Growth hormone axis in chronic kidney disease

Mahesh, Shefali; Kaskel, Frederick J.

doi:10.1007/s00467-007-0527-x

Cited by 136 publications

(128 citation statements)

References 41 publications

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“…Although growth must be interpreted within the context of the patient' s genetic potential, nutritional status, and neonatal history, practitioners should be alert to the possibility that abnormal growth may reflect CKD. Children with CKD can have impaired linear growth even when the GFR is only mild to moderately impaired, 75,76 and both LBW and SGA status were risk factors for impaired linear growth in…”

Section: Practice and Policy Implications: What Are Pediatricians To Do?mentioning

confidence: 98%

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

2013

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Thanks to remarkable advances in neonatal intensive care, infants who once had little chance for survival can now enter adulthood. Yet the consequences of premature birth or low birth weight (LBW) on nephrogenesis, final nephron number, and long-term kidney function are unclear. This review focuses on the theory, experimental evidence, and observational data that suggest an increased risk of chronic kidney disease (CKD) for infants born prematurely. Many premature and LBW infants begin life with an incomplete complement of immature nephrons. They are then exposed to a variety of external stressors that can hinder ongoing kidney development or cause additional nephron loss such as hemodynamic alterations, nephrotoxic medications, infections, and suboptimal nutrition. Acute kidney injury, in particular, may be a significant risk factor for the development of CKD. According to Brenner' s hypothesis, patients with decreased nephron number develop hyperfiltration that results in sodium retention, hypertension, nephron loss, and CKD due to secondary focal segmental glomerulosclerosis. Because the risk of CKD in premature and LBW infants has not been accurately determined, there are no evidence-based recommendations for screening or management. Yet with the first generation of infants from the surfactant era only now reaching adulthood, it is possible that there is already an unrecognized epidemic of CKD. We suggest individualized, risk-based assessments of premature and LBW infants due to the increased risk of CKD and call for additional research into the long-term risk for CKD these infants face.

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Section: Practice and Policy Implications: What Are Pediatricians To Do?mentioning

confidence: 98%

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

2013

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“…Impairment of linear growth velocity is a prominent clinical feature of CKD in children (1)(2)(3) and has been linked to decreased quality of life (4,5) and increased morbidity (6). In pediatric ESRD, poor growth has also been linked to mortality (7).…”

Section: Introductionmentioning

confidence: 99%

Medication Adherence and Growth in Children with CKD

Akchurin¹,

Schneider²,

Mulqueen³

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Poor growth is a consequence of CKD, but can often be partially or fully prevented or corrected with the use of a number of medications. The extent of nonadherence with medications used to treat or mitigate growth failure in CKD has not been examined prospectively in children with CKD.Design, setting, participants, & measurements The prevalence of both prescription of and nonadherence to recombinant human growth hormone (rhGH), phosphate binders, alkali, active vitamin D, nutritional vitamin D, iron, and erythrocyte-stimulating agents was summarized over the first seven visits of the Chronic Kidney Disease in Children cohort study. The association between self-reported nonadherence to each medication group and the mean annual change in age-and sex-specific height z score was quantified using seven separate linear regression models with generalized estimating equations.Results Of 834 participants, 597 reported use of at least one of these medication groups and had adherence data available. Nonadherence ranged from 4% over all visits for erythrocyte-stimulating agents to 22% over all visits for nutritional vitamin D. Of the study participants, 451 contributed data to at least one of the analyses of adherence and changes in height z score. Children nonadherent to rhGH had no change in height z score, whereas those adherent to rhGH had a significant improvement of 0.16 SDs (95% confidence interval, 0.05 to 0.27); the effect size was slightly larger and remained significant after adjustment. Among participants with height#3rd percentile and after adjustment, adherence to rhGH was associated with a 0.33 SD (95% confidence interval, 0.10 to 0.56) greater change in height z score. Nonadherence with other medication groups was not significantly associated with a change in height z score.Conclusions Self-reported nonadherence to rhGH was associated with poorer growth velocity in children with CKD, suggesting an opportunity for intervention and improved patient outcome.

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“…A number of observations suggest that hypothalamicpituitary regulation of GH is perturbed in chronic kidney disease [12,13]. Plasma GH levels falls off to low normal values after the institution of maintenance dialysis, an effect that may be mediated in part by acetate in the dialysis bath.…”

Section: Resultsmentioning

confidence: 99%

Effect of Growth Hormone on Plasminogen Activator and Inhibitor Activity in Rat

et al. 2012

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Growth retardation is one of the significant changes in chronic kidney disease (CKD) and is associated with increased morbidity and mortality. Disturbances in growth hormone (GH) are held responsible for several complications in CKD. GH is a protein based peptide hormone which directly or indirectly regulates renal functions to ensure homeostasis. We investigated the effects of growth hormone on plasminogen activators (PA) in rat kidney, PA and plasminogen activator inhibitor (PAI), glucose and fibrinogen in plasma and serum lipid profile. Rats were injected daily with 250 mU GH kg-1 body weight subcutaneously for one week. Growth hormone treatment increased PA activity significantly in rat kidneys as compared to controls. No changes were seen in PA, PAI and fibrinogen levels in the plasma of two groups of rats. There was significant decrease in plasma glucose, total cholesterol and LDL-cholesterol levels in serum of treated group resulting in the decrease of HDL/LDL and total cholesterol/cholesterol ratios. However, triglycerides and VLDL showed significant higher activity in the serum of treated group as compared to controls. Our data suggests that GH administration might improve renal function by increasing PA activity in kidney as well as by reducing the cholesterol content in blood. GH may be effective in improving growth failure as it helps to maintain the normal homeostatic balance.

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Growth hormone axis in chronic kidney disease

Cited by 136 publications

References 41 publications

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

Medication Adherence and Growth in Children with CKD

Effect of Growth Hormone on Plasminogen Activator and Inhibitor Activity in Rat

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