Comparison of surgically removed cardiac valves of patients with ESRD with those of the general population.
BACKGROUND
Patients with end-stage renal disease (ESRD) have increased vascular and valvular calcification compared with the general population. Recently, 44% of renal transplant recipients were found to have vascular calcification of the medial layer of the inferior epigastric artery that was associated with deposition of bone matrix proteins. Similar findings have been reported for native and bioprosthetic cardiac valves surgically removed from patients without ESRD.


METHODS
To determine whether valvular calcification in patients with ESRD is similar to that in patients without ESRD, we retrospectively examined surgically excised native cardiac valves of all hemodialysis patients and compared them pathologically with those of matched controls without renal failure. Valves were examined by using routine stains and immunohistochemistry for markers to endothelial cells, macrophages, B and T lymphocytes, alkaline phosphatase, osteopontin, and bone morphogenic protein 4.


RESULTS
Histologically, 7 of 10 valves from patients with ESRD had moderate to severe inflammation compared with 1 of 10 valves from control patients. Patients with ESRD had more endothelial cells/vascularity (P = 0.002) and macrophages (P = 0.069). There was no difference between the 2 groups with respect to B and T lymphocytes, alkaline phosphatase, osteopontin, or bone morphogenic protein 4.


CONCLUSIONS
The noncollagenous proteins bone morphogenic protein and osteopontin have been shown in surgically removed cardiac valves of patients with ESRD and the general population. However, valvular calcification in patients with ESRD is associated with enhanced inflammation, consistent with the previously reported greater C-reactive protein levels in this patient population and their increased risk for death.
Ottawa Hospital, Ottawa, Ontario, Canada.
Sahar
S
Kajbaf
John P
JP
Veinot
Andrew
A
Ha
Deborah
D
Zimmerman
D000469:Alkaline Phosphatase / Q000032:analysis; D015415:Biomarkers; D055415:Bone Morphogenetic Protein 4; D019485:Bone Morphogenetic Proteins / Q000032:analysis; D002114:Calcinosis / Q000150:complications / Q000473:pathology* / Q000601:surgery; D015897:Comorbidity; D042783:Endothelial Cells / Q000473:pathology; D005260:Female; D006349:Heart Valve Diseases / Q000150:complications / Q000473:pathology* / Q000601:surgery; D006351:Heart Valves / Q000737:chemistry / Q000473:pathology* / Q000601:surgery; D006801:Humans; D007249:Inflammation; D007676:Kidney Failure, Chronic / Q000150:complications / Q000473:pathology* / Q000628:therapy; D008017:Life Expectancy; D016131:Lymphocyte Subsets / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D053495:Osteopontin; D006435:Renal Dialysis; D012189:Retrospective Studies; D012795:Sialoglycoproteins / Q000032:analysis; D016037:Single-Blind Method
C525809:BMP4 protein, human; D015415:Biomarkers; D055415:Bone Morphogenetic Protein 4; D019485:Bone Morphogenetic Proteins; C506895:SPP1 protein, human; D012795:Sialoglycoproteins; D053495:Osteopontin; D000469:Alkaline Phosphatase