Growth Retardation in Children with Kidney Disease

Salas, Paulina; Pinto, Viola; Rodríguez, J; Zambrano, María José; Mericq, Verónica

doi:10.1155/2013/970946

Cited by 28 publications

(33 citation statements)

References 45 publications

(73 reference statements)

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“…Aggressive nutritional intervention, appropriate control of CKD-induced metabolic and bone mineral disorders, use of erythropoietin and iron supplements, administration of growth hormone, early kidney transplantation, and avoidance of inflammation are all measures able to exert a favorable effect on growth of children with CKD (18,19).…”

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confidence: 99%

Chronic kidney disease induced by adenine: a suitable model of growth retardation in uremia

Claramunt

Gil‐Peña

Fuente

et al. 2015

American Journal of Physiology-Renal Physiology

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Growth retardation is a major manifestation of chronic kidney disease (CKD) in pediatric patients. The involvement of the various pathogenic factors is difficult to evaluate in clinical studies. Here, we present an experimental model of adenine-induced CKD for the study of growth failure. Three groups (n = 10) of weaning female rats were studied: normal diet (control), 0.5% adenine diet (AD), and normal diet pair fed with AD (PF). After 21 days, serum urea nitrogen, creatinine, parathyroid hormone (PTH), weight and length gains, femur osseous front advance as an index of longitudinal growth rate, growth plate histomorphometry, chondrocyte proliferative activity, bone structure, aorta calcifications, and kidney histology were analyzed. Results are means ± SE. AD rats developed renal failure (serum urea nitrogen: 70 ± 6 mg/dl and creatinine: 0.6 ± 0.1 mg/dl) and secondary hyperparathyroidism (PTH: 480 ± 31 pg/ml). Growth retardation of AD rats was demonstrated by lower weight (AD rats: 63.3 ± 4.8 g, control rats: 112.6 ± 4.7 g, and PF rats: 60.0 ± 3.8 g) and length (AD rats: 7.2 ± 0.2 cm, control rats: 11.1 ± 0.3 cm, and PF rats: 8.1 ± 0.3 cm) gains as well as lower osseous front advances (AD rats: 141 ± 13 μm/day, control rats: 293 ± 16 μm/day, and PF rats: 251 ± 10 μm/day). The processes of chondrocyte maturation and proliferation were impaired in AD rats, as shown by lower growth plate terminal chondrocyte height (21.7 ± 2.3 vs. 26.2 ± 1.9 and 23.9 ± 1.3 μm in control and PF rats) and proliferative activity index (AD rats: 30 ± 2%, control rats: 38 ± 2%, and PF rats: 42 ± 3%). The bone primary spongiosa structure of AD rats was markedly disorganized. In conclusion, adenine-induced CKD in young rats is associated with growth retardation and disturbed endochondral ossification. This animal protocol may be a useful new experimental model to study growth in CKD.

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mentioning

confidence: 99%

Chronic kidney disease induced by adenine: a suitable model of growth retardation in uremia

Claramunt

Gil‐Peña

Fuente

et al. 2015

American Journal of Physiology-Renal Physiology

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“…These defects are consistent with Schaefer et al findings in experimental models in uremic rats, observing a decreased phosphorylation of JAK-2 and STAT-5; decreased translocation of phosphorylated STAT proteins to the nucleus and increased SOCS inhibitory proteins compared to healthy rats 43 . RhGH treatment has shown to significantly improve stature in these patients, with an increase of 0.73 SD in children under 5 years old and 0.26 SD in those older than 6 years old, after a year of treatment 4,7 ; however, this treatment does not completely reverse the growth deficit, resulting in a final stature shorter than the expected by genetics. This was corroborated in our study, as the children treated with rhGH did not present a significant increase of the Z H/A score.…”

Section: Discussionmentioning

confidence: 94%

“…Finally, during puberty, through the GH/ insulin-like growth factor1 axis, IGF1, and initiated by sex hormones, the puberty growth spurt is stimulated 2 , but delayed in CKD due to a pulsatile secretion loss of the hypothalamic gonadotrophin hormone (GnRH) 2,3 . CKD is characterized by delayed growth not being able to reach the final adult size estimated by genetics 4 . According to data from the North American Pediatric Renal Trials and Collaborative Studies in 2011, 36.9% of children with CKD have a delayed growth, and the extent correlates with the deterioration of kidney function, with an average height of -1.85 SD.…”

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confidence: 99%

“…According to data from the North American Pediatric Renal Trials and Collaborative Studies in 2011, 36.9% of children with CKD have a delayed growth, and the extent correlates with the deterioration of kidney function, with an average height of -1.85 SD. In Chile, according to the 2007 National Registry of the disease, 50% of patients with CKD have a delayed growth 4 . The etiology of under height for age in CKD is multifactorial.…”

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confidence: 99%

See 1 more Smart Citation

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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“…8 However, post transplant, the steroidal therapy often included in immunosuppression regimens can affect longitudinal growth and calcium/ phosphorous metabolism. 9,10 Aetiology, pathology and prognosis…”

Section: Clinical Effectiveness Systematic Reviewmentioning

confidence: 99%

Immunosuppressive therapy for kidney transplantation in children and adolescents: systematic review and economic evaluation

Haasova

Snowsill

Jones-Hughes

et al. 2016

Health Technol Assess

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BackgroundEnd-stage renal disease is a long-term irreversible decline in kidney function requiring kidney transplantation, haemodialysis or peritoneal dialysis. The preferred option is kidney transplantation followed by induction and maintenance immunosuppressive therapy to reduce the risk of kidney rejection and prolong graft survival.ObjectivesTo systematically review and update the evidence for the clinical effectiveness and cost-effectiveness of basiliximab (BAS) (Simulect,®Novartis Pharmaceuticals) and rabbit antihuman thymocyte immunoglobulin (Thymoglobuline,®Sanofi) as induction therapy and immediate-release tacrolimus [Adoport®(Sandoz); Capexion®(Mylan); Modigraf®(Astellas Pharma); Perixis®(Accord Healthcare); Prograf®(Astellas Pharma); Tacni®(Teva); Vivadex®(Dexcel Pharma)], prolonged-release tacrolimus (Advagraf,®Astellas Pharma); belatacept (BEL) (Nulojix,®Bristol-Myers Squibb), mycophenolate mofetil (MMF) [Arzip®(Zentiva), CellCept®(Roche Products), Myfenax®(Teva), generic MMF is manufactured by Accord Healthcare, Actavis, Arrow Pharmaceuticals, Dr Reddy’s Laboratories, Mylan, Sandoz and Wockhardt], mycophenolate sodium, sirolimus (Rapamune,®Pfizer) and everolimus (Certican,®Novartis Pharmaceuticals) as maintenance therapy in children and adolescents undergoing renal transplantation.Data sourcesClinical effectiveness searches were conducted to 7 January 2015 in MEDLINE (via Ovid), EMBASE (via Ovid), Cochrane Central Register of Controlled Trials (via Wiley Online Library) and Web of Science [via Institute for Scientific Information (ISI)], Cochrane Database of Systematic Reviews, Database of Abstracts of Reviews of Effects and Health Technology Assessment (HTA) (The Cochrane Library via Wiley Online Library) and Health Management Information Consortium (via Ovid). Cost-effectiveness searches were conducted to 15 January 2015 using a costs or economic literature search filter in MEDLINE (via Ovid), EMBASE (via Ovid), NHS Economic Evaluation Databases (via Wiley Online Library), Web of Science (via ISI), Health Economic Evaluations Database (via Wiley Online Library) and EconLit (via EBSCOhost).Review methodsTitles and abstracts were screened according to predefined inclusion criteria, as were full texts of identified studies. Included studies were extracted and quality appraised. Data were meta-analysed when appropriate. A new discrete time state transition economic model (semi-Markov) was developed; graft function, and incidences of acute rejection and new-onset diabetes mellitus were used to extrapolate graft survival. Recipients were assumed to be in one of three health states: functioning graft, graft loss or death.ResultsThree randomised controlled trials (RCTs) and four non-RCTs were included. The RCTs only evaluated BAS and tacrolimus (TAC). No statistically significant differences in key outcomes were found between BAS and placebo/no induction. Statistically significantly higher graft function (p < 0.01) and less biopsy-proven acute rejection (odds ratio 0.29, 95% confidence interval 0.15 to 0.57) was found between TAC and ciclosporin (CSA). Only one cost-effectiveness study was identified, which informed NICE guidance TA99. BAS [with TAC and azathioprine (AZA)] was predicted to be cost-effective at £20,000–30,000 per quality-adjusted life year (QALY) versus no induction (BAS was dominant). BAS (with CSA and MMF) was not predicted to be cost-effective at £20,000–30,000 per QALY versus no induction (BAS was dominated). TAC (with AZA) was predicted to be cost-effective at £20,000–30,000 per QALY versus CSA (TAC was dominant). A model based on adult evidence suggests that at a cost-effectiveness threshold of £20,000–30,000 per QALY, BAS and TAC are cost-effective in all considered combinations; MMF was also cost-effective with CSA but not TAC.LimitationsThe RCT evidence is very limited; analyses comparing all interventions need to rely on adult evidence.ConclusionsTAC is likely to be cost-effective (vs. CSA, in combination with AZA) at £20,000–30,000 per QALY. Analysis based on one RCT found BAS to be dominant, but analysis based on another RCT found BAS to be dominated. BAS plus TAC and AZA was predicted to be cost-effective at £20,000–30,000 per QALY when all regimens were compared using extrapolated adult evidence. High-quality primary effectiveness research is needed. The UK Renal Registry could form the basis for a prospective primary study.Study registrationThis study is registered as PROSPERO CRD42014013544.FundingThe National Institute for Health Research HTA programme.

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Growth Retardation in Children with Kidney Disease

Cited by 28 publications

References 45 publications

Chronic kidney disease induced by adenine: a suitable model of growth retardation in uremia

Chronic kidney disease induced by adenine: a suitable model of growth retardation in uremia

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

Immunosuppressive therapy for kidney transplantation in children and adolescents: systematic review and economic evaluation

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