Marín C, Mosquera J, Rodríguez-Iturbe B
Servicio de Nefrología, Hospital Universitario, Maracaibo, Venezuela.
Clin Nephrol. 1997 Apr;47(4):217-21.
Serum neuraminidase (NA, sialidase) activity has been demonstrated in acute poststreptococcal glomerulonephritis (APSGN) and implicated in the pathogenesis of the disease. Recent investigations show that neuraminidase-treated leukocytes accumulate preferentially in kidneys; therefore, we were interested in knowing if desialized cells infiltrate the kidney in APSGN. We first tested the capacity of peanut agglutinin lectin (PNA) to detect injected NA-treated leukocytes in the kidney of rats. NA-treated leukocytes were transfused and desialized cells were identified with fluorescein-conjugated peanut lectin (FITC-PNA) in renal tissue. PNA positive cells were identified in rat kidneys 3 hours after injection (glomeruli: 1.67 +/- 0.19 cells/g.c.s.; interstitium: 0.50 +/- 0.12 cells/int). Sections from available renal biopsy material of APSGN (n = 11), other glomerulonephritis (n = 28) and normal kidneys (n = 5) were double-stained with FITC-PNA and with monoclonal antibody to the CD11b molecule, which is expressed on polymorphonuclear and monocytes the main types of infiltrating cells during APSGN. Desialized (FITC-PNA positive) cells were found in the glomeruli (2.17 +/- SEM 0.22 cells per glomerular cross section, g.c.s.) and interstitium (0.61 +/- 0.15 cells per 0.0625 mm2, int) in all biopsies of APSGN. Only in 2 of 28 other glomerulonephritis showed desialized cells. More than 80% of the PNA positive cells in APSGN expressed the CD11b molecule and the infiltration was more intense in early biopsies. In conclusion, desialized leukocytes represent a significant part of the inflammatory infiltrate in APSGN. This finding gives support for a role of NA in the disease and provides clinical validation for a mechanism of renal cellular infiltration suggested by experimental observations.
血清神经氨酸酶(NA,唾液酸酶)活性已在急性链球菌感染后肾小球肾炎(APSGN)中得到证实,并与该疾病的发病机制有关。最近的研究表明,经神经氨酸酶处理的白细胞优先在肾脏中积聚;因此,我们想了解去唾液酸化细胞是否会在APSGN中浸润肾脏。我们首先测试了花生凝集素(PNA)检测注射了经NA处理的白细胞的大鼠肾脏中的能力。将经NA处理的白细胞进行输血,并在肾组织中用荧光素偶联花生凝集素(FITC-PNA)鉴定去唾液酸化细胞。注射后3小时在大鼠肾脏中鉴定出PNA阳性细胞(肾小球:1.67±0.19个细胞/g.c.s.;间质:0.50±0.12个细胞/间质)。对APSGN(n = 11)、其他肾小球肾炎(n = 28)和正常肾脏(n = 5)的可用肾活检材料切片进行FITC-PNA和抗CD11b分子单克隆抗体双重染色,CD11b分子在多形核细胞和单核细胞上表达,是APSGN期间浸润细胞的主要类型。在所有APSGN活检中,在肾小球(每个肾小球横截面2.17±SEM 0.22个细胞,g.c.s.)和间质(每0.0625平方毫米0.61±0.15个细胞,间质)中发现了去唾液酸化(FITC-PNA阳性)细胞。在28例其他肾小球肾炎中只有2例显示有去唾液酸化细胞。APSGN中超过80%的PNA阳性细胞表达CD11b分子,并且在早期活检中浸润更强烈。总之,去唾液酸化白细胞是APSGN中炎症浸润的重要组成部分。这一发现支持了NA在该疾病中的作用,并为实验观察所提示的肾细胞浸润机制提供了临床验证。