acid-phosphatase has been researched along with Aortic-Diseases* in 6 studies
6 other study(ies) available for acid-phosphatase and Aortic-Diseases
Article | Year |
---|---|
[Relationship between coronary and abdominal calcification score, serum osteoprotegerin (OPG), and serum tartrate-resistant acid phosphatase (TRACP) -5b in pre-dialysis CKD patients].
Osteoprotegerin (OPG) inhibits interaction of the receptor-activator of nuclear factor-kappaB (RANK) ligand (RANKL) with its receptor RANK, which is expressed on osteoclasts. OPG appeared to accelerate vascular calcification in vitro by the inhibition of vascular osteoclast-like cells. On the contrary, early-onset arterial calcification was observed in OPG-deficient mice. We measured the coronary artery calcification score (CACS) and abdominal aortic calcification score (AAoCS) by multi-detector computed tomography in 30 pre-dialysis CKD patients (eGFR 20 mL/min on average). Biomarkers were measured, including serum OPG, soluble RANKL (sRANKL) and tartrate-resistant acid phosphatase (TRACP) -5b (the biomarker of osteoclasts independent of renal function). The median values of CACS and AAoCS were 54.4 and 1,088 Agatston units (AU), respectively. Serum OPG was increased and serum sRANKL was decreased. In a multivariate logistic regression analysis using CACS > or = 100 AU as the outcome variable, CACS was found to be positively correlated with serum corrected Ca x iP product and serum OPG, though it was not correlated with serum TRACP-5b. ROC curve analysis showed that the serum OPG cutoff value predicting CACS > or = 100 AU was 5.2 pmol/L (624 pg/mL). In a stepwise regression analysis, log (AAoCS + 1) was positively correlated with serum OPG alone, but it was not correlated with age, eGFR, serum albumin and bone alkaline phosphatase (BAP). No correlation was found between serum OPG and serum TRACP-5b. In conclusion, vascular calcification in pre-dialysis CKD patients was correlated with an increase in OPG, but was independent of serum TRACP-5b. The decrease in serum sRANKL may have been caused by the increase in OPG production. Topics: Acid Phosphatase; Aorta, Abdominal; Aortic Diseases; Biomarkers; Calcinosis; Coronary Disease; Coronary Vessels; Dialysis; Female; Humans; Isoenzymes; Logistic Models; Male; Osteoclasts; Osteoprotegerin; RANK Ligand; Tartrate-Resistant Acid Phosphatase | 2010 |
Aortic medial calcification in progeria-like syndrome.
Aortic medial calcification was investigated in rats in which the progeria-like syndrome (PLS) was evoked by administering dihydrotachysterol. In 35 experimental rats and 15 controls, calcification was studied morphologically by light and electron microscopy, and by enzyme histochemistry. Body weight, food intake and serum calcium levels were also determined. Calcification occurred along and on the elastic lamellae in association with the accumulation of ground substance. In the smooth-muscle cells surrounding the calcified foci, the activities of various lysosomal enzymes increased concomitantly with a tendency toward transformation of smooth-muscle cells to a modified form. From these observations, the role of ground-substance formation by smooth-muscle cells is postulated, and participation in the catabolism of ground substance by the lysosomal enzymes of these cells is suggested. It appears the increased activity of adenosine monophosphatase should be linked to the calcification. The etiology of weight loss, skin manifestations and aortic calcification in PLS rats seems to be different from that in human progeric diseases. Therefore, the PLS rat should not be readily accepted as an animal model for the study of progeric diseases. Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Aorta; Aortic Diseases; Apyrase; Body Weight; Calcinosis; Calcium; Dihydrotachysterol; Female; Glucuronidase; Hexosaminidases; Histocytochemistry; Phosphoric Monoester Hydrolases; Rats; Werner Syndrome | 1977 |
Increased activity of lysosomal enzymes in human atherosclerotic aortas.
Topics: Acid Phosphatase; Aorta; Aortic Diseases; Arteriosclerosis; Cathepsins; DNA; Glucuronidase; Humans; Sulfatases | 1969 |
Clinical and experimental studies on acid adenosine triphosphatase, with special reference to lysosomes and isozyme.
Topics: Acid Phosphatase; Adenosine Triphosphatases; Adult; Alkaline Phosphatase; Angina Pectoris; Animals; Aortic Diseases; Blood Proteins; Chromatography; Chromatography, Gel; Diabetes Mellitus; Dogs; Electrocardiography; Electrophoresis; Female; Heart Failure; Humans; Hypertension; Isoenzymes; Kidney; Kidney Diseases; Liver; Liver Diseases; Lysosomes; Male; Mesenteric Arteries; Middle Aged; Mitochondria; Muscles; Myocardium; Potassium; Radionuclide Imaging; Rats; Sodium; Transaminases | 1968 |
[Histochemical studies of aortic lesions following experimental hypertension].
Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Aortic Diseases; Edema; Enzymes; Esterases; Glucosephosphate Dehydrogenase; Glycosaminoglycans; Histocytochemistry; Hypertension; Lipase; Nucleotidases; Rabbits; Sulfatases | 1966 |
Distributions of succinic dehydrogenase, acid phosphatase and alkaline phosphatase in the kidneys of rats made hypertensive by partial constriction of the abdominal aorta.
Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Aorta; Aorta, Abdominal; Aortic Diseases; Constriction; Disease; Electron Transport Complex II; Hypertension; Kidney; Phosphoric Monoester Hydrolases; Rats; Succinate Dehydrogenase | 1957 |