Effects of maternal vitamin A status on kidney development: a pilot study

Goodyer, Paul; Kurpad, Anura V; Rekha, Swarna; Muthayya, Sumitra; Dwarkanath, Pratibha; Iyengar, Arpana; Philip, Babu; Mhaskar, A; Benjamin, Alice; Maharaj, Suran; Laforte, Diane; Raju, Chandhana; Phadke, Kishore

doi:10.1007/s00467-006-0213-4

Cited by 70 publications

(49 citation statements)

References 19 publications

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“…In humans, maternal protein and micronutrient deficiencies are common in developing countries, and maternal malnutrition, underweight, iron deficiency and anemia are all recognized risk factors for LBW 35 . Vitamin A deficiency is also highly prevalent among pregnant women world-wide ( Figure 2 (Table 1) 38 .…”

Section: Developmental Determinants Of Low Nephron Numbermentioning

confidence: 99%

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

et al. 2013

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Developmental programming of non-communicable diseases is now an established paradigm. With respect to hypertension and chronic kidney disease, adverse events experienced in utero can affect development of the fetal kidney and reduce final nephron number. Low birth weight and prematurity are the most consistent clinical surrogates for a low nephron number, and are associated with increased risk of hypertension, proteinuria and kidney disease in later life. Rapid weight gain in childhood or adolescence further compounds these risks. Low birth weight, prematurity and rapid childhood weight gain should alert clinicians to an individual's life-long risk of hypertension and kidney disease, prompting education to minimize additional risk factors and ensuring follow-up. Birth weight and prematurity are significantly impacted by maternal nutrition and health during pregnancy. Optimization of maternal health and early childhood nutrition could therefore attenuate this programming cycle and reduce the global burden of hypertension and kidney disease in the future.

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Section: Developmental Determinants Of Low Nephron Numbermentioning

confidence: 99%

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

et al. 2013

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“…122 Vitamin A is an important regulator of cell proliferation and differentiation and plays a critical role in the determination of nephron mass. [123][124][125] Vitamin A deficiency is also common in premature infants 126 due in part to increased urinary losses of vitamin A. 127 Although vitamin A supplementation appears to be beneficial in the lung, another branching organ that develops in late gestation, in protecting against chronic lung disease, 128 there are no clinical data on renal outcomes in humans.…”

Section: Research Horizons Nephrogenesismentioning

confidence: 99%

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

2013

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Thanks to remarkable advances in neonatal intensive care, infants who once had little chance for survival can now enter adulthood. Yet the consequences of premature birth or low birth weight (LBW) on nephrogenesis, final nephron number, and long-term kidney function are unclear. This review focuses on the theory, experimental evidence, and observational data that suggest an increased risk of chronic kidney disease (CKD) for infants born prematurely. Many premature and LBW infants begin life with an incomplete complement of immature nephrons. They are then exposed to a variety of external stressors that can hinder ongoing kidney development or cause additional nephron loss such as hemodynamic alterations, nephrotoxic medications, infections, and suboptimal nutrition. Acute kidney injury, in particular, may be a significant risk factor for the development of CKD. According to Brenner' s hypothesis, patients with decreased nephron number develop hyperfiltration that results in sodium retention, hypertension, nephron loss, and CKD due to secondary focal segmental glomerulosclerosis. Because the risk of CKD in premature and LBW infants has not been accurately determined, there are no evidence-based recommendations for screening or management. Yet with the first generation of infants from the surfactant era only now reaching adulthood, it is possible that there is already an unrecognized epidemic of CKD. We suggest individualized, risk-based assessments of premature and LBW infants due to the increased risk of CKD and call for additional research into the long-term risk for CKD these infants face.

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“…Vitamin A and its derivatives play a vital role in the development and homeostasis of almost every organ of the body by regulating embryogenesis, including kidney development, cell differentiation, proliferation, apoptosis, immune regulation, and metabolism [1][2][3]. Recent studies have revealed that vitamin A also has an effect on energy metabolism, adipocyte differentiation, and lipid metabolism [4][5][6].…”

Section: Introductionmentioning

confidence: 98%

Vitamin A deficiency results in dysregulation of lipid efflux pathway in rat kidney

et al. 2010

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The mechanisms of action of vitamin A deficiency (VAD) on lipid metabolism in the rat kidney were investigated in adult female rats and their offspring. The rats were randomized into three groups: (1) control, in which the mother and offspring received a normal diet (4000 retinol IU/kg diet) for 8 weeks; (2) VAD group, in which the mothers and offspring received a VAD diet (400 retinol IU/kg diet) for 8 weeks; (3) vitamin A-refed group, in which a group of pups on a VAD diet for 8 weeks received a complete diet (6500 retinol IU/kg diet) for 15 days. The lipid metabolism of the offsprings' kidneys and its relation to the expression of apolipoprotein B100 (Apo-B100), liver X receptor alpha (LXRalpha), and retinoid X receptor-alpha/beta (RXRalpha/beta) mRNA was analyzed. VAD was found to alter renal lipid metabolism and its immune environment due to the expression of Apo-B100. Compared with the control, VAD rats had significantly higher levels of transforming growth factor-beta 1 and lower levels of ABCA1, a key gene involved in cholesterol efflux and tissue lipid homeostasis. The expression of LXRalpha and RXRalpha/beta mRNA also decreased in the VAD rat kidney. Vitamin A refeeding reversed all of the changes. Lipid metabolism involved in renal reverse cholesterol transport may be mediated by decreasing the signaling through the ABCA1 cholesterol efflux pathway, which is significantly modified in kidneys of vitamin A-deficient rats.

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Effects of maternal vitamin A status on kidney development: a pilot study

Cited by 70 publications

References 19 publications

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

Vitamin A deficiency results in dysregulation of lipid efflux pathway in rat kidney

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