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http://purl.uniprot.org/citations/17389622http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Background

Chronic kidney disease (CKD) is associated with vascular and tissue calcification. The extent of vascular calcification has been identified as an independent risk factor of cardiovascular death in patients on haemodialysis.

Methods

We studied the role of fetuin-A in CKD-associated calcification using a mouse model of graded renal insufficiency generated by nephrectomy and high phosphate diet. We used wild-type and fetuin-A-deficient mice on the calcification resistant genetic background C57BL/6 to study the influence on calcification of CKD, dietary phosphate and fetuin deficiency. Hyperphosphataemia, elevated BUN, hyperparathyroidism and von Kossa histochemistry served as indicators of calcification disease. The expression of osteopontin, a marker of osteoblast-like cell differentiation was analyzed by realtime PCR and immunohistochemistry.

Results

We detected tissue and genotype-specific susceptibility for calcification. Fetuin-A-deficient mice with CKD and high phosphate diet had only a moderately elevated serum calcium phosphate product (6.9 +/-1.4 mmol(2)/l(2)), but suffered severe calcification of kidney, heart and lung. In contrast, wild-type mice under the same conditions developed renal calcinosis only despite an elevated serum calcium phosphate product (9.6 +/-0.9 mmol(2)/l(2)). Calcification was preceded by the local induction of osteopontin, a marker for osteoblast-like cell differentiation.

Conclusion

Fetuin-A deficiency, CKD and high phosphate diet act synergistically in the pathogenesis of extraosseous calcification."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.org/dc/terms/identifier"doi:10.1093/ndt/gfm094"xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Smeets R."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Jahnen-Dechent W."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Schafer C."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Floege J."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Ketteler M."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Westenfeld R."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/author"Brandenburg V.M."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/name"Nephrol Dial Transplant"xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/pages"1537-1546"xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/title"Fetuin-A (AHSG) prevents extraosseous calcification induced by uraemia and phosphate challenge in mice."xsd:string
http://purl.uniprot.org/citations/17389622http://purl.uniprot.org/core/volume"22"xsd:string
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