Download Chronic Kidney Disease by Monika Göőz PDF

By Monika Göőz

ISBN-10: 9535101714

ISBN-13: 9789535101710

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Additional resources for Chronic Kidney Disease

Sample text

As a result, FGF-23 increases urinary phosphate excretion and decreases gastrointestinal phosphate absorption directly and through inhibition of 1a-hydroxylase and reduction of circulating calcitriol levels indirectly. Oversecretion of FGF-23 allows the body to maintain phosphate levels within a ‘physiological’ range until very advanced CKD stages (Miyamoto K et al. 2004). 4. CKD – MBD – and vascular calcification Tissue calcification is a complex and highly regulated process in bone and teeth, and also at extraosseous sites.

2008). ; 23(10):3050-2. Foley RN, Parfrey PS et al. (1998). “Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis; 32 (5 Suppl 3):S112-9. , Y. Hamada, et al. (2006). “The kidney and bone metabolism: Nephrologists' point of view”. J Bone Miner Metab. 24(6): 434-8. Ganesh SK, Stack AG et al. (2001). ;12(10): 2131-8. Gao P, and D'Amour P (2005). ; 51(1-2): 21-9. Giachelli CM. (2004). ;15(12): 295964. Hollis BW and Napoli JL. (1985). ; 31(11): 1815-9. Huan J, Olgaard K, et al.

2008). It has been shown that the serum calcium level is a poor reflection of overall total body calcium. Only 1% of total body calcium is measurable in the extracellular compartment while the most important part of calcium is stored in the bones. Serum ionized calcium, generally 40–50% of total serum calcium, is physiologically active, while non-ionized calcium is bound to albumin or anions such as citrate, bicarbonate, and The New Kidney and Bone Disease: Chronic Kidney Disease – Mineral and Bone Disorder (CKD–MBD) 27 phosphate, and is therefore not physiologically active.

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Chronic Kidney Disease by Monika Göőz

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