Alterations of the growth plate in chronic renal failure

Santos, Fernando; Carbajo-Pérez, E; Rodríguez, Julián; Fernández-Fuente, Marta; Molinos, Inés; Amil, Benito; García, Eva

doi:10.1007/s00467-004-1652-4

Cited by 24 publications

(19 citation statements)

References 24 publications

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“…D and E. representative images of the growth cartilage of the proximal tibiae of the 4 groups of animals after immunohistochemical procedure to demonstrate IGF-I or IGFI-R protein pattern distribution which was mostly confined to the hypertrophic zone in the 4 groups of rats. metaphysis to epiphysis and represents the vascular invasion phenomenon and cartilage replacement by new bone (28). This apposition bone vector reflects the longitudinal growth rate, and the association of reduced growth velocity and diminished cartilage height, as happened in the KD group, suggests that the process of progression and hypertrophy of chondrocytes became more damaged than the rate of new bone formation.…”

Section: Discussionmentioning

confidence: 97%

Alterations of growth plate and abnormal insulin-like growth factor I metabolism in growth-retarded hypokalemic rats: effect of growth hormone treatment

Gil‐Peña¹,

García-López²,

Álvarez-García³

et al. 2009

American Journal of Physiology-Renal Physiology

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of growth plate and abnormal insulin-like growth factor I metabolism in growth-retarded hypokalemic rats: effect of growth hormone treatment. Am J Physiol Renal Physiol 297: F639-F645, 2009. First published July 8, 2009 doi:10.1152/ajprenal.00188.2009.-Hypokalemic tubular disorders may lead to growth retardation which is resistant to growth hormone (GH) treatment. The mechanism of these alterations is unknown. Weaning female rats were grouped (n ϭ 10) in control, potassium-depleted (KD), KD treated with intraperitoneal GH at 3.3 mg ⅐ kg Ϫ1 ⅐ day Ϫ1during the last week (KDGH), and control pair-fed with KD (CPF). After 2 wk, KD rats were growth retarded compared with CPF rats, the osseous front advance (ϮSD) being 67. . GH administration normalized these changes except for the distal chondrocyte height. Quantitative PCR of insulin-like growth factor I (IGF-I), IGF-I receptor, and GH receptor genes in KD growth plates showed downregulation of IGF-I and upregulation of IGF-I receptor mRNAs, without changes in their distribution as analyzed by immunohistochemistry and in situ hybridization. GH did not further modify IGF-I mRNA expression. KD rats had normal hepatic IGF-I mRNA levels and low serum IGF-I values. GH increased liver IGF-I mRNA, but circulating IGF-I levels remained reduced. This study discloses the structural and molecular alterations induced by potassium depletion on the growth plate and shows that the lack of response to GH administration is associated with persistence of the disturbed process of chondrocyte hypertrophy and depressed mRNA expression of local IGF-I in the growth plate.tubulopathies; chondrocyte; cartilage GROWTH RETARDATION IS FREQUENTLY found in primary hypokalemic tubular disorders (32). Potential pathogenic factors of growth impairment in these tubulopathies include maintained metabolic acidosis, polyuria with decreased food intake and repeated dehydration episodes, disturbed bone mineralization, sodium deficit, and potassium depletion. In children with renal tubular acidosis, growth retardation is common and is ameliorated or reversed after sustained correction of metabolic acidosis (29). Metabolic acidosis disturbs normal growth through various mechanisms such as the stimulation of protein catabolism (18), interference with growth hormone (GH) action (21), and the alteration of the structure and dynamics of growth cartilage (5). In hypokalemic tubulopathies associated with alkalosis, Bartter's or Gitelman's syndromes, the adverse effect on growth is not well documented and the response of growth to treatment is rather unpredictable. Growth impairment is frequently described in Bartter's syndrome (22). Gitelman's syndrome, traditionally considered as asymptomatic or responsible for mild clinical manifestations (9), has been reported to be accompanied by short stature in over 30% of children (8).Although clinical cases of isolated GH deficiency as well as improvement of growth rate following administration of indomethacin have been reported in patients with Gitelman's syndrome, the...

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Section: Discussionmentioning

confidence: 97%

Alterations of growth plate and abnormal insulin-like growth factor I metabolism in growth-retarded hypokalemic rats: effect of growth hormone treatment

Gil‐Peña¹,

García-López²,

Álvarez-García³

et al. 2009

American Journal of Physiology-Renal Physiology

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“…Vulnerable periods are the first 2 years of life and puberty, when children lose growth potential [38]. Growth retardation is preventable and can be reversed in patients who develop CRI in infancy [39].…”

Section: Growth (Richard Fine Md)mentioning

confidence: 99%

Report of an NIH task force on research priorities in chronic kidney disease in children

et al. 2005

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“…The reasons for these differences are not clear, but the degree and length of time with CKD and the type of ROD have been shown to affect the thickness of the growth plate [46]. Obviously, little is known about the specifics of PTH activity in the growth plate in man, but animal studies suggest PTH is associated with differing effects on the growth plate.…”

Section: Other Aspectsmentioning

confidence: 98%

Parathyroid hormone and growth in chronic kidney disease

Waller

2010

Pediatr Nephrol

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Growth failure is common in children with chronic kidney disease, and successful treatment is a major challenge in the management of these children. The aetiology is multi-factorial with "chronic kidney disease-metabolic bone disorder" being a key component that is particularly difficult to manage. Parathyroid hormone is at the centre of this mineral imbalance, consequent skeletal disease and, ultimately, growth failure. When other aetiologies are treated, good growth can be achieved throughout the course of the disease when parathyroid hormone (PTH) levels are in the normal range or slightly elevated. A direct correlation between PTH levels and growth has not been convincingly established, and the direct effect of PTH on growth has not been adequately described; furthermore, direct actions of PTH on the growth plate are unproven. The effects of PTH on growth stem from the pivotal role that PTH plays in the development of renal osteodystrophy. In severe secondary hyperparathyroidism, the growth plate is altered and growth is affected. At the other end of the spectrum, with an over-suppressed parathyroid gland, the rate of bone turnover and remodelling is markedly diminished, and some data suggest this is associated with poor growth. Most of the data available suggests that avoiding the development of significant bone disease through the strict control of PTH levels permits good growth. Absolute optimal ranges for PTH that maximise growth or minimise growth failure are not yet established.

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Alterations of the growth plate in chronic renal failure

Cited by 24 publications

References 24 publications

Alterations of growth plate and abnormal insulin-like growth factor I metabolism in growth-retarded hypokalemic rats: effect of growth hormone treatment

Alterations of growth plate and abnormal insulin-like growth factor I metabolism in growth-retarded hypokalemic rats: effect of growth hormone treatment

Report of an NIH task force on research priorities in chronic kidney disease in children

Parathyroid hormone and growth in chronic kidney disease

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