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.
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.
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.
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.
"The pathophysiology underlying the rapid progression of aortic stenosis in dialysis patients has not been fully elucidated. A reduced aortic valve area at baseline, preexisting valvular calcification, and high levels of circulating calcium-phosphate product and parathyroid hormone have all been proposed to contribute to the progression of stenosis [3, 16–19]. Data on progression of prosthetic aortic valve stenosis in renal failure patients are scarce. "
[Show abstract][Hide abstract] ABSTRACT: Although renal failure is one of the known comorbidities associated with rapid progression of aortic stenosis, it is unclear whether hemodialysis alters the progression of prosthetic aortic valve stenosis. We describe a 79-year-old female who underwent bioprosthetic aortic valve replacement 8 years ago with stable prosthetic valve area for the initial 6 years. In the last two years, coinciding with the initiation of maintenance hemodialysis, she developed progressive prosthetic valve stenosis to the point of clinical decompensation. She underwent a second prosthetic aortic valve replacement with symptom resolution. This case suggests that circulating milieu in end-stage renal failure and dialysis can accelerate the progression of prosthetic aortic valve stenosis. More frequent clinical followup and surveillance echocardiogram for dialysis patients with bioprosthetic aortic valve may facilitate timely management of valvular stenosis.
"We found inflammation, neovascularization, and bone morphogenic proteins in degenerative valves from both the normal and the dialysis populations (Fig. 2). Interestingly, when the results were unblinded, the patients with dialysis seemed to have more neovascularization and chronic inflammation than the nondialysis patients . Enhanced inflammation in patients with ESRD is consistent with the marked elevation of acutephase reactants in patients with ESRD compared to the general population. "
[Show abstract][Hide abstract] ABSTRACT: Rheumatic disease is an important cause of inflammatory native heart valve disease. However, with increased understanding of the pathoetiology of valve disease and valve injury, it is evident that inflammation may play a role in many valve disorders. We are only beginning to understand these complex processes. With increasing knowledge that many of these processes are active, there may be opportunity for intervention or even prevention.
"Data providing contribution of serum CRP to valve calcification in the clinical setting is available in patients with renal failure. Valvar calcification in patients with renal failure is associated with enhanced inflammation . Furthermore, in chronic hemodyalisis patients in steady clinical conditions with no clinical evidence of either infectious or inflammatory diseases, a high CaxPO4 is associated with high CRP concentrations and hence associated with valvar calcification [13,14]. "
[Show abstract][Hide abstract] ABSTRACT: Degenerative aortic valve stenosis includes a range of disorder severity from mild leaflet thickening without valve obstruction, "aortic sclerosis", to severe calcified aortic stenosis. It is a slowly progressive active process of valve modification similar to atherosclerosis for cardiovascular risk factors, lipoprotein deposition, chronic inflammation, and calcification. Systemic signs of inflammation, as wall and serum C-reactive protein, similar to those found in atherosclerosis, are present in patients with degenerative aortic valve stenosis and may be expression of a common disease, useful in monitoring of stenosis progression.
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