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신장질환 환자에서의 혈청 Procollagen Ⅲ Aminopeptide치의 변화

Other Titles
 Serum procollagen Ⅲ aminopeptide levels in patients with kidney disease 
Authors
 조한선 
Issue Date
1992
Description
의학과/석사
Abstract
[한글] 정상적인 신장의 조직에서 대부분의 세포외 간질의 성분은 mesangial cell로부터 합성 유리되며 이 세포로부터 제 Ⅰ형, Ⅲ형, Ⅳ형의 collagen과 laminin, fibronectin, 및 glycosaminoglycan이 분비된다. 이 중 제 Ⅳ형 collagen은 신사구체 기저막에서 많은 양이 생성되며 존재하는 것으로 알려져 있다. 이에 반해 신장 질환 환자에 있어서 제 Ⅲ형 collagen에 대한 보고는 거의 없는 상태로서 신장 질환의 연구에 있어서도 양측 신의 크기, 신기능 검사 등 고식적인 방법이 이용될 뿐이며, 결체 조직 증식과 신장질환과의 상호 관계는 알려지지 않은 상태이다. 본 연구에서는 신장 질환 환자군에 있어서 제 Ⅲ형 collagen의 생성과 연관이 있는지를 알아보고 정상 성인과 비교하기 위하여 collagen의 생합성을 대변하는 전구 물질 특이 분절의 하나인 procollagen Ⅲ aminopeptide를 측정하고 신장 질환 환자군에서 혈청 procollagen Ⅲ aminopeptide가 다른 변수들과 상관관계가 있는지를 조사하여 다음과 같은 결과를 얻었다. 1. 헐청 procollagen Ⅲ aminopeptide의 농도는 신장 질환 환자군에서 정상 성인 대조군에 비하여 통계학적으로 유의하게 높았다. 2. 급성 신부전 , 만성 말기성 신부전 및 원발성 사구체 신염환자군들의 비교 결과, 혈청procollagen Ⅲ aminopeptide는 급성신부전 환자군에서 통계학적으로 유의하게 높았다. 3. 신장 질환 환자들에 있어서 혈청procollagen Ⅲ aminopeptide의 농도는 혈청 creatinine phosphokinase, lactic dehydrogenase, C-reactive protein, 24시간 뇨의 procollagen Ⅲ aminopeptide의 농도, procollagen Ⅲ aminopeptide의 사구체 여과율, 크레아티닌 제거율에 대한 procollagen Ⅲ aminopeptide의 사구체 여과율에 대한 비와 의미 있는 양의 상관 관계가 있었다. 이상의 결과로서 신장 질환 환자에서 혈청의 procollagen Ⅲ aminopeptide의 농도는 정상 성인 대조군에 비하여 유의하게 높았고 이것은 신장에서의 제 Ⅲ형 collagen의 합성 및 혈중으로의 유리가 증가됨으로써 일어난 결과로 사료되며, 혈청 농도는 사구체 신염이 나 만성 말기성 신부전등 그 진행 속도가 느리거나 정체되어 있는 경우보다는 급성 진행상태를 보이는 급성 신부전에서 더욱 높은 겅향을 보였다. 또한 혈청 procollagen Ⅲ aminopeptide의 농도는 질병의 급성 시기 혹은 초기에 혈청 농도가 증가하는 여러 변수들과 양의 상관 관계를 보였다. Serum procollagen Ⅲ aminopeptide levels in patients with kidney disease Han Sun Cho Department of Medical Science, The Graduate School, Yonsei University (Directed by professor Young Hak Shim, M.D.) Collagens are the main structural proteins of the extracellular matrix. Their biochemistry has become increasingly interesting for the study of various diseases. Different formation and degradation products of collagen metabolism can be detected and quantified in serum. Type Ⅲ collagen is a major constituent of most dense and loose connective tissues in the body except bone, tendon and cartilage. Type Ⅲ collagen is synthesized as a procollagen which contains propeptide extensions at both ends of the molecule. The amino terminal propeptide is partially set free during the aynthesis and deposition of type Ⅲ collagen and partially retained in the molecules which remain on the surface of the collagen fibrils. The type Ⅲ amino terminal propeptide, when found in serum, can, in principlel, thus be derived from the synthesis of new tripe Ⅲ collagen in the organism or from the degradation of existing type Ⅲ collagen fibrils. Smaller degradation products related to procollagen Ⅲ aminopeptide (PIINP) are found in serum and excreted in urine. Serum PIIINP is increases in various such as myeloproliferative disease, liver fibrosis, a number of connective tissue disease, several malignant diseases and thyroid diseases. But it has not been proved yet whether the serum concentration is increased or not in kidder disease. The present study investigated serum and urinary PIIINP levels in patients with various type of kidney disease, but without, evidence of hepatic or any other disease. Serum PlIINP levels were compared with the conventional parameters of renal function and other conventional variables of patients with kidney disease. The results are as follows : 1. The mean level of PlIINP in kidney patients was 3 times as high as that of a normal control group, and the difference was stastically significant (student t-test, p<0.001). 2. Statistically significant differences for the PlIINP levels were obtained among patients with various kidney diseases, such as acute renal failure, chronic end-stage renal failure and primary glomerulonephritis. The PlIINP level is highest in the patient group with acute renal failure (One Way ANOVA test, p<0.01). 3. Positive correlations were established between PIIINP and various variables for kidney disease, such as CPK, LDH, CRP, and PIIIN excretion in 24hr urine (correlation analysis, r<0.5). It is concluded that, the serum concentration of PIIINP is increased in various kidney diseases as compared to normal control subjects. The high serum concentration of PlIINP does not seem to be influenced by renal excretion or tubular reabsorption. And, it suggests that type Ⅲ collagen production is increased in the renal tissue. Since the PIIINP level was highest in the patients with acute renal failure as compared to those with end stage renal failure or primary glomerulonephritis, it can be concluded that PIIINP production is much more increased in the acute and early phase of the disease process, not in the slow or static process of the disease. Since the serum concentration of PlIINP correlated with the serum concentration of various variable that increase in the acute or active process of disease, there is an indication that PIIINP increases in the acute or active process rather than in the chronic or atatic process.
[영문] Collagens are the main structural proteins of the extracellular matrix. Their biochemistry has become increasingly interesting for the study of various diseases. Different formation and degradation products of collagen metabolism can be detected and quantified in serum. Type Ⅲ collagen is a major constituent of most dense and loose connectiveb tissues in the body except bone, tendon and cartilage. Type Ⅲ collagen is synthesized as a procollagen which contains propeptide extensions at both ends of the molecule. The amino terminal propeptide is partially set free during the aynthesis and deposition of type Ⅲ collagen and partially retained in the molecules which remain on the surface of the collagen fibrils. The type Ⅲ amino terminal propeptide, when found in serum, can, in principlel, thus be derived from the synthesis of new tripe Ⅲ collagen in the organism or from the degradation of existing type Ⅲ collagen fibrils. Smaller degradation products related to procollagen Ⅲ aminopeptide (PIINP) are found in serum and excreted in urine. Serum PIIINP is increases in various such as myeloproliferative disease, liver fibrosis, a number of connective tissue disease, several malignant diseases and thyroid diseases. But it has not been proved yet whether the serum concentration is increased or not in kidder disease. The present study investigated serum and urinary PIIINP levels in patients with various type of kidney disease, but without, evidence of hepatic or any other disease. Serum PlIINP levels were compared with the conventional parameters of renal function and other conventional variables of patients with kidney disease. The results are as follows : 1. The mean level of PlIINP in kidney patients was 3 times as high as that of a normal control group, and the difference was stastically significant (student t-test, p<0.001). 2. Statistically significant differences for the PlIINP levels were obtained among patients with various kidney diseases, such as acute renal failure, chronic end-stage renal failure and primary glomerulonephritis. The PlIINP level is highest in the patient group with acute renal failure (One Way ANOVA test, p<0.01). 3. Positive correlations were established between PIIINP and various variables for kidney disease, such as CPK, LDH, CRP, and PIIIN excretion in 24hr urine (correlation analysis, r<0.5). It is concluded that, the serum concentration of PIIINP is increased in various kidney diseases as compared to normal control subjects. The high serum concentration of PlIINP does not seem to be influenced by renal excretion or tubular reabsorption. And, it suggests that type Ⅲ collagen production is increased in the renal tissue. Since the PIIINP level was highest in the patients with acute renal failure as compared to those with end stage renal failure or primary glomerulonephritis, it can be concluded that PIIINP production is much more increased in the acute and early phase of the disease process, not in the slow or static process of the disease. Since the serum concentration of PlIINP correlated with the serum concentration of various variable that increase in the acute or active process of disease, there is an indication that PIIINP increases in the acute or active process rather than in the chronic or atatic process.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/117076
Appears in Collections:
2. 학위논문 > 1. College of Medicine (의과대학) > 석사
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