Abstract: FR-PO131

Vitamin D Deficiency Prevalent in Pediatric Patients with Severe AKI on Prolonged Continuous Renal Replacement Therapy

Session Information

Category: Acute Kidney Injury

  • 003 AKI: Clinical and Translational


  • Akcan Arikan, Ayse, Baylor College of Medicine, Houston, Texas, United States
  • Tufan Pekkucuksen, Naile, texas childrens hospial, Houston, Texas, United States
  • Vega, Molly Rw, Texas Children''s Hospital/Baylor College of Medicine, Houston, Texas, United States
  • Imani, Peace D., Texas Children's Hospital , Houston, Texas, United States
  • Brewer, Eileen D., Baylor College of Medicine and Texas Children's Hospital, Houston, Texas, United States
  • Srivaths, Poyyapakkam, Texas Children's Hospital , Houston, Texas, United States

Vitamin D deficiency is reported in critically ill children and pediatric chronic kidney disease (CKD) patients (pts) with associated with adverse outcomes. Children on continuous renal replacement therapy(CRRT) are at risk of micronutrient deficiencies; however, serum vitamin D profiles in children with severe acute kidney injury on CRRT are unreported. We aimed to describe vitamin D levels and frequency of vitamin D deficiency in pediatric pts requiring prolonged CRRT(>28days).


Our center utilizes continuous venovenous hemodiafiltration with regional citrate anticoagulation per institutional protocol for CRRT. Calcium is infused postfilter to keep serum ionized calcium levels in the normal range. All prolonged CRRT pts are assumed to be at risk of CKD and undergo monthly monitoring for CKD labs, including vitD(25;1,25) and parathyroid hormone(PTH) levels. All pts receiving prolonged CRRT during 2015-2017 were included in this study.


16 patients, 56% male received prolonged CRRT for acute kidney injury; CRRT duration was 60±34 days. First vitD levels were obtained after 28 days on CRRT; 4 pts (25%) were vitD deficient (<20), 7(44%) were insufficient (<30). Mean vitD25 level was 25.4 ± 7.5 ng/ml, mean vitD1,25 level was 47 ± 55 pg/ml; total calcium was10 ±1.5 mg/dl, ionized calcium was 1.23(1.16-1.28) mmol/L, phosphorus was 4.2 ±1.3 mg/dl. Despite routine vitD supplementation in total parenteral nutrition and additional oral supplementation when needed, all 4 patients with normal vitD25 levels became insufficient over time, 6 deficient or insufficient pts never had vitD25 levels>30. There was a negative correlation between vitD25 and PTH levels which did not reach statistical significance (Spearman r=-0.28, p=0.08). Despite strict control of serum ionized calcium and phosphorus levels in the normal range, 4/6 patients who became vitD deficient/insufficient developed rising PTH levels(from 52 (45-176) to 434 (348-656) pg/ml,p=0.06).


Vit D deficiency/insufficiency is prevalent in pediatric prolonged CRRT, and might worsen despite usual pharmacological supplementation. Our preliminary data suggesting vitamin D abnormalities might be related to developing bone mineral disease in prolonged CRRT require confirmation through further studies.