Kidney dysfunction leads to many different diseases, including chronic kidney disease (CKD) (Kendrick & Choncol, 2008). In the USA alone, 11.5% of the population suffers from CKD (Kendrick & Choncol, 2008). The main cause of death in the CKD population, before these patients reach end-stage renal failure, is cardiovascular disease (CVD) (Karras et al., 2012; Gansveroot et al., 2013).
A chronic inflammatory state in the blood vessels is a hallmark of CKD leading to CVD (Kendrick & Choncol, 2008). This inflammatory state leads to endothelial dysfunction, a non-traditional risk factor for CVD (Kendrick & Choncol, 2008). Therefore, severity of the dysfunction can provide important information on a patient’s risk for CVD (Kendrick & Choncol, 2008). Endothelial dysfunction can be measured using bio-inflammatory markers such as NF-kB (Kendrick, 2014).
NF-kB is a transcription factor that regulates the transcription of inflammatory cytokines in blood vessels (Kempe, 2005). Overexpression of NF-kB can lead to a chronic inflammatory state, a symptom of CKD and CVD (Kempe, 2005). Kendrick (2014) and Ingauma (2008) found that CKD patients seemed to have low serum levels of vitamin D. When these patients were treated with vitamin D supplements, bio-inflammatory markers such as interleukin-6 and NF-kB were markedly reduced (Kendrick, 2014; Inaguma, 2008).
We are examining the relationship between vitamin D treatments and endothelial dysfunction by examining the inflammatory protein NF-kB in endothelial cells using immunofluorescent antibody staining. Endothelial cells were collected from 128 stage IIIB to IV CKD patients using cannulation before and after treatment with two different types of vitamin D supplements, calcitriol (active form of vitamin D) and cholecalciferol (dietary supplement). The purpose of this study is to compare the efficacy of calcitriol to cholecalciferol in treating inflammation in CKD patients. If these treatments reduce inflammation as assessed by our biomarkers, then vitamin D may be used to treat CKD patients for chronic inflammation to prevent cardiovascular events in the future.
Sarah Calhoun, ’16
Biochemistry & Molecular Biology
Sponsor: Craig Tepper