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More than 30 ng of vitamin D is sometimes needed (Kidney needs 50 ng) – March 2019

Rationale for Raising Current Clinical Practice Guideline Target for Serum 25-Hydroxyvitamin D in Chronic Kidney Disease.

Am J Nephrol. 2019;49(4):284-293. doi: 10.1159/000499187

Vitamin D Life

Participants with Chronic Kidney Disease who had low vitamin D levels
Gave extended release vitamin D (in the form of calcifediol)
Those who achieved more than 50 ng/ml had much better outcomes
It is not clear that the extended release type (patented and very expensive) is needed


Previous Vitamin D level conclusions for Kidneys


Is 50 ng of vitamin D too high, just right, or not enough has the following
50 - 60 ng

> 60 ng


Kidney category starts with

Kidney category listing has 193 items

see also Overview Kidney and vitamin D
Search Vitamin D Life for dialysis OR haemodialysis 878 items not in PDF as of Aug 2020
Search Vitamin D Life for kidney transplant 798 items as of June 2019
"Chronic Kidney Disease" OR CKD 874 items as of Jan 2018

Calcitriol category listing has 46 items along with related searches

Kidney Intervention trials using Vitamin D:


Overview Kidney and vitamin D contains the following summary

  • FACT: Kidney is the primary way to activate vitamin D
  • FACT: When the Kidney has problems, there is less active vitamin D (Calcitriol) for the body
  • FACT: When the Kidney has problems, there is increased death due to many factors - many of which are associated with lack of Calcitriol
  • FACT: There are many on-going intervention clinical trials trying to determine how much of what kind of vitamin D is needed to treat the problem
  • FACT: One Randomized Controlled Trial has proven that Vitamin D treats CKD
  • FACT: Taking extra Vitamin D, in various forms, does not cause health problems - even if poor kidney
  • Suggestion: Increase vitamin D getting into body now - and increase co-factors so that the vitamin D can be better used
      Sun, UV lamp, Vitamin D supplement - probably > 5,000 IU,
    Calcitriol - which bypasses the need for the kidney to activate vitamin D
      Problems with Calcitriol however: typically only lasts for a few hours, also, possible complications
        Update: Pre-cursor of active vitamin D made from plants is better than calcitriol – Sept 2012
  • Category Kidney and Vitamin D contains 193 items


Getting Vitamin D into your body has the following grapbical summary
http://vitad.org/tiki-index.php?page_id=5644

Image
CTx-1 = Serum collagen type 1 C-telopeptide
P1NP = Intact procollagen type 1 N-terminal propeptide

Strugnell SA1, Sprague SM2, Ashfaq A3, Petkovich M4, Bishop CW3.
1 Renal Division, OPKO Health, Inc., Miami, Florida, USA, sstrugnell at opko.com.
2 Department of Medicine, NorthShore University HealthSystem, Evanston, Illinois, USA.
3 Renal Division, OPKO Health, Inc., Miami, Florida, USA.
4 Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.

BACKGROUND:
Vitamin D repletion is recommended for secondary hyperparathyroidism (SHPT) and associated vitamin D insufficiency (VDI) in chronic kidney disease (CKD), but optimal levels of serum total 25-hydroxyvitamin D remain undefined. Clinical practice guidelines target sufficiency, whereas recent data indicate that higher levels are required to control the elevation of intact parathyroid hormone (iPTH) as CKD advances. This secondary analysis of 2 randomized controlled trials seeks to identify the minimum level of mean serum 25-hydroxyvitamin D required to control SHPT arising from VDI in stage 3 or 4 CKD.

METHODS:
Adult subjects (n = 429) with SHPT, VDI, and stage 3 or 4 CKD were stratified by stage and treated daily with either extended-release calcifediol (ERC) or placebo in 2 identical, parallel, randomized, double-blind studies. After treatment for 26 weeks, all subjects were ranked by the level of serum total 25-hydroxyvitamin D and divided into quintiles in order to examine the relationships between the degree of vitamin D repletion and the associated changes in plasma iPTH, serum bone turnover markers, calcium, phosphorus, intact fibroblast growth factor 23 (FGF23) and vitamin D metabolites, estimated glomerular filtration rate (eGFR), and urine calcium:creatinine (Ca:Cr) ratio.

RESULTS:
Progressive increases in serum 1,25-dihydroxyvitamin D and reductions in plasma iPTH and serum bone turnover markers were observed as mean posttreatment serum 25-hydroxyvitamin D rose from 13.9 ng/mL (in Quintile 1) to 92.5 ng/mL (in Quintile 5), irrespective of CKD stage. Mean serum calcium, phosphorus and FGF23, eGFR, and urine Ca:Cr ratio (collectively "safety parameters") did not significantly change from Quintile 1. Suppression of iPTH and bone turnover markers was not observed until serum 25-hydroxyvitamin D rose to at least 50.8 ng/mL (Quintile 3).

CONCLUSION:
ERC therapy produced exposure-dependent reductions in plasma iPTH and bone turnover markers only when mean serum total 25-hydroxyvitamin D reached at least 50.8 ng/mL, indicating that current targets for vitamin D repletion therapy in CKD are too low. Gradual elevation of mean serum 25-hydroxyvitamin D to 92.5 ng/mL was not associated with significant adverse changes in safety parameters.


Created by admin. Last Modification: Sunday November 3, 2019 23:55:45 GMT-0000 by admin. (Version 9)

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