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 tendon and cartilage. Type III collagen is synthesized as a procollagen which
contasins propeptide extensions at both ends of the ends fo the molecule. The amino terminal propeptide is partially set free during the synthesis and deposition of type. III collagen and partially collagen fibrils. The type III amino terminal
propeptide, when found in serum, can, in principle, thus be derived from the synthesis of new type III collagen in the organism or from the degradation of existing type III collagen fibrils.
Smaller degradation products related to procollagen III aminpeptide (PIIINP) are found in serum and excreted in urine. Serum PIINP is increased in various diseases such as myeloproliferative disease, liver fibrosis and cirrhosis, a number of
connective
tissue diseases, several malignant diseases and thyroid diseases. But it has not been proved yet whether the serum cncentration is increased or not in kidney disease.
The present study investitgated serum and urinary PIIINP levels in patients with various type of kidney disease, but without evidence of hepatic or any other desease. Serum PIIINP levels were compared with the conventional parameterds of renal
function
and other conventional variables of patients with kidney disease.
@ES The results are as follows:
@EN 1) The mean level of PIIINP 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 PIIINP levels were obtaned among patients with various kistage renal failure and primary glomerulonephritis. The PIIINP 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 PIIINP excretion I 24 hr urine (correlation analysis, r<0.5).
4) It is concluded that, the serum concentration of PIIINPO is increased in various kidney discases as compared to normal control subjects. The high serum concentration of PIIINP does not seem to ve 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 cooncentraiton of PIIINP correlated with
the
serum concentration of various variables 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 static process.
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