Applying the Growth Failure in CKD Consensus Conference: Evaluation and treatment algorithm in children with chronic kidney disease

Mahan, John D.

doi:10.1016/j.ghir.2006.04.005

Cited by 9 publications

(8 citation statements)

References 48 publications

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“…44,45 Fortunately, this noxious effect seems to be limited to rodents, because prolonged treatment of children with uremia has not been associated with adverse renal effects. 46 Because of its physiologic role in regulating cardiac structure and function, there has been interest in evaluating whether GH might be beneficial in cardiac disease treatment. Several studies suggested that GH may have a salutary effect on cardiac disease, although this is not a uniform finding.…”

Section: Tgf-␤ Immunostaining Was Markedly Increased In Crf Heart (Crmentioning

confidence: 99%

Low-Dose Growth Hormone is Cardioprotective in Uremia

Rabkin

Awwad

Chen

et al. 2008

Journal of the American Society of Nephrology

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Growth hormone (GH) is required to maintain normal cardiac structure and function and has a positive effect on cardiac remodeling in experimental and possibly human disease. Cardiac resistance to GH develops in the uremic state, perhaps predisposing to the characteristic cardiomyopathy associated with uremia. It was hypothesized that administration of low-dosage GH may have a salutary effect on the cardiac remodeling process in uremia, but because high levels of GH have adverse cardiac effects, administration of high-dosage GH may worsen uremic cardiomyopathy. In rats with chronic renal failure, quantitative cardiac morphology revealed a decrease in total capillary length and capillary length density and an increase in mean intercapillary distance and fibroblast volume density evident. Low-dosage GH prevented these changes. Collagen and TGF-␤ immunostaining, increased in chronic renal failure, were also reduced by GH, suggesting a mechanism for its salutary action. Low-dosage GH also prevented thickening of the carotid artery but did not affect aortic pathology. In contrast, high-dosage GH worsened several of these variables. These results suggest that low-dosage GH may benefit the heart and possibly the carotid arteries in chronic renal failure.

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Section: Tgf-␤ Immunostaining Was Markedly Increased In Crf Heart (Crmentioning

confidence: 99%

Low-Dose Growth Hormone is Cardioprotective in Uremia

Rabkin

Awwad

Chen

et al. 2008

Journal of the American Society of Nephrology

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“…The binding of GH to its receptor in tissues stimulates receptor dimerization and autophosphorylation of tyrosinkinases, Janus kinase 2, phosphorylating the transcription signal proteins, STAT (1, 3 and 5). The phosphorylated STAT (STATp) are translocated to the nucleus, activating the gene expression regulated by GH 1,2,6,7 . GH has an effect through IGF-1 produced in the liver.…”

mentioning

confidence: 99%

“…However, IGF-1 is also secreted locally in the growth plate, acting as a paracrine/autocrine factor 6,7 . In CKD, plasma IGF-1 levels may be normal or decreased, but its bioactivity is low 6,7 . This protein is carried through plasma by binding proteins, IGF -BPs (1 to 6), which prevent rapid metabolism.…”

mentioning

confidence: 99%

“…This protein is carried through plasma by binding proteins, IGF -BPs (1 to 6), which prevent rapid metabolism. 99% of IGF-1 is bound to IGFBP-3 8 and to acid-labile subunit (ALS) 7 7 , forming a ternary complex. In CKD, these IGFBPs are increased due to a decreased clearance.…”

mentioning

confidence: 99%

“…However, despite its use, a final height close to -2 SD is still observed in all populations studied 1 . According to an international consensus published in 2006 9 , a treatment with rhGH should be considered in all patients with glomerular filtration rate < 75 ml/ min/1.73 m 2 , undergoing medical or dialytic treatment or kidney transplant recipients the year following the intervention, with a ZT/E score of <-1, 88 (<p3) or growth rate (GR) SD <-2 7 . The greatest effect on GR is achieved at the first year of therapy, to decline thereafter 10 .…”

mentioning

confidence: 99%

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Eje somatotrópico y marcadores moleculares del metabolismo mineral en niños en diálisis peritoneal crónica

Osorio

Schuffeneger

2016

Revista Chilena de Pediatría

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Eje somatotrópico y marcadores moleculares del metabolismo mineral en niños en diálisis María Luisa Ceballos Osorio, Francisco Cano Schuffeneger AbstractGrowth failure is one of the most relevant complications in children with chronic kidney disease (CKD). Among others, growth hormone (GH) resistance and bone mineral disorders have been identified as the most important causes of growth retardation. Objectives: 1. To characterize bone mineral metabolism and growth hormone bio-markers in CKD children treated with chronic peritoneal dialysis (PD). 2. To evaluate height change with rhGH treatment. Patients and Method: A longitudinal 12-month follow-up in prepuberal PD children. Exclusion criteria: Tanner stage > 1, nephrotic syndrome, genetic disorders, steroids, intestinal absorption disorders, endocrine disturbances, treatment with GH to the entry of the study. Demographic and anthropometric data were registered. FGF23, Klotho, VitD, IGF-1, IGFBP3, and GHBP were measured to evaluate mineral and growth metabolism. Results: 15 patients, 7 male, age 6.9 ± 3.0 y were included. Time on PD was 14.33 ± 12.26 months. Height/age Z score at month 1 was -1.69 ± 1.03. FGF23 and Klotho: 131.7 ± 279.4 y 125.9 ± 24.2 pg/ml, respectively. 8 patients were treated with GH during 6-12 months, showing a non-significant increase in height/age Z-score during the treatment period. Bivariate analysis showed a positive correlation between Klotho and delta ZT/E, and between GHBP vs growth velocity index (p < .05). Conclusions: FGF23 values were high and Klotho values were reduced in children with CKD in PD, comparing to healthy children. Somatotropic axis variables were normal or elevated. rhGH tends to improve height and there is a positive correlation of GHBP and growth velocity in these children.

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Inflammation and linear bone growth: the inhibitory role of SOCS2 on GH/IGF-1 signaling

Farquharson

Ahmed

2012

Pediatr Nephrol

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Linear bone growth is widely recognized to be adversely affected in children with chronic kidney disease (CKD) and other chronic inflammatory disorders. The growth hormone (GH)/insulin-like growth factor-1 (IGF-1) pathway is anabolic to the skeleton and inflammatory cytokines compromise bone growth through a number of different mechanisms, which include interference with the systemic as well as the tissue-level GH/IGF-1 axis. Despite attempts to promote growth and control disease, there are an increasing number of reports of the persistence of poor growth in a substantial proportion of patients receiving rhGH and/or drugs that block cytokine action. Thus, there is an urgent need to consider better and alternative forms of therapy that are directed specifically at the mechanism of the insult which leads to abnormal bone health. Suppressor of cytokine signaling 2 (SOCS2) expression is increased in inflammatory conditions including CKD, and is a recognized inhibitor of GH signaling. Therefore, in this review, we will focus on the premise that SOCS2 signaling represents a critical pathway in growth plate chondrocytes through which pro-inflammatory cytokines alter both GH/IGF-1 signaling and cellular function.

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Applying the Growth Failure in CKD Consensus Conference: Evaluation and treatment algorithm in children with chronic kidney disease

Cited by 9 publications

References 48 publications

Low-Dose Growth Hormone is Cardioprotective in Uremia

Low-Dose Growth Hormone is Cardioprotective in Uremia

Eje somatotrópico y marcadores moleculares del metabolismo mineral en niños en diálisis peritoneal crónica

Inflammation and linear bone growth: the inhibitory role of SOCS2 on GH/IGF-1 signaling

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