No juvenile arterial hypertension in sheep multiples despite reduced nephron numbers

Mühle, Anja; Mühle, Christiane; Amann, Kerstin; Dötsch, Jörg; Nüsken, Kai-Dietrich; Boltze, Johannes; Schneider, Holm

doi:10.1007/s00467-010-1512-3

Cited by 15 publications

(13 citation statements)

References 41 publications

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“…In the same way, we have observed that renal function and structure were unaffected in ageing IUGR offspring with a slow postnatal growth [16]. Such a considerable influence of early growth and nutrition on long term blood pressure in rats has been observed in other species, especially in sheep [78, 79]. Finally, adult hypertension and salt sensitive hypertension (52-week-old animals) could be prevented by placing IUGR rat offspring on a low salt diet just 3 weeks after weaning [80].…”

Section: Developmental Origins Of Ckdmentioning

confidence: 64%

Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

Boubred

Saint-Faust

Buffat

et al. 2013

International Journal of Nephrology

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Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the “early programming” of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a “factor of vulnerability” when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways.

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Section: Developmental Origins Of Ckdmentioning

confidence: 64%

Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

Boubred

Saint-Faust

Buffat

et al. 2013

International Journal of Nephrology

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“…Consistent with this, a recent Swedish study of 16,265 twins found a correlation between LBW and later life hypertension within dizygotic and monozygotic twin pairs, suggesting that individual fetal growth is an important factor, independent of genetic background, impacting developmental programming of adult disease 83. Not all studies confirm the association between birth weight and subsequent blood pressures, however 84–86. The relationship appears to be least consistent among US black children but is maintained in African and Caribbean black children, suggesting that genetic and/or environmental factors may be more pivotal in the US population 75,77,78,87…”

Section: Clinical Consequences Of Impaired Developmental Programming mentioning

confidence: 81%

Inborn Nephron Diversity and Its Clinical Consequences

Luyckx¹,

Shukha²,

Brenner³

2011

Rambam Maimonides Med J

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Epidemiologic studies now strongly support the hypothesis, proposed over two decades ago, that developmental programming of the kidney impacts an individual’s risk for hypertension and renal disease in later life. Low birth weight is the strongest current clinical surrogate marker for an adverse intrauterine environment and, based on animal and human studies, is associated with a low nephron number. Other clinical correlates of low nephron number include female gender, short adult stature, small kidney size, and prematurity. Low nephron number in Caucasian and Australian Aboriginal subjects has been shown to be associated with higher blood pressures, and, conversely, hypertension is less prevalent in individuals with higher nephron numbers. In addition to nephron number, other programmed factors associated with the increased risk of hypertension include salt sensitivity, altered expression of renal sodium transporters, altered vascular reactivity, and sympathetic nervous system overactivity. Glomerular volume is universally found to vary inversely with nephron number, suggesting a degree of compensatory hypertrophy and hyperfunction in the setting of a low nephron number. This adaptation may become overwhelmed in the setting of superimposed renal insults, e.g. diabetes mellitus or rapid catch-up growth, leading to the vicious cycle of on-going hyperfiltration, proteinuria, nephron loss and progressive renal functional decline. Many millions of babies are born with low birth weight every year, and hypertension and renal disease prevalences are increasing around the globe. At present, little can be done clinically to augment nephron number; therefore adequate prenatal care and careful postnatal nutrition are crucial to optimize an individual’s nephron number during development and potentially to stem the tide of the growing cardiovascular and renal disease epidemics worldwide.

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“…These results support findings in our laboratory and in others, and suggest that neonatal nutrition/growth has to be taken into account in the long-term effects of IUGR in this model. The considerable influence of neonatal growth on long-term diseases in rat has been observed in other species, especially in sheep [145,146].…”

Section: Experimental Studiesmentioning

confidence: 98%

Adverse consequences of accelerated neonatal growth: cardiovascular and renal issues

et al. 2010

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Epidemiological and experimental studies show that the risk of cardiovascular and metabolic diseases at adulthood is inversely related to the weight at birth. Although with less evidence, low birth weight has been suggested to increase the risk of chronic kidney disease (CKD). It is well established that the developmental programming of arterial hypertension and of renal disease involves in particular renal factors, especially nephron endowment, which is reduced in low birth weight and maternal diabetes situations. Experimental studies, especially in rodents, have demonstrated the long-term influence of postnatal nutrition and/or postnatal growth on cardiovascular, metabolic and renal functions, while human data are scarce on this issue. Vascular and renal diseases appear to have a "multihits" origin, with reduced nephron number the initial hit and rapid postnatal growth the second hit. This review addresses the current understanding of the role of the kidney, both as a mechanism and as a target, in the developmental origins of adult disease theory, with a particular focus on the long-term effects of postnatal growth and nutrition.

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No juvenile arterial hypertension in sheep multiples despite reduced nephron numbers

Cited by 15 publications

References 41 publications

Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

Inborn Nephron Diversity and Its Clinical Consequences

Adverse consequences of accelerated neonatal growth: cardiovascular and renal issues

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