Hypocalcemia with hyperphosphatemia are seen in.
<p>Improved medical management of chronic kidney disease now allows many patients to survive for decades and hence time enough to develop features of renal osteodystrophy, which must be controlled to avoid additional morbidity. Impaired production of 1,25(OH) 2 D is now thought to be the principal factor that causes calcium deficiency, secondary hyperparathyroidism, and bone disease; hyperphosphatemia typically occurs only in the later stages of CKD. Low levels of 1,25(OH) 2 D due to increased FGF23 production in bone are critical in the development of hypocalcemia. The uremic state also causes impairment of intestinal absorption by mechanisms other than defects in vitamin D metabolism. Nonetheless, treatment with supraphysiologic amounts of vitamin D or calcitriol corrects the impaired calcium absorption. Since increased FGF23 levels are seen even in early stages of renal failure in some patients, and have been repoed to correlate with increased moality, there is current interest in methods (lowering phosphate absorption) to lower FGF23 levels and concern as to whether vitamin D supplementation (known physiologically to increase FGF23) increases FGF23 in CKD. Hyperphosphatemia in renal failure lowers blood calcium levels by several mechanisms, including extraosseous deposition of calcium and phosphate, impairment of the bone-resorbing action of PTH, and reduction in 1,25(OH) 2 D production by remaining renal tissue(harrison 18 pg 3116)</p>
CRF
Pseudobypoparathyoidsm
Vit-D deficiency
Vit-D deficiency
Endocrinology