A new dimension to the Barker hypothesis: Low birthweight and susceptibility to renal disease

Hoy, W. E.; Rees, Megan; Kile, Emma; Mathews, John D.; Wang, Zhiqiang

doi:10.1046/j.1523-1755.1999.00633.x

Cited by 294 publications

(264 citation statements)

References 38 publications

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“…These results are similar to findings in infants without CCHD 11. In infants without CCHD, SGA has been linked to the development of early systemic hypertension,27 type 2 diabetes mellitus,28 hyperlipidemia,28 and reduced renal function 29, 30. We hypothesize that this link is even more apparent in infants with CCHD.…”

Section: Discussionsupporting

confidence: 87%

Effect of Fetal Growth on 1‐Year Mortality in Neonates With Critical Congenital Heart Disease

Steurer

Baer

Burke

et al. 2018

JAHA

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BackgroundInfants with critical congenital heart disease (CCHD) are more likely to be small for gestational age (GA). It is unclear how this affects mortality. The authors investigated the effect of birth weight Z score on 1‐year mortality separately in preterm (GA <37 weeks), early‐term (GA 37–38 weeks), and full‐term (GA 39–42 weeks) infants with CCHD.Methods and ResultsLive‐born infants with CCHD and GA 22 to 42 weeks born in California 2007–2012 were included in the analysis. The primary predictor was Z score for birth weight and the primary outcome was 1‐year mortality. Multivariable logistic regression was used. Results are presented as adjusted odds ratios and 95% confidence intervals (CIs). The authors identified 6903 infants with CCHD. For preterm and full‐term infants, only a Z score for birth weight <−2 was associated with increased mortality compared with the reference group (Z score 0–0.5, adjusted odds ratio, 2.15 [95% CI, 1.1–4.21] and adjusted odds ratio, 3.93 [95% CI, 2.32–6.68], respectively). In contrast, in early‐term infants, the adjusted odds ratios for Z scores <−2, −2 to −1, and −1 to −0.5 were 3.42 (95% CI, 1.93–6.04), 1.78 (95% CI, 1.12–2.83), and 2.03 (95% CI, 1.27–3.23), respectively, versus the reference group.Conclusions GA seems to modify the effect of birth weight Z score on mortality in infants with CCHD. In preterm and full‐term infants, only the most severe small‐for‐GA infants (Z score <−2) were at increased risk for mortality, while, in early‐term infants, the risk extended to mild to moderate small‐for‐GA infants (Z score <−0.5). This information helps to identify high‐risk infants and is useful for surgical planning.

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Section: Discussionsupporting

confidence: 87%

Effect of Fetal Growth on 1‐Year Mortality in Neonates With Critical Congenital Heart Disease

Steurer

Baer

Burke

et al. 2018

JAHA

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“…Epidemiological studies have suggested that individuals with a birthweight <2.5 kg are at increased risk of developing end-stage renal disease [7,34] or albuminuria [6] compared to those with a birthweight >2.5 kg. Low birthweight, with fewer glomeruli, may provide a partial explanation for the excess end-stage renal disease in African Americans compared to Caucasians [7].…”

Section: Discussionmentioning

confidence: 99%

“…This combination of reduced glomerular number, reduced filtration surface area and hypertension is believed to result in an increased incidence and accelerated progression of non-diabetic renal diseases [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

The effect of intrauterine environment and low glomerular number on the histological changes in diabetic glomerulosclerosis

et al. 2005

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Aims/hypothesis: We tested the hypothesis that diabetic glomerulosclerosis would develop more rapidly in animals with fewer glomeruli. Methods: We studied the female offspring of Wistar rats that had been fed a low-protein diet (LPD) containing 6% protein or a normal-protein diet (NPD) containing 18% protein during pregnancy. Streptozotocin diabetes was induced at 12 weeks and animals were killed at 40 weeks. Results: Non-diabetic LPD offspring were of lower birthweight than the NPD offspring (5.19± 0.64 vs 6.45±0.67 g, p<0.001) and had fewer glomeruli (27,402±3,137 vs 34,203±6,471, p<0.05). Glomerular volume correlated inversely with glomerular number (r=−0.64, p=0.035), but total glomerular filtration surface area was reduced in the LPD animals (4,770±541 vs 5,779±1,302 mm 2 , p=0.05). Other renal structural and functional parameters were similar. In LPD and NPD diabetic animals, glomerular volume and basement membrane width were significantly increased compared to their respective controls. Podocyte density was lowest in the LPD diabetic animals (not significant), and the area covered by each podocyte was greater in the LPD diabetic group (2.40±0.693 ×10 −3 mm 2 ) than in the LPD control group (1.68±0.374 ×10 −3 mm 2 , p<0.001) and in the NPD diabetic animals (1.71±0.291 ×10 −3 mm 2 , p<0.05). There was no difference in any other structural or functional parameter between the LPD and NPD diabetic animals. Conclusions/ interpretation: A decrease in glomerular number was not deleterious to renal structure and function over 40 weeks in this animal model. Further work in models with progressive renal impairment and hypertension is necessary to clarify the impact of glomerular number on the development of renal disease.

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“…Hoy et al, first reported an odds ratio of 2.8 (95% CI, 1.26 -6.31) of macroalbuminuria among Aboriginal Australians who had been of LBW compared to NBW 68 . In this population, albuminuria was associated with a significant increase in cardiovascular and renal deaths, emphasising its' clinical relevance 69 .…”

Section: Renal Function Birth Weight and Nephron Massmentioning

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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A new dimension to the Barker hypothesis: Low birthweight and susceptibility to renal disease

Cited by 294 publications

References 38 publications

Effect of Fetal Growth on 1‐Year Mortality in Neonates With Critical Congenital Heart Disease

Effect of Fetal Growth on 1‐Year Mortality in Neonates With Critical Congenital Heart Disease

The effect of intrauterine environment and low glomerular number on the histological changes in diabetic glomerulosclerosis

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

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