Growth failure in children with renal diseases study: An overview from the National Institutes of Health and the Advisory Committee

Gladys H. Hirschman; Gary E. Striker; Robert L. Vernier; Russell W. Chesney; Malcolm A. Holliday; Julie R. Ingelfinger; Joel D. Kopple; Stephen S. Rich; George W. Williams

doi:10.1016/S0022-3476(05)82916-6

Growth failure in children with renal diseases study: An overview from the National Institutes of Health and the Advisory Committee

Gladys H. Hirschman, Gary E. Striker, Robert L. Vernier, Russell W. Chesney, Malcolm A. Holliday, Julie R. Ingelfinger, Joel D. Kopple, Stephen S. Rich, George W. Williams

Research output: Contribution to journal › Article › peer-review

5 Scopus citations

Original language	English
Pages (from-to)	S8-S10
Journal	Journal of Pediatrics
Volume	116
Issue number	2
DOIs	https://doi.org/10.1016/S0022-3476(05)82916-6
State	Published - Feb 1990
Externally published	Yes

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10.1016/S0022-3476(05)82916-6

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Hirschman, G. H., Striker, G. E., Vernier, R. L., Chesney, R. W., Holliday, M. A., Ingelfinger, J. R., Kopple, J. D., Rich, S. S., & Williams, G. W. (1990). Growth failure in children with renal diseases study: An overview from the National Institutes of Health and the Advisory Committee. Journal of Pediatrics, 116(2), S8-S10. https://doi.org/10.1016/S0022-3476(05)82916-6

@article{ccbd52284b444ffea8912cf4ad451cfc,

title = "Growth failure in children with renal diseases study: An overview from the National Institutes of Health and the Advisory Committee",

author = "Hirschman, {Gladys H.} and Striker, {Gary E.} and Vernier, {Robert L.} and Chesney, {Russell W.} and Holliday, {Malcolm A.} and Ingelfinger, {Julie R.} and Kopple, {Joel D.} and Rich, {Stephen S.} and Williams, {George W.}",

note = "Funding Information: During the past two decades, important insights have been gained into vitamin D metabolism. 13 Vitamin D is first activated in the skin by ultraviolet irradiation, then hydroxylated to 25-hydroxyvitamin D3 in liver microsomes and mitochondria, and finally hydroxylated to both 1,25-dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 by mitochondrial enzymes at the renal proximal convoluted and straight tubules. In children with chronic renal failure, growth failure may be caused by calorie-protein deficiency, metabolic acidosis, anemia, azotemic anorexia, and other factors. However, even when these potential causes are eradicated, growth failure usually persists. Recent evidence suggests that inadequate renal synthesis of 1,25-dihydroxyvitamin D3 leads to renal osteodystrophy, which in turn may cause growth failure in the child with uremia. Growth failure will persist unless the bone lesions heal. l{"}herefore vitamin D metabolites, which are essential to skeletal mineralization, must be an integral part of the treatment of renal osteodystrophy in children. Several recent studies have suggested that the use of vitamin D metabolites in renal failure may cause deterioration of renal function. 4,5 Other researchers have not confirmed these observations. 6-8 Thes e conflicting reports, coupled with the potential benefits of vitamin D metabolites Supported by National Institutes of Health grants R01 DK 31370 and R01 DK 32431. Reprint requests: Gladys H. Hirschman, MD, National Institutes of Health, Federal Building, Room 102, Bethesda, MD 20892.",

year = "1990",

month = feb,

doi = "10.1016/S0022-3476(05)82916-6",

language = "English",

volume = "116",

pages = "S8--S10",

journal = "Journal of Pediatrics",

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TY - JOUR

T1 - Growth failure in children with renal diseases study

T2 - An overview from the National Institutes of Health and the Advisory Committee

AU - Hirschman, Gladys H.

AU - Striker, Gary E.

AU - Vernier, Robert L.

AU - Chesney, Russell W.

AU - Holliday, Malcolm A.

AU - Ingelfinger, Julie R.

AU - Kopple, Joel D.

AU - Rich, Stephen S.

AU - Williams, George W.

N1 - Funding Information: During the past two decades, important insights have been gained into vitamin D metabolism. 13 Vitamin D is first activated in the skin by ultraviolet irradiation, then hydroxylated to 25-hydroxyvitamin D3 in liver microsomes and mitochondria, and finally hydroxylated to both 1,25-dihydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 by mitochondrial enzymes at the renal proximal convoluted and straight tubules. In children with chronic renal failure, growth failure may be caused by calorie-protein deficiency, metabolic acidosis, anemia, azotemic anorexia, and other factors. However, even when these potential causes are eradicated, growth failure usually persists. Recent evidence suggests that inadequate renal synthesis of 1,25-dihydroxyvitamin D3 leads to renal osteodystrophy, which in turn may cause growth failure in the child with uremia. Growth failure will persist unless the bone lesions heal. l"herefore vitamin D metabolites, which are essential to skeletal mineralization, must be an integral part of the treatment of renal osteodystrophy in children. Several recent studies have suggested that the use of vitamin D metabolites in renal failure may cause deterioration of renal function. 4,5 Other researchers have not confirmed these observations. 6-8 Thes e conflicting reports, coupled with the potential benefits of vitamin D metabolites Supported by National Institutes of Health grants R01 DK 31370 and R01 DK 32431. Reprint requests: Gladys H. Hirschman, MD, National Institutes of Health, Federal Building, Room 102, Bethesda, MD 20892.

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