Chronic Kidney Disease by M. Gooz

By M. Gooz

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2 Bone mineralization It is a parameter which reflects the amount of unmineralized osteoid. Mineralization is measured by the osteoid maturation time or by mineralization lag time, both of which depend heavily on the osteoid width as well as on the distance between tetracycline labels. The classic disease with an abnormality of mineralization is osteomalacia, in which the bone-formation rate is low and the osteoid volume is high. Some patients have a modest increase in osteoid, which is a result of high bone formation rates.

Hyalinosis of afferent arterioles, in diabetes, and damage to the post-glomerular arteriole and peritubular capillaries cause interstitial ischemia and fibrosis. Fig. 2. Role of Intrinsic Cells in Kidney Damage. 2 Role of extrinsic cells in kidney damage Infiltration of inflammatory cells into the glomeruli and the renal interstitium is the hallmark of glomerulosclerosis and tubuloiterstitial fibrosis. Severity and Stages of Chronic Kidney Disease 19 Platelets and coagulation: Platelets and their release products within the damaged glomeruli stimulate a coagulation cascade which activate the mesangial cells to induce sclerosis.

Some of these markers are excreted by the kidneys, so in CKD, the serum concentrations may merely represent accumulation instead of bone turnover (Rogers and Eastell, 2005). Renal phosphate excretion is physiologically regulated mainly by proximal tubular cells, which express Na/Pi Type II cotransporters at their apical membrane that control phosphate reclamation. Renal phosphate reabsorption is mediated primarily through the Na/Pi IIa co-transporter, whereas approximately one-third of phosphate ions are reabsorbed through the Na/Pi IIc cotransporter.

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