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

2006 ◽  
Vol 16 ◽  
pp. 68-78 ◽  
Author(s):  
John D. Mahan
2007 ◽  
Vol 97 (2) ◽  
pp. 232-238 ◽  
Author(s):  
R. Rashid ◽  
E. Neill ◽  
H. Maxwell ◽  
S. F. Ahmed

Growth failure is a common yet complex problem of childhood chronic kidney disease caused by multiple factors encountered due to the primary disease or secondary to the renal impairment. This review seeks to describe the various patho-physiological mechanisms contributing to growth failure in the various stages of childhood with particular emphasis on nutritional problems and endocrine dysfunction encountered whilst managing these children. In addition, we shall examine the role of body composition in chronic kidney disease, their relationship with growth and nutrition and the potential effect of abnormalities in fat mass and lean mass on long-term morbidity and mortality.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Susan R. Mendley ◽  
Fotios Spyropoulos ◽  
Debra R. Counts

We describe an alternative strategy for management of severe growth failure in a 14-year-old child who presented with advanced chronic kidney disease close to puberty. The patient was initially treated with growth hormone for a year until kidney transplantation, followed immediately by a year-long course of an aromatase inhibitor, anastrozole, to prevent epiphyseal fusion and prolong the period of linear growth. Outcome was excellent, with successful transplant and anticipated complete correction of height deficit. This strategy may be appropriate for children with chronic kidney disease and short stature who are in puberty.


2021 ◽  
Vol 8 (Supplement_1) ◽  
pp. S273-S274
Author(s):  
Taryn A Eubank ◽  
Katherine Perez ◽  
William L Musick ◽  
Kevin W Garey

Abstract Background The coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), spread globally throughout late 2019. During this pandemic, concern for bacterial and fungal superinfections has been present during the treatment of these patients. Methods Hospitalized, adult patients with laboratory confirmed and symptomatic COVID-19 disease admitted between March 12, 2020 and May 31, 2020 were eligible for inclusion in this study. Data was obtained from electronic medical records and the hospital system’s clinical surveillance program including demographics, comorbidities, hospitalization dates, laboratory values, mechanical ventilation, positive blood and respiratory cultures, treatment administration for COVID-19 as defined by the system’s fluid treatment algorithm, and discharge disposition. Outcomes of this analysis include overall bacterial and fungal superinfection occurrence rate within 28 days of admission, patient characteristics that correlate with a higher risk of a superinfection, and the effect on 28-day mortality. Patient Population Flow diagram of patient inclusion. Results A total of 404 patients were included in the study analyses of which 56 (13.9%) had a documented superinfection within 28-days from admission. The most common superinfection organisms observed were Staphylococcus spp. (36.9%), Candida spp. (16.7%), and Klebsiella spp. (13.1%). Mortality was significantly higher in patients with superinfections (12.1% vs 5.8%, p < 0.001). To best assess characteristics that place patients at a higher risk of superinfection, a backwards, stepwise, multivariable logistic regression was performed. Black ethnicity, chronic kidney disease, intensive care unit (ICU) upon admission, lymphocytopenia, and receipt of tocilizumab were found to more likely have a superinfection within 28-days from admission. Baseline Characteristics Comparison and analysis of baseline characteristics in patients with or without superinfection present. 28-day Mortality Day-28 mortality comparison in patients with or without superinfection. Mortality was observed in 7/58 patients with a superinfection versus 20/346 patients without superinfection present (p < 0.001). Multivariable analysis results for increased superinfection risk. All baseline characteristics with univariate analysis resulting in a p value of < 0.2 were included in the backwards, stepwise logistic regression model. Conclusion In conclusion, our retrospective cohort study reports a superinfection rate of 13.9%. Presence of a superinfection significantly increases the likelihood of mortality within 28-days from admission. Characteristics that have a significant correlation to increased risk of superinfections include Black ethnicity, chronic kidney disease, ICU upon admission, and receipt of tocilizumab. Disclosures Kevin W. Garey, Pharm.D., M.S., FASHP, Summit Therapeutics (Research Grant or Support)


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Maren Leifheit-Nestler ◽  
Dieter Haffner

AbstractChronic kidney disease (CKD) is associated with distinct alterations in mineral metabolism in children and adults resulting in multiple organ dysfunctions. Children with advanced CKD often suffer from impaired bone mineralization, bone deformities and fractures, growth failure, muscle weakness, and vascular and soft tissue calcification, a complex which was recently termed CKD-mineral and bone disorder (CKD-MBD). The latter is a major contributor to the enhanced cardiovascular disease comorbidity and mortality in these patients. Elevated circulating levels of the endocrine-acting phosphaturic hormone fibroblast growth factor (FGF) 23 are the first detectable alteration of mineral metabolism and thus CKD-MBD. FGF23 is expressed and secreted from osteocytes and osteoblasts and rises, most likely due to increased phosphate load, progressively as kidney function declines in order to maintain phosphate homeostasis. Although not measured in clinical routine yet, CKD-mediated increased circulating levels of FGF23 in children are associated with pathological cardiac remodeling, vascular alterations, and increased cognitive risk. Clinical and experimental studies addressing other FGF23-mediated complications of kidney failure, such as hypertension and impaired bone mineralization, show partly conflicting results, and the causal relationships are not always entirely clear. This short review summarizes regulators of FGF23 synthesis altered in CKD and the main CKD-mediated organ dysfunctions related to high FGF23 levels.


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