Early postnatal overfeeding induces early chronic renal dysfunction in adult male rats

Low birth weight is associated with an increased risk of hypertension and renal dysfunction at adulthood. Such an association has been shown to involve a reduction of nephron endowment and to be enhanced by accelerated postnatal growth in humans. However, while low-birth-weight infants often undergo catch-up growth, little is known about the long-term vascular and renal effects of accelerated postnatal growth. We surimposed early postnatal overfeeding (OF; reduction of litter size during the suckling period) to appropriate-birth-weight (NBW+OF) and intrauterine growth restriction (IUGR; IUGR+OF) pups, obtained after a maternal gestational low-protein diet. Blood pressure (systolic blood pressure; SBP) and renal function (glomerular filtration rate; GFR) were measured in young and aging offspring. Glomerulosclerosis and nephron number were determined in aging offspring (22 mo). Nephron number was reduced in both IUGR and IUGR+OF male offspring (by 24 and 26%). GFR was reduced by 40% in 12-mo-old IUGR+OF male offspring, and both NBW+OF and IUGR+OF aging male offspring had sustained hypertension (+25 mmHg) and glomerulosclerosis, while SBP and renal function were unaffected in IUGR aging offspring. Female offspring were unaffected. In conclusion, in this experimental model, early postnatal OF in the neonatal period has major long-lasting effects. Such effects are gender dependent. Reduced nephron number alone, associated with IUGR, may not be sufficient to induce long-lasting physiological alterations, and early postnatal OF acts as a “second hit.” Early postnatal OF is a suitable model with which to study the long-term effects of postnatal growth in the pathogenesis of vascular disorders and renal disease.

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Correlation of renal volume to renal function and blood pressures in low birth weight children

Paediatrica Indonesiana ◽

10.14238/pi54.2.2014.73-6 ◽

2014 ◽

Vol 54 (2) ◽

pp. 73

Author(s):

Ekawaty Larope ◽

Adrian Umboh ◽

Rocky Wilar

Keyword(s):

Blood Pressure ◽

Renal Function ◽

Birth Weight ◽

Low Birth Weight ◽

Renal Volume ◽

Nephron Number ◽

Blood Pressures ◽

Relationship Of ◽

The Relationship ◽

Renal Length

Background Disruption of nephrogenesis in low birth weight(LBW) infant leads to decreases in nephron number andrenal volume, resulting in renal hyperfunction and eventually,hypertension.Objective To assess for a possible correlation of renal volume torenal function and blood pressures in low birth weight childrenaged 7 -8 years.Methods We conducted a retrospective cohort study on childrenaged 7-8 years in Manado, who were born LBW or n ormalbirth weight (NBW). Renal function was assessed by measuringblood cyctatin-C level while renal volume was determined usingultrasound measurements of renal length x width x thickness(cm3). Ttest was used to compare renal volume and cystatin-Clevels in LBW children to NBW children. Pearson's correlationtest was used to assess the relationship of renal volume to renalfunction and blood pressure in low birth weight children.Results Subjects were 48 LBW and 48 NBW children. Meanrenal volumes were 7 8.28 (SD 7 .96) cm3 in the LBW group and103.68 (SD 12.52) cm3 in the NBW group (P< 0.01). The meancystatin-C levels, as a measure of renal function, were 0.81 (SD0.07) mg/Lin the LBW group and in 0.73 (SD 0.06) mg/Linthe NBW group (P< 0.01). There was no correlation betweenrenal volume and cystatin-C level (r=-0.169; P>0,05) as wellas between renal volume and systolic (r=-0.07, P>0.05) anddias tolic blood pressure (r=-0.123, P>0.05).Conclusion Mean renal volume is lower in the LBW groupthan in the NBW group, but is not correlated to decreased renalfunction or blood pressures.

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Long-Term Effects of Maternal Diabetes on Blood Pressure and Renal Function in Rat Male Offspring

PLoS ONE ◽

10.1371/journal.pone.0088269 ◽

2014 ◽

Vol 9 (2) ◽

pp. e88269 ◽

Cited By ~ 25

Author(s):

Jie Yan ◽

Xin Li ◽

Rina Su ◽

Kai Zhang ◽

Huixia Yang

Keyword(s):

Blood Pressure ◽

Renal Function ◽

Maternal Diabetes ◽

Male Offspring ◽

Long Term Effects

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Low Birth Weight Is Associated with Reduced Nephron Number and Increased Blood Pressure in Adulthood in a Novel Spontaneous Intrauterine Growth-Restricted Model in Yucatan Miniature Swine

Neonatology ◽

10.1159/000326341 ◽

2011 ◽

Vol 100 (4) ◽

pp. 380-386 ◽

Cited By ~ 23

Author(s):

Semone B. Myrie ◽

Leslie L. McKnight ◽

Bruce N. Van Vliet ◽

Robert F. Bertolo

Keyword(s):

Blood Pressure ◽

Birth Weight ◽

Low Birth Weight ◽

Nephron Number ◽

Miniature Swine ◽

Intrauterine Growth ◽

Restricted Model

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Developmental Origins of Chronic Renal Disease: An Integrative Hypothesis

International Journal of Nephrology ◽

10.1155/2013/346067 ◽

2013 ◽

Vol 2013 ◽

pp. 1-12 ◽

Cited By ~ 34

Author(s):

F. Boubred ◽

M. Saint-Faust ◽

C. Buffat ◽

I. Ligi ◽

I. Grandvuillemin ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Birth Weight ◽

Kidney Disease ◽

Molecular Mechanisms ◽

Chronic Renal Disease ◽

Postnatal Growth ◽

Nephron Number ◽

Nephron Endowment ◽

Causes Of Mortality

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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