Effect of early postnatal nutrition on chronic kidney disease and arterial hypertension in adulthood: a narrative review

Juvet, Christian; Simeoni, Umberto; Yzydorczyk, Catherine; Siddeek, Bénazir; Jb, Armengaud; Nardou, Katya; Juvet, Par Gustave; Benahmed, Mohamed; Cachat, François; Chehade, Hassib

doi:10.1017/s2040174418000454

Cited by 10 publications

(6 citation statements)

References 120 publications

(232 reference statements)

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“…We initially hypothesised that low podocyte endowment may be an important mechanism that leads to the onset of podocyte-associated glomerular pathology later in life. However, our findings suggest that LPD offspring with low nephron endowment and a 9% lower podocyte endowment at 6 months do not develop significant albuminuria or glomerulosclerosis despite accelerated early postnatal growth (catch-up growth), a known risk factor for renal disease and hypertension (16). This may be due in part to their still smaller body size (despite significant catch-up growth) and/or with the timing of our analysis, given that 6 months is a relatively young age in rats (48).…”

Section: Discussionmentioning

confidence: 63%

Podocyte endowment and the impact of adult body size on kidney health

Cullen‐McEwen

Wolde

Haruhara

et al. 2021

American Journal of Physiology-Renal Physiology

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Low birth weight is a risk factor for chronic kidney disease (CKD), while adult podocyte depletion is a key event in the pathogenesis of glomerulosclerosis. However, whether low birth weight due to poor maternal nutrition is associated with low podocyte endowment and glomerulosclerosis in later life is not known. Female Sprague-Dawley rats were fed a normal (NPD, 20%) or low (LPD, 8%) protein diet from 3 weeks before mating until postnatal day 21 (PN21), when kidneys from some male offspring were taken for quantitation of podocyte number and density in whole glomeruli using immunolabeling, tissue clearing and confocal microscopy. Remaining offspring were fed a normal or high fat diet until 6 months to induce catch-up growth and excessive weight gain, respectively. At PN21, podocyte number per glomerulus was 15% lower in low birth weight (LPD) than normal birthweight (NPD) offspring, with this deficit greater in outer glomeruli. Surprisingly, podocyte number in LPD offspring increased in outer glomeruli between PN21 and 6 months, although an overall 9% podocyte deficit persisted. Postnatal fat feeding to LPD offspring did not alter podometric indices or result in glomerular pathology at 6 months, whereas fat feeding in NPD offspring was associated with far greater body and fat mass as well as podocyte loss, reduced podocyte density, albuminuria and glomerulosclerosis. This is the first report that maternal diet can influence podocyte endowment. Our findings provide new insights into the impact of low birth weight, podocyte endowment and postnatal weight on podometrics and renal health in adulthood.

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Section: Discussionmentioning

confidence: 63%

Podocyte endowment and the impact of adult body size on kidney health

Cullen‐McEwen

Wolde

Haruhara

et al. 2021

American Journal of Physiology-Renal Physiology

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“…Caroline Abitbol et al in Miami found a link between the appearance of proteinuria and its subsequent increase, as measured by the protein/creatinine ratio in urine, and a subsequent deterioration of glomerular filtration ( r = 0.8, p = 0.0001) and a tendency toward obesity with a body mass index (BMI) greater than the 85th percentile (89 percent sensitivity, PPV: 67%, p = 0.03) in newborns under 1,000 g. A subsequent study by the same center looked at the effects of obesity and prematurity on renal disease progression in a retrospective cohort of these children (44 obese and 36 non-obese). When compared to obese children born at term, patients who became obese after being born extremely preterm had a higher risk of impaired kidney function during childhood (hazard ratio 2.4; 95% CI: 1.1–7.1; p = 0.04) ( 60 ).…”

Section: Impact Of Lbw In Pediatrics and Obstetricsmentioning

confidence: 99%

Low Birthweight as a Risk Factor for Non-communicable Diseases in Adults

Bianchi

Restrepo

2022

Front. Med.

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According to studies undertaken over the past 40 years, low birthweight (LBW) is not only a significant predictor of perinatal death and morbidity, but also increases the risk of chronic non-communicable diseases (NCDs) in adulthood. The purpose of this paper is to summarize the research on LBW as a risk factor for NCDs in adults. The Barker hypothesis was based on the finding that adults with an LBW or an unhealthy intrauterine environment, as well as a rapid catch-up, die due to NCDs. Over the last few decades, terminology such as thrifty genes, fetal programming, developmental origins of health and disease (DOHaD), and epigenetic factors have been coined. The most common NCDs include cardiovascular disease, diabetes mellitus type 2 (DMT2), hypertension (HT), dyslipidemia, proteinuria, and chronic kidney disease (CKD). Studies in mothers who experienced famine and those that solely reported birth weight as a risk factor for mortality support the concept. Although the etiology of NCD is unknown, Barry Brenner explained the notion of a low glomerular number (nGlom) in LBW children, followed by the progression to hyperfiltration as the physiopathologic etiology of HT and CKD in adults based on Guyton's renal physiology work. Autopsies of several ethnic groups have revealed anatomopathologic evidence in fetuses and adult kidneys. Because of the renal reserve, demonstrating renal function in proportion to renal volume in vivo is more difficult in adults. The greatest impact of these theories can be seen in pediatrics and obstetrics practice.

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“…Indeed, recent studies have highlighted the potential role of intrauterine growth restriction (IUGR) in the pathophysiology of psychiatric neurodevelopment diseases, such as SZ [17][18][19]. IUGR [20] is widely considered to be a predisposing factor to several non-transmissible diseases such as cardiovascular and renal disorders [21][22][23]. In addition to significantly impacting birth weight [20,24], IUGR has also been correlated with impaired cerebral development [20,25,26] and adverse cognitive outcomes, such as lower IQ and reduced working memory [24,27], occurring even many years after the adverse environmental exposure.…”

Section: Introductionmentioning

confidence: 99%

Low protein-induced intrauterine growth restriction as a risk factor for schizophrenia phenotype in a rat model: assessing the role of oxidative stress and neuroinflammation interaction

Allgäuer

Cabungcal²,

Yzydorczyk³

et al. 2023

Transl Psychiatry

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A large body of evidence suggests that intrauterine growth restriction (IUGR) impedes normal neurodevelopment and predisposes the offspring to cognitive and behavioral deficits later in life. A significantly higher risk rate for schizophrenia (SZ) has been reported in individuals born after IUGR. Oxidative stress and neuroinflammation are both involved in the pathophysiology of SZ, particularly affecting the structural and functional integrity of parvalbumin interneurons (PVI) and their perineuronal nets (PNN). These anomalies have been tightly linked to impaired cognition, as observed in SZ. However, these pathways remain unexplored in models of IUGR. New research has proposed the activation of the MMP9-RAGE pathway to be a cause of persisting damage to PVIs. We hypothesize that IUGR, caused by a maternal protein deficiency during gestation, will induce oxidative stress and neuroinflammation. The activation of these pathways during neurodevelopment may affect the maturation of PVIs and PNNs, leading to long-term consequences in adolescent rats, in analogy to SZ patients. The level of oxidative stress and microglia activation were significantly increased in adolescent IUGR rats at postnatal day (P)35 as compared to control rats. PVI and PNN were decreased in P35 IUGR rats when compared to the control rats. MMP9 protein level and RAGE shedding were also increased, suggesting the involvement of this mechanism in the interaction between oxidative stress and neuroinflammation. We propose that maternal diet is an important factor for proper neurodevelopment of the inhibitory circuitry, and is likely to play a crucial role in determining normal cognition later in life, thus making it a pertinent model for SZ.

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Effect of early postnatal nutrition on chronic kidney disease and arterial hypertension in adulthood: a narrative review

Cited by 10 publications

References 120 publications

Podocyte endowment and the impact of adult body size on kidney health

Podocyte endowment and the impact of adult body size on kidney health

Low Birthweight as a Risk Factor for Non-communicable Diseases in Adults

Low protein-induced intrauterine growth restriction as a risk factor for schizophrenia phenotype in a rat model: assessing the role of oxidative stress and neuroinflammation interaction

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