"Virtually, the only way to confirm the presence of arterial calcification is through radiological imaging modalities. X-rays, ultrasonography and non-contrast CT may be used to detect macrocalcifications, whilst 18F-NaF PET scans are able to assess microcalcifications and angiography aids to visualise vascular stenosis 39. MRI is of limited value in the detection of calcifications, as they are proton-poor and diamagnetic, thus inconspicuous on conventional sequences 13,14."
"PET using 18F-NaF, a detector of cellular mechanisms related to bone formation 45,46, is significantly helpful for the assessment of microcalcification, since the pathophysiological mechanism of vascular calcifications connects the procedure to osteoblast-related mechanisms. Despite its low spatial resolution, PET has excellent sensitivity for calcifications."
"Contrary to conventional CT, 18F-NaF PET can detect early active calcium deposition on arterial walls in the form of microcalcifications, due to significantly higher resolution 47-49."
"When in doubt, alizarin red stain can be used to verify 18F-NaF in sites suspicious for microscopic calcification 50."
"leptin deficiency (in ob/ob mice), especially when high doses of vitamin D3 are administered 8"
"In diabetic patients, calcification sites upregulate the expression of ALP, Runx2 and annexin II, while downregulating annexin V. Alizarin red stain was found to be able to reveal calcium deposition in resected aortic valves of patients with diabetes mellitus 29."
"As one of the main causes of renal artery calcification is a disequilibrium in mineral-bone metabolism, the levels of certain serological markers are expected to be disturbed in affected patients. More notably, serum osteoprotegerin, bone-specific alkaline phosphatase (BAP), intact PTH, phosphorus and osteocalcin levels are usually elevated, while 25[OH]D3, 1,25[OH]2D3 and fetuin A levels are usually reduced 34."
"As one of the main causes of renal artery calcification is a disequilibrium in mineral-bone metabolism, the levels of certain serological markers are expected to be disturbed in affected patients. More notably, serum osteoprotegerin, bone-specific alkaline phosphatase (BAP), intact PTH, phosphorus and osteocalcin levels are usually elevated, while 25[OH]D3, 1,25[OH]2D3 and fetuin A levels are usually reduced 34."
"As one of the main causes of renal artery calcification is a disequilibrium in mineral-bone metabolism, the levels of certain serological markers are expected to be disturbed in affected patients. More notably, serum osteoprotegerin, bone-specific alkaline phosphatase (BAP), intact PTH, phosphorus and osteocalcin levels are usually elevated, while 25[OH]D3, 1,25[OH]2D3 and fetuin A levels are usually reduced 34."
Expected headings
"Associations"
"PET"
"Conventional calcifications, of renal or extrarenal location, are generally a result of the conversion of vascular smooth muscle cells to osteoblasts, due to retention of phosphate, hypercalcaemia, previous dialysis treatment, active vitamin D administration or calcification inhibitor deficiency among other causal factors 15."
"As one of the main causes of renal artery calcification is a disequilibrium in mineral-bone metabolism, the levels of certain serological markers are expected to be disturbed in affected patients. More notably, serum osteoprotegerin, bone-specific alkaline phosphatase (BAP), intact PTH, phosphorus and osteocalcin levels are usually elevated, while 25[OH]D3, 1,25[OH]2D3 and fetuin A levels are usually reduced 34."
"In diabetic patients, calcification sites upregulate the expression of ALP, Runx2 and annexin II, while downregulating annexin V. Alizarin red stain was found to be able to reveal calcium deposition in resected aortic valves of patients with diabetes mellitus 29."
"In cases of increased osteoblast activity and/or transformation of vascular smooth muscles cells to osteoblasts, markers such as osteoprotegerin, osteopontin, osteocalcin, MGP and bone matrix protein (BMP) are expected to be overexpressed 31. The more atherosclerotic plaques progress to type V and of fibrocalcific type, the more markers like BMP2 and transcription factors such as Cbfa1 and osterix are expressed 33."
"As one of the main causes of renal artery calcification is a disequilibrium in mineral-bone metabolism, the levels of certain serological markers are expected to be disturbed in affected patients. More notably, serum osteoprotegerin, bone-specific alkaline phosphatase (BAP), intact PTH, phosphorus and osteocalcin levels are usually elevated, while 25[OH]D3, 1,25[OH]2D3 and fetuin A levels are usually reduced 34."
"Virtually, the only way to confirm the presence of arterial calcification is through radiological imaging modalities. X-rays, ultrasonography and non-contrast CT may be used to detect macrocalcifications, whilst 18F-NaF PET scans are able to assess microcalcifications and angiography aids to visualise vascular stenosis 39. MRI is of limited value in the detection of calcifications, as they are proton-poor and diamagnetic, thus inconspicuous on conventional sequences 13,14."
"The main ultrasonographic appearance of vascular calcification is that of hyperechoic foci accompanied by acoustic shadowing 41. Its pattern of sound reflection allows an echogenicity seven times greater than that of the normal vessel wall and three times greater than uncalcified (lipid-rich, haemorrhagic or fibrotic) atherosclerotic plaques 42."
"Calcium appears white on non-contrast CT images due to its high attenuation (Hounsfield unit, HU) 38, diagnostically accepted when equal to, or greater than, 130 HU. These hyperdense lesions are typically found on the arterial walls in any plane, and the combination of coronal, axial and sagittal views offer an excellent 3D anatomical topographic localisation."
"Angiographic techniques are unable to depict macrocalcification, microcalcification or atherosclerotic plaques. They employ the excellent vascular imaging potential of contrast media to visualise arteries and all their branches, to assess any possible narrowing. It is known that calcifications are a causal factor of arterial stenosis, hence acting as a surrogate marker for the presence of vascular calcium deposition 44."