Romão E A, Coimbra T M, Costa R S, Vieira Neto O M, Reis M A, Rodrigues Júnior A L, Ribeiro R A, Ravinal R C, Dantas M
University of São Paulo, Brazil.
Clin Nephrol. 2009 Dec;72(6):473-81.
The protein alpha1-microglobulin (alpha1-microg) is filtered by the glomeruli and fully reabsorbed by the proximal tubules, and tubulointerstitial injury compromises its reabsorption. The aim of this study was to determine which functional, morphological and inflammatory renal disorders associated with tubulointerstitial damage interfere with urinary excretion of alpha1-microg in patients with glomerulopathies.
38 patients (33.6 +/- 11.3 years) with primary or secondary glomerulopathies diagnosed by renal biopsies were studied. The urinary fractional excretion of alpha1-microg (FEalpha1-microg), the urinary monocyte chemoattractant protein-1/urinary creatinine (UMCP-1) index and 24-h proteinuria were determined. In the cortex of renal biopsies, the number of macrophages/104 microm2 of glomerular tuft (GT) and tubulointerstitial (TI) areas, the relative interstitial area (RCIA), and the relative interstitial fibrosis area (CIF) were measured. Results are reported as median and range and the Spearman non-parametric test was used to determine the correlations.
FEalpha1-microg was 0.165% (0.008% - 14,790.0%) in patients with glomerulopathies and 0.065% (0.010% - 0.150%) in the control group (p < 0.05; Mann-Whitney U-Test). FEalpha1-microg was correlated with creatinine clearance (r = -0.4396; p = 0.0358), UMCP-1 index (r = 0.5978; p < 0.0001), number of macrophages/TI area (r = 0.5634; p = 0.0034) and RCIA (r = 0.7436; p < 0.0001). However, FEa1-microg was not correlated with proteinuria (r = 0.1465; p = 0.5153) or with CIF (r = 0.0039; p = 0.98).
renal MCP-1 and the expansion and number of macrophages of the tubulointerstitial area participate in the increase of urinary excretion of alpha1-microg in patients with glomerulopathies. Although proteinuria and interstitial fibrosis have not been associated with this effect, the present study does not exclude some of these disorders in the pathophysiology of urinary excretion of alpha1-microg.
蛋白质α1 - 微球蛋白（α1 - microg）经肾小球滤过并被近端小管完全重吸收，而肾小管间质损伤会损害其重吸收功能。本研究的目的是确定在患有肾小球疾病的患者中，哪些与肾小管间质损伤相关的功能、形态和炎症性肾脏疾病会干扰α1 - microg的尿排泄。
对38例经肾活检确诊为原发性或继发性肾小球疾病的患者（33.6±11.3岁）进行研究。测定了α1 - microg的尿分数排泄（FEα1 - microg）、尿单核细胞趋化蛋白 - 1/尿肌酐（UMCP - 1）指数和24小时蛋白尿。在肾活检的皮质中，测量了肾小球簇（GT）和肾小管间质（TI）区域每104平方微米的巨噬细胞数量、相对间质面积（RCIA）和相对间质纤维化面积（CIF）。结果以中位数和范围表示，并使用Spearman非参数检验来确定相关性。
肾小球疾病患者的FEα1 - microg为0.165%（0.008% - 14,790.0%），对照组为0.065%（0.010% - 0.150%）（p < 0.05；Mann - Whitney U检验）。FEα1 - microg与肌酐清除率（r = -0.4396；p = 0.0358）、UMCP - 1指数（r = 0.5978；p < 0.0001）、巨噬细胞/TI区域数量（r = 0.5634；p = 0.0034）和RCIA（r = 0.7436；p < 0.0001）相关。然而，FEα1 - microg与蛋白尿（r = 0.1465；p = 0.5153）或CIF（r = 0.0039；p = 0.98）无关。
肾脏MCP - 1以及肾小管间质区域巨噬细胞的扩张和数量参与了肾小球疾病患者α1 - microg尿排泄的增加。虽然蛋白尿和间质纤维化与这种效应无关，但本研究并未排除这些疾病在α1 - microg尿排泄病理生理学中的某些作用。
