Low molecular weight proteinuria in human immunodeficiency virus-infected patients
Low molecular weight proteinuria in human immunodeficiency virus-infected patients
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DOI：
10.1016/s0272-6386(96)90517-x
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发表时间：
1996-06-01
影响因子：
13.2
通讯作者：
deStrihou, CV
中科院分区：
文献类型：
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作者：
Kabanda, A;Vandercam, B;deStrihou, CV
为了确定人类免疫缺陷病毒（HIV）感染是否与早期肾小管或肾小球缺陷相关，我们测定了四种低分子量蛋白（LMWP）的尿液排泄量； β(2)-微球蛋白 (U-beta(2)-m)、胱抑素 C (U-cyst C)、克拉拉细胞蛋白 (U-CC16) 和视黄醇结合蛋白 (U-RBP)，肾小管功能障碍的标志物，白蛋白 (U-Alb) 的排泄，肾小球缺陷的标志物，以及 N-乙酰基-β-D-氨基葡萄糖苷酶 (U-NAG)，近端肾小管上皮结构损伤的标志物。使用年龄、性别、血清-β(2)-m (S-β(2)-m)、CD4 淋巴细胞计数或 HIV 感染阶段和治疗作为可能的预测因子，通过逐步回归分析对其决定因素进行了评估。该研究涉及 76 名无肾病的 HIV 感染患者，其中 56 名 S-β(2)-m < 5 mg/L（B-1 组），20 名 S-beta(2)-m 大于或等于 5 mg/L（B-2 组），以及 30 名 HIV 阴性对照。 14 名患者 (18.4%) 没有异常尿蛋白丢失，62 名患者 (81.6%) 至少一种蛋白质（Alb、LMWP 或 NAG）的尿排泄量升高。 21 名患者中有单一尿蛋白异常（U-beta(2)-m，n = 9；U-RBP，n = 2；U-CC16，n = 4；U-Alb，n = 6）。 23 名患者中至少有 2 名 LMWP 异常，但 U-Alb 未升高（12 名 U-NAG 升高，11 名 U-NAG 正常）。 10 名患者尿中至少一种 LMWP 与 U-Alb 的排泄量增加（5 名患者 U-NAG 增加，5 名患者 U-NAG 正常）。在最后 8 名患者中观察到所有蛋白质的尿排泄增加。 HIV 组中所有蛋白质（囊肿 C 除外）的平均尿排泄量显着高于对照组。正如预期的那样，B-2 组的 U-β(2)-m 值和异常 U-β(2)-m 值的发生率高于 B-1 组 (P = 0.0001)，而平均尿排泄量和 Alb、LMWP（β(2)-m 除外）或 NAG 值升高的发生率在两个 HIV 组中相同。通过逐步回归分析，年龄成为尿中 β(2)-m 和 CC16 排泄的重要决定因素，而男性与 U-CC16 增加相关。由于 S-beta(2)-m 与 HIV 感染阶段 (r = -0.52，P = 0.0001) 或 CD4 计数 (r = -0.45，P = 0.0002) 之间密切相关，因此 S-beta(2)-m、CD4 淋巴细胞计数或 HIV 感染阶段仅成为 U-beta(2)-m 的重要决定因素。超过 80% 的无明显肾脏疾病的 HIV 感染患者有肾小球通透性缺陷或肾小管功能障碍的证据，无论疾病处于哪个阶段。 U-Alb、RBP 和 CC16 似乎是这些异常最敏感和最可靠的早期标志物。它们的原因和预后价值仍有待确定。 (C) 1996 年，国家肾脏基金会 (National Kidney Foundation, Inc.)
To determine whether human immunodeficiency virus (HIV) infection is associated with incipient tubular or glomerular defects, we determined the urinary excretion of four low molecular weight proteins (LMWP); beta(2)-microglobulin (U-beta(2)-m), cystatin C (U-cyst C), Clara cell protein (U-CC16), and retinol-binding protein (U-RBP), the markers of tubular dysfunction, the excretion of albumin (U-Alb), a marker of glomerular defect, and the excretion of N-acetyl-beta-D-glucosaminidase (U-NAG), a marker of structural damage of the proximal tubular epithelium. Their determinants have been assessed by stepwise regression analysis using as possible predictors age, sex, serum-beta(2)-m (S-beta(2)-m), CD4 lymphocyte count, or HIV infection stage and therapy. The study involved 76 HIV-infected patients without renal disease, 56 with S-beta(2)-m < 5 mg/L (Group B-1), 20 with S-beta(2)-m greater than or equal to 5 mg/L (Group B-2), and 30 HIV-negative controls. Fourteen patients (18.4%) had no abnormal urinary protein loss, and 62 (81.6%) had elevated urinary excretion of at least one protein (Alb, LMWP, or NAG). A single urinary protein was abnormal in 21 patients (U-beta(2)-m, n = 9; U-RBP, n = 2; U-CC16, n = 4; and U-Alb, n = 6). At least two LMWP were abnormal without increased U-Alb in 23 patients (12 with increased and 11 with normal U-NAG). Ten patients had an increased urinary excretion of at least one LMWP together with U-Alb (5 with increased and 5 with normal U-NAG). An increased urinary excretion of all proteins was observed in the last 8 patients. The average urinary excretion of all proteins (except cyst C) was significantly higher in HIV than in the control group. As expected, U-beta(2)-m and the prevalence of abnormal U-beta(2)-m values were higher in the B-2 than in the B-1 group (P = 0.0001), whereas the average urinary excretion and the prevalence of elevated values of Alb, LMWP (except beta(2)-m) or NAG were the same in both HIV groups. By stepwise regression analysis, age emerged as a significant determinant of urinary excretion of beta(2)-m and CC16, whereas male sex was associated with increased U-CC16. S-beta(2)-m, CD4-lymphocyte count, or HIV infection stage emerged as significant determinants only for U-beta(2)-m as a consequence of a close correlation between S-beta(2)-m and either HIV infection stage (r = -0.52, P = 0.0001), or CD4 count (r = -0.45, P = 0.0002). Over 80% of HIV-infected patients without overt renal disease have evidence of glomerular permeability defects or tubular dysfunction, whatever the stage of the disease. U-Alb, RBP, and CC16 appear as the most sensitive and reliable early markers of these abnormalities. Their cause and prognostic value remain to be determined. (C) 1996 by the National Kidney Foundation, Inc.