“…12,13 By contrast, some studies did not identify an increased risk of kidney stone after exposure to vitamin D alone (without calcium supplementation) during a median follow-up of 3.3 years. 25 Interventional studies remain sparse but recent observations show that some kidney stone formers may develop hypercalciuria after vitamin D "repletion". 26,27 An important point to take into consideration is the time required to develop Randall's plaque, which precede stone formation.…”
Most of kidney stones are made of calcium oxalate crystals. Randall's plaque, an apatite deposit at the tip of the renal papilla is considered to be at the origin of these stones. Hypercalciuria may promote Randall's plaque formation and growth. We analysed whether long-term exposure of Abcc6-/mice (a murine model of Randall's plaque) to vitamin D supplementation, with or without calcium-rich diet, would accelerate the formation of Randall's plaque. Eight groups of mice (including Abcc6-/and wild-type) received vitamin D alone (100,000 UI/Kg every 2 weeks), a calcium-enriched diet alone (calcium gluconate 2g/l in drinking water), both vitamin D supplementation and calcium rich diet, or a standard diet (controls) for 6 months. Kidney calcifications were assessed by 3Dmicro-computed tomography, µ-Fourier transform infrared spectroscopy, field emissionscanning electron microscopy, transmission electron microscopy and Yasue staining. At 6 months, Abcc6-/mice exposed to vitamin D and calcium supplementation developed massive Randall's plaque when compared to control Abcc6-/mice (p<0.01). Wild-type animals did not develop significant calcifications when exposed to vitamin D. Combined administration of vitamin D and calcium accelerates significantly Randall's plaque formation in a murine model. This original model raises concerns about the cumulative risk of vitamin D supplementation and calcium intakes in Randall's plaque formation.
“…12,13 By contrast, some studies did not identify an increased risk of kidney stone after exposure to vitamin D alone (without calcium supplementation) during a median follow-up of 3.3 years. 25 Interventional studies remain sparse but recent observations show that some kidney stone formers may develop hypercalciuria after vitamin D "repletion". 26,27 An important point to take into consideration is the time required to develop Randall's plaque, which precede stone formation.…”
Most of kidney stones are made of calcium oxalate crystals. Randall's plaque, an apatite deposit at the tip of the renal papilla is considered to be at the origin of these stones. Hypercalciuria may promote Randall's plaque formation and growth. We analysed whether long-term exposure of Abcc6-/mice (a murine model of Randall's plaque) to vitamin D supplementation, with or without calcium-rich diet, would accelerate the formation of Randall's plaque. Eight groups of mice (including Abcc6-/and wild-type) received vitamin D alone (100,000 UI/Kg every 2 weeks), a calcium-enriched diet alone (calcium gluconate 2g/l in drinking water), both vitamin D supplementation and calcium rich diet, or a standard diet (controls) for 6 months. Kidney calcifications were assessed by 3Dmicro-computed tomography, µ-Fourier transform infrared spectroscopy, field emissionscanning electron microscopy, transmission electron microscopy and Yasue staining. At 6 months, Abcc6-/mice exposed to vitamin D and calcium supplementation developed massive Randall's plaque when compared to control Abcc6-/mice (p<0.01). Wild-type animals did not develop significant calcifications when exposed to vitamin D. Combined administration of vitamin D and calcium accelerates significantly Randall's plaque formation in a murine model. This original model raises concerns about the cumulative risk of vitamin D supplementation and calcium intakes in Randall's plaque formation.
“…A recent article on a high-dose vitamin D supplementation trial in New Zealand involving 5110 participants reported that, over a median of 3.3 years, monthly supplementation with 100,000 IU of vitamin D 3 did not affect the incidence rate of kidney stone events or hypercalcemia [144].…”
The world is in the grip of the COVID-19 pandemic. Public health measures that can reduce the risk of infection and death in addition to quarantines are desperately needed. This article reviews the roles of vitamin D in reducing the risk of respiratory tract infections, knowledge about the epidemiology of influenza and COVID-19, and how vitamin D supplementation might be a useful measure to reduce risk. Through several mechanisms, vitamin D can reduce risk of infections. Those mechanisms include inducing cathelicidins and defensins that can lower viral replication rates and reducing concentrations of pro-inflammatory cytokines that produce the inflammation that injures the lining of the lungs, leading to pneumonia, as well as increasing concentrations of anti-inflammatory cytokines. Several observational studies and clinical trials reported that vitamin D supplementation reduced the risk of influenza, whereas others did not. Evidence supporting the role of vitamin D in reducing risk of COVID-19 includes that the outbreak occurred in winter, a time when 25-hydroxyvitamin D (25(OH)D) concentrations are lowest; that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome; and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration. To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D 3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d. The goal should be to raise 25(OH)D concentrations above 40-60 ng/mL (100-150 nmol/L). For treatment of people who become infected with COVID-19, higher vitamin D 3 doses might be useful. Randomized controlled trials and large population studies should be conducted to evaluate these recommendations.
“…A recent article on high-dose vitamin D supplementation trial in New Zealand involving 5110 participants reported that over a median of 3.3 years, monthly supplementation with 100,000 IU of vitamin D3 did not affect the incidence rate of kidney stone events or hypercalcemia [144].…”
The world is in the grips of the COVID-19 pandemic. Public health measures that can reduce the risk of infection and death in addition to quarantines are desperately needed. This article reviews the roles of vitamin D in reducing risk of respiratory tract infections, knowledge about the epidemiology of influenza and COVID-19, and how vitamin D supplementation might be a useful measure to reduce risk. Through several mechanisms, vitamin D can reduce risk of infections. Those mechanisms include inducing cathelicidins and defensins that can lower viral replication rates and reducing concentrations of pro-inflammatory cytokines that produce the inflammation that injures the lining of the lungs, leading to pneumonia, as well as increase concentrations of anti-inflammatory cytokines. Several observational studies and clinical trials reported that vitamin D supplementation reduced risk of influenza, whereas others did not. Evidence supporting the role of vitamin D in reducing risk of COVID-19 includes that the outbreak occurred in winter, a time when 25-hydroxyvitamin D [25(OH)D] concentrations are lowest; that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome, and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration. To reduce risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d. The goal should be to raise 25(OH)D concentrations above 40–60 ng/ml (100–150 nmol/l). For treatment of people who become infected with COVID-19, higher vitamin D3 doses might be useful. Randomized controlled trials and large population studies should be conducted to evaluate these recommendations.
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