The pathogenesis of rickets or "osteodystrophy" in various forms of renal disease has been subject to considerable debate. In renal diseases with glomerular failure, osteodystrophy has been explained on the basis of hyperfunctioning parathyroid glands "... stimulated by retention of phosphorus, poor dietary intake of calcium in these chronically ill patients, and increased fecal and urinary losses of calcium because of persistent acidosis." 1 In renal tubular disease, excessive tubular loss of phosphate has generally been considered to be responsible for the demineralization of bone.
Studies in two siblings with azotemic renal osteodystrophy2 and in two patients with long-standing nephrotic syndrome complicated by tubular dysfunction and osteodystrophy 3,4 have demonstrated increased fecal losses of calcium and phosphorus in contrast to low levels of urinary excretion of these ions. Following administration of large doses of vitamin D, the fecal losses of calcium and phosphorus decreased, and the urinary output of these
STRICKLER GB, BURKE EC. External Calcium and Phosphorus Balances: A Comparative Study of Renal Disease and the Celiac Syndrome. Am J Dis Child. 1963;106(2):154–160. doi:10.1001/archpedi.1963.02080050156006
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