title: Difference in coronary artery intima and media calcification in autopsied patients with chronic kidney disease.
abstract: BACKGROUND
  In patients with chronic kidney disease (CKD), coronary artery calcification occurs at two distinct sites in the vessel wall: the intima and the media. Arterial media calcification (AMC), a nonocclusive condition, affects hemodynamics differently compared to arterial intima calcification (AIC), which occurs in atherosclerotic plaques. Arterial calcification is considered a cell-regulated process resembling intramembranous bone formation. The purpose of this retrospective observational study was to clarify the morphological differences between AIC and AMC and to evaluate the role of vascular smooth muscle cells (VSMCs) and macrophages in AIC and AMC formation.
  
  
  METHODS
  We histologically analyzed 14 tissue specimens from 14 autopsies of patients with CKD Stage 5D who underwent hemodialysis and 5 specimens from 5 patients with CKD Stage 2 - 3 (90 ml/min/1.73 m2 > estimated GFR >= 30 ml/min/1.73 m2). We performed immunohistochemical staining of osteopontin (OPN) as a marker for bone matrix protein, alpha-smooth muscle actin (alphaSMA) for VSMCs, Cbfa1/Runx2 as a marker for osteoblastic differentiation of VSMCs, and CD68 for macrophages.
  
  
  RESULTS
  In the CKD 2/3 group, we also found AIC and AMC. OPN and CD68 expression in the CKD 2/3 group was similar to that in the CKD 5D group. Although we did not find Cbfa1/Runx2 positive cell expression in the CKD 2/3 group, we did find it in the CKD 5D group. We found CD68-positive cells predominantly in AIC and absent in AMC in both groups.
  
  
  CONCLUSIONS
  These findings suggest that the influence of Cbfa1/Runx2 pathway in coronary artery calcification depends on the CKD Stage. Expression of CD68-positive cells depends on the location of the coronary artery calcification.
authors.affiliation: Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan. hiraku@jikei.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Yoshida
authors.forename: K
authors.initials: K
authors.lastname: Yokoyama
authors.forename: T
authors.initials: T
authors.lastname: Yaginuma
authors.forename: I
authors.initials: I
authors.lastname: Ohkido
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Utsunomiya
authors.forename: M
authors.initials: M
authors.lastname: Kawakami
authors.forename: T
authors.initials: T
authors.lastname: Hosoya
mesh_terms: D000199:Actins / Q000032:analysis; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001344:Autopsy; D015415:Biomarkers / Q000032:analysis; D002114:Calcinosis / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D002908:Chronic Disease; D050659:Core Binding Factor Alpha 1 Subunit / Q000032:analysis; D003324:Coronary Artery Disease / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D003331:Coronary Vessels / Q000737:chemistry / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007674:Kidney Diseases / Q000150:complications* / Q000378:metabolism / Q000628:therapy; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D053495:Osteopontin / Q000032:analysis; D006435:Renal Dialysis; D012189:Retrospective Studies; D012720:Severity of Illness Index; D017539:Tunica Intima / Q000737:chemistry / Q000473:pathology*; D017540:Tunica Media / Q000737:chemistry / Q000473:pathology*; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D050659:Core Binding Factor Alpha 1 Subunit; D053495:Osteopontin; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C493709:RUNX2 protein, human; C506895:SPP1 protein, human