By Monika Göőz

ISBN-10: 9535101714

ISBN-13: 9789535101710

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Its extracellular concentration is strictly regulated by several enzymes. It is generated by PC-1 nucleotide triphosphate pyrophosphohydrolase and metabolized to inorganic phosphate by nucleotide pyrophosphatase/phosphodiesterase (NPP1), in addition to Tnap. Its hydrolysis to inorganic phosphate actually transforms it from a calcification inhibitor to a promoter. , 2005). 3 Contribution of experimental models in vascular calcification Arterial calcification assessed by all the available imaging studies cannot accurately differentiate calcification that is localized to the intima from calcification in the media adjacent to the internal elastic lamina, or in the medial layer (Figure 1 and 2).

4. CKD – MBD – and vascular calcification Tissue calcification is a complex and highly regulated process in bone and teeth, and also at extraosseous sites. The most threatening localization of unwanted calcification is at vascular sites, where it may manifest as both medial and intimal calcification of arteries. Studies in the general population have identified calcification in most of atherosclerotic plaques. Calcification seems to be a part of the natural development of atherosclerotic plaques, with extensive calcification associated with late-stage atherosclerosis.

Discontinue NSAIDs, correct volume depletion and treat BPH (men) and bladder dysfunction (women). Treat hypertension. Goal of therapy is <130/80. Use ACE, ARB, both, renin blockers, calcium channel blockers, aldosterone antagonists, loop diuretics as needed. Measure (spot urine protein /creatinine) and treat proteinuria. The goal is<300mg/day. Maximize the dose of an ACE inhibitor, then add an ARB at ½ full dose and increase to reach goal. Loop diuretics are essential to manage edema fluid and offset the development of hyperkalemia.

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Chronic Kidney Disease by Monika Göőz

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