Maternal vitamin D deficiency programmes adult renal renin gene expression and renal function

Boyce, A; Palmer-Aronsten, B. J.; Kim, M. Y.; Gibson, Karen J.

doi:10.1017/s2040174413000342

Cited by 15 publications

(21 citation statements)

References 34 publications

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“…Although offspring nephron number was increased by maternal vitamin D deficiency, these additional nephrons could be abnormal. Boyce et al (2013) found that adult male offspring of vitamin D deficient dams who ate normal chow from weaning had a reduced creatinine clearance and others have reported high blood pressure and ventricular hypertrophy in young offspring maintained on a vitamin D deficient diet ( Gezmish et al, 2010 ; Tare et al, 2011 ).…”

Section: Abnormal Renal Developmentmentioning

confidence: 99%

Programming of Renal Development and Chronic Disease in Adult Life

et al. 2020

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Chronic kidney disease (CKD) can have an insidious onset because there is a gradual decline in nephron number throughout life. There may be no overt symptoms of renal dysfunction until about two thirds or more of the nephrons have been destroyed and glomerular filtration rate (GFR) falls to below 25% of normal (often in mid-late life) ( Martinez-Maldonaldo et al., 1992 ). Once End Stage Renal Disease (ESRD) has been reached, survival depends on renal replacement therapy (RRT). CKD causes hypertension and cardiovascular disease; and hypertension causes CKD. Albuminuria is also a risk factor for cardiovascular disease. The age of onset of CKD is partly determined during fetal life. This review describes the mechanisms underlying the development of CKD in adult life that results from abnormal renal development caused by an adverse intrauterine environment. The basis of this form of CKD is thought to be mainly due to a reduction in the number of nephrons formed in utero which impacts on the age dependent decline in glomerular function. Factors that affect the risk of reduced nephron formation during intrauterine life are discussed and include maternal nutrition (malnutrition and obesity, micronutrients), smoking and alcohol, use of drugs that block the maternal renin-angiotensin system, glucocorticoid excess and maternal renal dysfunction and prematurity. Since CKD, hypertension and cardiovascular disease add to the disease burden in the community we recommend that kidney size at birth should be recorded using ultrasound and those individuals who are born premature or who have small kidneys at this time should be monitored regularly by determining GFR and albumin:creatinine clearance ratio. Furthermore, public health measures aimed at limiting the prevalence of obesity and diabetes mellitus as well as providing advice on limiting the amount of protein ingested during a single meal, because they are all associated with increased glomerular hyperfiltration and subsequent glomerulosclerosis would be beneficial.

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Section: Abnormal Renal Developmentmentioning

confidence: 99%

Programming of Renal Development and Chronic Disease in Adult Life

et al. 2020

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“…Vitamin D deficiency in rats during the nephrogenic period leads to renal disorders in adulthood, such as a 20% increase in glomerular numbers, associated with a significant reduction in renal corpuscle volume [126,132]. Maternal vitamin D deficiency leads to elevated fetal renal renin mRNA level and this persists in adulthood, associated with impaired renal function [133]. Vitamin D deficiency in rats during renal development causes disturbances in renal microvasculature that are persistent in adulthood, accompanied by increased plasma levels of ANGII.…”

Section: Impact Of Environmental Factors On Renin-angiotensin System mentioning

confidence: 99%

Role of the renin–angiotensin system in kidney development and programming of adult blood pressure

et al. 2020

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Adverse events during fetal life such as insufficient protein intake or elevated transfer of glucocorticoid to the fetus may impact cardiovascular and metabolic health later in adult life and are associated with increased incidence of type 2 diabetes, ischemic heart disease and hypertension. Several adverse factors converge and suppress the fetal renin-angiotensin-aldosterone system (RAAS). The aim of this review is to summarize data on the significance of RAAS for kidney development and adult hypertension. Genetic inactivation of RAAS in rodents at any step from angiotensinogen to angiotensin II (ANGII) type 1 receptor (AT 1 ) receptors or pharmacologic inhibition leads to complex developmental injury to the kidneys that has also been observed in human case reports. Deletion of the 'protective' arm of RAAS, angiotensin converting enzyme (ACE) 2 (ACE-2) and G-protein coupled receptor for Angiotensin 1-7 (Mas) receptor does not reproduce the AT 1 phenotype. The changes comprise fewer glomeruli, thinner cortex, dilated tubules, thicker arterioles and arteries, lack of vascular bundles, papillary atrophy, shorter capillary length and volume in cortex and medulla. Altered activity of systemic and local regulators of fetal-perinatal RAAS such as vitamin D and cyclooxygenase (COX)/prostaglandins are associated with similar injuries. ANGII-AT 1 interaction drives podocyte and epithelial cell formation of vascular growth factors, notably vascular endothelial growth factor (VEGF) and angiopoietins (Angpts), which support late stages of glomerular and cortical capillary growth and medullary vascular bundle formation and patterning. RAAS-induced injury is associated with lower glomerular filtration rate (GFR), lower renal plasma flow, kidney fibrosis, up-regulation of sodium transporters, impaired sodium excretion and salt-sensitive hypertension. The renal component and salt sensitivity of programmed hypertension may impact dietary counseling and choice of pharmacological intervention to treat hypertension.

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“…Vit.D-pups also had lower BWs, confirming the results of previous studies. 11 However, these rats presented with a higher BW compared with the CG group in adulthood. Wen et al demonstrated that Vit.D deficiency during pregnancy stimulates the proliferation and differentiation of pre-adipocytes, which may be associated with the alteration in the methylation of genes, such as Vldlr and Hif1α, leading to offspring obesity.…”

Section: Discussionmentioning

confidence: 84%

“…Vessel rarefaction in the medulla, which is associated with increased ANGII due to renal development disorders, may have contributed to the changes in urinary concentration. 20,11 It has been shown that ANGII increases differentiation and branched ureteric buds in vivo and is responsible for renal vessel formation during kidney development. 9 Increased ANGII during renal development can lead to imbalanced angiogenesis factors for vascular branches, which impairs renal vessel maturation, promotes arteriolar wall thickening and reduces inner medulla volume.…”

Section: Discussionmentioning

confidence: 99%

“…9 Pups from mothers subjected to a vitamin D 3 (Vit.D 3 )-deficient diet during pregnancy and lactation exhibit changes in kidney development associated with alterations in the RAS. 10,11 This study investigates the influence of Vit.D 3 deficiency on changes in kidney development in female rats, the morphological and functional consequences in adulthood and the mechanisms involved in this process.…”

Section: Introductionmentioning

confidence: 99%

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Renal developmental disturbances and their long-term consequences in female pups from vitamin D-deficient mothers: involved mechanisms

Almeida

Francescato

Silva

et al. 2019

J Dev Orig Health Dis

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The mechanisms involved in kidney disturbances during development, induced by vitamin D3 deficiency in female rats, that persist into adulthood were evaluated in this study. Female offspring from mothers fed normal (control group, n=8) or vitamin D-deficient (Vit.D-, n=10) diets were used. Three-month-old rats had their systolic blood pressure (SBP) measured and their blood and urine sampled to quantify vitamin D3 (Vit.D3), creatinine, Na+, Ca+2 and angiotensin II (ANGII) levels. The kidneys were then removed for nitric oxide (NO) quantification and immunohistochemical studies. Vit.D- pups showed higher SBP and plasma ANGII levels in adulthood (P<0.05) as well as decreased urine osmolality associated with increases in urinary volume (P<0.05). Decreased expression of JG12 (renal cortex and glomeruli) and synaptopodin (glomeruli) as well as reduced renal NO was also observed (P<0.05). These findings showed that renal disturbances in development in pups from Vit.D- mothers observed in adulthood may be related to the development of angiogenesis, NO and ANGII alterations.

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Maternal vitamin D deficiency programmes adult renal renin gene expression and renal function

Cited by 15 publications

References 34 publications

Programming of Renal Development and Chronic Disease in Adult Life

Programming of Renal Development and Chronic Disease in Adult Life

Role of the renin–angiotensin system in kidney development and programming of adult blood pressure

Renal developmental disturbances and their long-term consequences in female pups from vitamin D-deficient mothers: involved mechanisms

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