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Cozzolino, M.
[FGF-23: a new player in CKD-MBD]
G Ital Nefrol, 26(3):292
ISSN: 0393-5590 (Print) 0393-5590 (Linking)

Keywords: Bone Diseases/*etiology Fibroblast Growth Factors/*physiology Humans Hyperparathyroidism/etiology Kidney Failure, Chronic/*etiology Uremia/complications

Cozzolino, M.
[KDIGO on CKD-MBD: a new classification for an old problem?]
G Ital Nefrol, 26(6):645
ISSN: 0393-5590 (Print) 0393-5590 (Linking)

Keywords: Bone Diseases, Metabolic/complications Chronic Disease Humans Kidney Diseases/*classification Metabolic Diseases/complications *Practice Guidelines as Topic

Cozzolino, M. and Mazzaferro, S.
[Introduction. CKD-MBD (Chronic kidney disease-Metabolic bone disease)]
G Ital Nefrol, 26 Suppl 49:S1
ISSN: 0393-5590 (Print) 0393-5590 (Linking)

Keywords: Bone Diseases, Metabolic/diagnosis/*etiology/prevention & control/therapy Chronic Disease Humans Hyperparathyroidism, Secondary/etiology/therapy Kidney Diseases/*complications/diagnosis/prevention & control/therapy

Schlieper, G., Brandenburg, V., Ketteler, M. and Floege, J.
Sodium thiosulfate in the treatment of calcific uremic arteriolopathy
Nat Rev Nephrol, 5(9):539-43
ISSN: 1759-507X (Electronic) 1759-5061 (Linking)

Keywords: Aged Calciphylaxis/*drug therapy/epidemiology/physiopathology Chelating Agents/*therapeutic use Female Humans Prevalence Risk Factors Thiosulfates/*therapeutic use Uremia/*drug therapy/epidemiology/physiopathology

Abstract: Calcific uremic arteriolopathy (CUA; also known as calciphylaxis) is a life-threatening condition observed mostly in patients on dialysis. The key histopathologic features of CUA include media calcification of small arteries, associated with endovascular fibrosis and thrombosis. Several risk factors for CUA are related to disturbances in bone and mineral metabolism; current treatments largely aim to normalize these disturbances by lowering serum calcium phosphate concentration and thereby preventing, or even reversing, calcium phosphate oversaturation, precipitation and, finally, calcification. Administration of sodium thiosulfate, which sequesters calcium ions to form highly soluble calcium thiosulfate complexes, can prevent calcium phosphate precipitation. As randomized controlled studies on sodium thiosulfate are lacking, this Perspectives article focuses on case reports and case series; in these reports the compound seemed to be effective and was not associated with serious short-term adverse events. Large clinical trials to evaluate the efficacy and long-term safety of sodium thiosulfate are clearly warranted.


Cranenburg, E. C., Vermeer, C., Koos, R., Boumans, M. L., Hackeng, T. M., Bouwman, F. G., Kwaijtaal, M., Brandenburg, V. M., Ketteler, M. and Schurgers, L. J.
The circulating inactive form of matrix Gla Protein (ucMGP) as a biomarker for cardiovascular calcification
J Vasc Res, 45(5):427-36
ISSN: 1423-0135 (Electronic) 1018-1172 (Linking)

Keywords: Adult Angioplasty Biological Markers/blood Calcinosis/*metabolism Calciphylaxis/*metabolism Calcium-Binding Proteins/*blood Coronary Artery Disease/*metabolism/surgery Down-Regulation Enzyme-Linked Immunosorbent Assay Extracellular Matrix Proteins/*blood Female Germany Humans Male Middle Aged Netherlands Predictive Value of Tests Reference Values Renal Dialysis Renal Insufficiency/*metabolism/therapy Reproducibility of Results

Abstract: OBJECTIVE: Matrix gamma-carboxyglutamate (Gla) protein (MGP) is a vitamin K-dependent protein and a strong inhibitor of vascular calcification. Vitamin K deficiency leads to inactive uncarboxylated MGP (ucMGP), which accumulates at sites of arterial calcification. We hypothesized that as a result of ucMGP deposition around arterial calcification, the circulating fraction of ucMGP is decreased. Here we report on the development of an ucMGP assay and the potential diagnostic utility of monitoring serum ucMGP levels. METHODS AND RESULTS: An ELISA-based assay was developed with which circulating ucMGP can be determined. Serum ucMGP levels were measured in healthy subjects (n = 165) and in four patient populations; patients who underwent angioplasty (n = 30), patients with aortic stenosis (n = 25), hemodialysis patients (n = 52), and calciphylaxis patients (n = 10). All four patient populations had significantly lower ucMGP levels. In angioplasty patients and in those with aortic stenosis, some overlap was observed with the control population. However, in the hemodialysis and calciphylaxis populations, virtually all subjects had ucMGP levels below the normal adult range. CONCLUSION: Serum ucMGP may be used as a biomarker to identify those at risk for developing vascular calcification. This assay may become an important tool in the diagnosis of cardiovascular calcification.


Schafer, C., Heiss, A., Schwarz, A., Westenfeld, R., Ketteler, M., Floege, J., Muller-Esterl, W., Schinke, T. and Jahnen-Dechent, W.
The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification
J Clin Invest, 112(3):357-66
ISSN: 0021-9738 (Print) 0021-9738 (Linking)

Keywords: Animals Blood Proteins/deficiency/genetics/*physiology Calcinosis/blood/etiology/pathology/*prevention & control Calciphylaxis/blood/etiology/prevention & control Diet/adverse effects Female Humans Kidney Failure, Chronic/complications Male Mice Mice, Inbred C57BL Mice, Inbred DBA Mice, Knockout Minerals/administration & dosage Species Specificity Vitamin D/administration & dosage alpha-2-HS-Glycoprotein

Abstract: Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein alpha2-Heremans-Schmid glycoprotein (Ahsg, also known as fetuin-A) as an important inhibitor of ectopic calcification acting on the systemic level. Ahsg-deficient mice are phenotypically normal, but develop severe calcification of various organs on a mineral and vitamin D-rich diet and on a normal diet when the deficiency is combined with a DBA/2 genetic background. This phenotype is not associated with apparent changes in calcium and phosphate homeostasis, but with a decreased inhibitory activity of the Ahsg-deficient extracellular fluid on mineral formation. The same underlying principle may contribute to many calcifying disorders including calciphylaxis, a syndrome of severe systemic calcification in patients with chronic renal failure. Taken together, our data demonstrate a critical role of Ahsg as an inhibitor of unwanted mineralization and provide a novel therapeutic concept to prevent ectopic calcification accompanying various diseases.

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