F
Frederick J. Kaskel
Researcher at Boston Children's Hospital
Publications - 78
Citations - 8079
Frederick J. Kaskel is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Kidney disease & Focal segmental glomerulosclerosis. The author has an hindex of 31, co-authored 65 publications receiving 6748 citations. Previous affiliations of Frederick J. Kaskel include Yeshiva University.
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Journal ArticleDOI
New Equations to Estimate GFR in Children with CKD
George J. Schwartz,Alvaro Muñoz,Michael F. Schneider,Robert H. Mak,Frederick J. Kaskel,Bradley A. Warady,Susan L. Furth +6 more
TL;DR: In a test set of 168 CKiD patients at 1 yr of follow-up, this formula compared favorably with previously published estimating equations for children, and with height measured in cm, a bedside calculation provides a good approximation to the estimated GFR formula.
Journal ArticleDOI
Focal segmental glomerulosclerosis.
TL;DR: Current approaches to diagnosis and management ofocal segmental glomerulosclerosis are considered, which is characterized by progressive glomerular scarring, in children and adults.
Journal ArticleDOI
Prevalence and Associations of 25-Hydroxyvitamin D Deficiency in US Children: NHANES 2001–2004
TL;DR: 25(OH)D deficiency is common in the general US pediatric population and is associated with adverse cardiovascular risks and was associated with elevated parathyroid hormone levels and high-density lipoprotein cholesterol levels.
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Differential gene expression following early renal ischemia/reperfusion
Suroj Supavekin,Weijia Zhang,Raju Kucherlapati,Frederick J. Kaskel,Leon C. Moore,Prasad Devarajan +5 more
TL;DR: The results indicate that apoptosis may represent an important mechanism for the early loss of tubule cells following ischemia/reperfusion injury and provide a molecular basis for the previous findings that significant intrarenal mechanisms exist to enable tubule cell repair and regeneration.
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Update on Inflammation in Chronic Kidney Disease
TL;DR: The variety of factors contribute to chronic inflammatory status in CKD, including increased production and decreased clearance of pro-inflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, including those related to dialysis access, altered metabolism of adipose tissue, and intestinal dysbiosis.