Clin Chim Acta. 2016 Jan 30;453:1-12. doi: 10.1016/j.cca.2015.11.029. Epub 2015 Dec 2.
Liu WC1, Wu CC2, Hung YM3, Liao MT4, Shyu JF5, Lin YF6, Lu KC7, Yeh KC8.
Abstract fails to mention the many ways to reduce vascular calcification
See also VitaminDWiki
- Overview Vitamin K and Vitamin D
- Cardiovascular calcification prevented by Omega-3, Magnesium, Vitamin K, and Vitamin D – April 2015
- If you must take statins and want to avoid hardening of arteries, take vitamin K2 – RCT May 2015
- Vitamin K2 decreases arterial stiffness (cleans arteries) – RCT Feb 2015
- Vascular calcification greatly reduced by 1000 ug of Vitamin K2 MK-7 – Dec 2013
Items in both Kidney and Calcitriol categories in VitaminDWiki:
- Fully-activated Vitamin D (Calcitriol) is produced inside and outside of the kidneys – July 2020
- Kidney patients who happened to be getting high-dose Calcitriol were 9X less likely to die of COVID-19 - April 6, 2021
- Chronic Kidney Disease (stage 3) slowed by 30 ng of Vitamin D and Calcitriol – Dec 2019
- Vitamin D for kidney disease – use native or active form – Jan 2016
- Kidney failure – still debating what form of vitamin D to use – April 2016
- Magnesium reduced calcitriol (active vitamin D) artery calcification in CKD by 50 percent – Oct 2015
- Not as much active vitamin D if poor kidney function and low vitamin D – March 2015
- Calcitriol (active Vitamin D) recommended after kidney transplant – March 2014
- Kidney disease helped by active or high dose Vitamin D - Feb 2014
- Chronic Kidney Disease study not aware of appropriate forms of vitamin D – March 2014
- Time-release form of active vitamin D granted a patent for chronic kidney disease – July 2014
- Omega 3 increased by 60 percent the ACTIVE vitamin D in the blood – Aug 2012
- Vitamin D3 vs serum D3 (Calcitriol, HyD) – Jan 2012
- Vitamin D3 becomes Calcidiol which becomes Calcitriol
- Overview Kidney and vitamin D
Low 25(OH)D levels are common in chronic kidney disease (CKD) patients and are implicated in all-cause mortality and morbidity risks. Furthermore, the progression of CKD is accompanied by a gradual decline in 25(OH)D production. Vitamin D deficiency in CKD causes skeletal disorders, such as osteoblast or osteoclast cell defects, bone turnover imbalance, and deterioration of bone quality, and nonskeletal disorders, such as metabolic syndrome, hypertension, immune dysfunction, hyperlipidemia, diabetes, and anemia. Extra-renal organs possess the enzymatic machinery for converting 25(OH)D to 1,25(OH)2D, which may play considerable biological roles beyond the traditional roles of vitamin D.
Pharmacological 1,25(OH)2D dose causes hypercalcemia and hyperphosphatemia as well as adynamic bone disorder, which intensifies vascular calcification. Conversely, native vitamin D supplementation reduces the risk of hypercalcemia and hyperphosphatemia, which may play a role in managing bone and cardio-renal health and ultimately reducing mortality in CKD patients. Nevertheless, the combination of native vitamin D and active vitamin D can enhance therapy benefits of secondary hyperparathyroidism because of extra-renal 1a-hydroxylase activity in parathyroid gland. This article emphasizes the role of native vitamin D replacements in CKD, reviews vitamin D biology, and summarizes the present literature regarding native vitamin D replacement in the CKD population.
PMID: 26656443 DOI: 10.1016/j.cca.2015.11.029