OPTIMAL MANAGEMENT OF RENAL OSTEODYSTROPHY IN CHILDREN TREATED WITH CAPD AND CCPD

[1] Lucas RC, (1993)

[2] Alexander SR, Sullivan EK, Harmon WH, Stablein DM, Tejani A., Maintenance dialysis in North American children and adolescents: A preliminary report, Kidney Int, 44, (1992)

[3] Goodman WG, Coburn JW, Ramirez JA, Slatopolsky E., Salusky IB, Renal osteodvstroohy in adult and wdiatric patients, Primer on the Metabolic Bone Disease and Disorders of Mineral Metabolism, (1993)

[4] Portale AA, Boothe BE, Tsai HC, Morris RC, Reduced plasma concentration of 1.25‐dihydroxy‐vitamin D in children with moderate renal insufficiency, Kidney Int, 21, pp. 627-632, (1982)

[5] Wilson L., Felsenfeld A., Drezner MK, Liach F., Altered divalent ion metabolism in early renal failure: Role of 1,25(OH)₂D, Kidney Int, 27, pp. 565-573, (1985)

[6] Reichel H., Deibart B., SchmidtGayk H., Ritz E., Calcium metabolism in early chronic renal failure: Implications for the pathogenesis of hyperparathyroidism, Nephrol Dial Transplant, 6, pp. 162-169, (1991)

[7] Silver J., Naveh-Many T., Mayer H., Schmelzer HJ, Popovtzer MM, Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat, J Clin Invest, 78, pp. 1296-1301, (1986)

[8] Szabo A., Merke J., Beier E., Et al., 1,25(OH)₂ vitamin D, Inhibits parathyroid cell proliferation in experimental uremia, Kidney Int, 35, pp. 1049-1056, (1989)

[9] Korkor AB, Reduced binding of 3H‐1,25‐dihydroxyvitamin D in the parathyroid glands of patients with renal failure, N Engl J Med, 316, pp. 1573-1577, (1987)

[10] Fukagawa M., Kitaoka M., Kaname S., Okazaki R., Matsumoto T., Ogata E., Hoshino M., Inada T., Sekine T., Kurokawa K., Suppression of parathyroid gland hyperplasia by 1,25(OH)₂D₃ pulse therapy, N Engl J Med, 315, pp. 421-422, (1990)

[1] Lucas RC, (1993)

[2] Alexander SR, Sullivan EK, Harmon WH, Stablein DM, Tejani A., Maintenance dialysis in North American children and adolescents: A preliminary report, Kidney Int, 44, (1992)

[3] Goodman WG, Coburn JW, Ramirez JA, Slatopolsky E., Salusky IB, Renal osteodvstroohy in adult and wdiatric patients, Primer on the Metabolic Bone Disease and Disorders of Mineral Metabolism, (1993)

[4] Portale AA, Boothe BE, Tsai HC, Morris RC, Reduced plasma concentration of 1.25‐dihydroxy‐vitamin D in children with moderate renal insufficiency, Kidney Int, 21, pp. 627-632, (1982)

[5] Wilson L., Felsenfeld A., Drezner MK, Liach F., Altered divalent ion metabolism in early renal failure: Role of 1,25(OH)₂D, Kidney Int, 27, pp. 565-573, (1985)

[6] Reichel H., Deibart B., SchmidtGayk H., Ritz E., Calcium metabolism in early chronic renal failure: Implications for the pathogenesis of hyperparathyroidism, Nephrol Dial Transplant, 6, pp. 162-169, (1991)

[7] Silver J., Naveh-Many T., Mayer H., Schmelzer HJ, Popovtzer MM, Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat, J Clin Invest, 78, pp. 1296-1301, (1986)

[8] Szabo A., Merke J., Beier E., Et al., 1,25(OH)₂ vitamin D, Inhibits parathyroid cell proliferation in experimental uremia, Kidney Int, 35, pp. 1049-1056, (1989)

[9] Korkor AB, Reduced binding of 3H‐1,25‐dihydroxyvitamin D in the parathyroid glands of patients with renal failure, N Engl J Med, 316, pp. 1573-1577, (1987)

[10] Fukagawa M., Kitaoka M., Kaname S., Okazaki R., Matsumoto T., Ogata E., Hoshino M., Inada T., Sekine T., Kurokawa K., Suppression of parathyroid gland hyperplasia by 1,25(OH)₂D₃ pulse therapy, N Engl J Med, 315, pp. 421-422, (1990)