소아 특발성 IgA 신병증에서 신 손상의 예후 인자로서 신세뇨관 ICAM-1의 발현
Expression of Tubular Intercellular Adhesion Molecule-1 (ICAM-1) as a Marker of Renal Injury in Children with IgA Nephropathy
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목 적:저자들은 소아 IgA 신병증 환자를 대상으로 세뇨관 상피세포에서 ICAM의 발현이 신 손상의 예후인자로서 역할을 할 수 있는지를 알아보기 위하여, 신세뇨관 ICAM-1 발현과 조직소견 및 임상소견과의 연관성을 조사하고자 본 연구를 시행하였다. 방 법:IgA 신병증으로 진단된 43명의 환자를 후향적으로 분석하였고, Haas가 제안한 분류법에 따라 subclasses에 따라 비교하였다. 그리고 LSAB kit를 이용하여 세뇨관 상피 세포의 ICAM-1의 발현도를 평가했다. 결 과:IgA 신병증으로 진단된 43명의 평균 연령은 12.2±2.2세였으며, 남자 28명, 여자 15명이었다. 육안적 혈뇨에 따른 신세뇨관 ICAM-1 발현의 차이는 발견할 수 없었다. 그러나 단백뇨가 동반되었던 환자의 신세뇨관 ICAM-1의 발현율은 단백뇨가 없었던 환자들의 발현율에 비해 통계적으로 유의하게 높았다(78.72±14.19% vs. 55.80±32.20%, P<0.05). Haas의 조직학적 분류의 subclasses에 따른 ICAM-1의 발현율은 subclass가 증가할수록 ICAM-1의 발현율도 증가하였다. 신세뇨관 ICAM-1의 발현과 24시간 채집뇨의 총단백량 그리고 신세뇨관 ICAM-1의 발현과 조직학적 분류간의 상관성은 Spearmann 상관분석상 각각 통계적으로 유의한 상관관계를 보였다. 그러나 간질 염증세포 침윤, 섬유화, 신세뇨관 위축 정도와는 통계학적으로 유의한 상관 관계를 보이지 않았다. 결 론:소아 특발성 IgA 신병증에서 신세뇨관 ICAM-1의 발현은 신 손상 특히 사구체 손상의 정도를 잘 반영하고 있으며 예후 인자로서도 유용하게 이용할 수 있다고 생각한다.
Abstract
Purpose:In order to evaluate the value of the renal expression of ICAM-1 as a marker of renal injury, we analyzed the relationship between abnormal tubular expression of ICAM-1 and histopathological features and clinical manifestations in children with IgA nephropathy (IgAN). Methods:The clinical data from 43 patients with IgAN were analyzed retrospectively and compared to the histopathologic subclassification proposed by Haas. ICAM-1 in tubular epithelium was assessed using the LSAB(Labeled streptavidine biotin) kit on the renal biopsy specimens. Results:In 43 patients with primary IgAN, 28 males and 15 females aged 12.2±2.2 years were studied. There were no differences of renal tubular expression of ICAM-1 between patients with gross hematuria and without gross hematuria. But renal tubular expression of ICAM-1 in patients with proteinuria was significantly higher than that of in patients without proteinuria(78.72±14.19% vs. 55.80±32.20%, P<0.05). Renal tubular expression of ICAM-1 was also associated with the severity of histopathological degree using Haas classification method. In subclass I, renal tubular expression of ICAM-1 was significantly lower than those of other subclasses. A significant correlation was found between the tubular expression of ICAM-1 and the total amount of protein in 24 hour collected urine(rs=0.47236, P<0.05). But there were no significant correlations between the renal tubular expression of ICAM-1 and interstitial cellular infiltration, tubular atrophy, and interstitial fibrosis respectively(F=0.89, P>0.05; F=0.31, P>0.05; F=0.21, P>0.05). Conclusion:Renal tubular expression of ICAM-1 can be a useful marker of renal injury in children with IgAN.
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