 pg/mL vs. 84.9 pg/mL, p = 0.0176; urine average 28.7 pg/mg vs. 0.18 pg/mg, p = 0.0011). Urine IP-10 levels are significantly higher in patients with proliferative LN (PLN) than those with membranous LN (MLN) (average 32.8 pg/mg vs. 7.6 pg/mg, p = 0.0155). Urine IP-10 levels are also higher in MLN versus primary membranous nephropathy (MN) (average 7.6 pg/mg vs. 0.2 pg/mg, p = 0.0193). Importantly, serum IP-10 levels remain elevated during active LN and LN remission, but urine IP-10 levels are decreased from active LN to remission in 72% of our patients. Lastly, serum, but not urine IP-10 levels are significantly higher in African American than White American LN patients in active LN (average 227.8 pg/mL vs. 103.4 pg/mL, p = 0.0309) and during LN remission (average 254.6 pg/mL vs. 89.2 pg/mL, p = 0.0399). Conclusions: Our findings suggest that serum and urine IP-10 measurements provide promising tests for monitoring LN activity, differentiation between classifications of LN, and differentiation between LN and other forms of glomerular disease. We also conclude that further assessment of elevated IP-10 levels in the serum and urine of high-risk populations (i.e., African American) could be beneficial in determining why many of these patients have worse outcomes and are non-responsive to standard therapeutics.
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