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  • Review Article
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Prenatal programming—effects on blood pressure and renal function

Abstract

Impaired intrauterine nephrogenesis—most clearly illustrated by low nephron number—is frequently associated with low birthweight and has been recognized as a powerful risk factor for renal disease; it increases the risks of low glomerular filtration rate, of more rapid progression of primary kidney disease, and of increased incidence of chronic kidney disease or end-stage renal disease. Another important consequence of impaired nephrogenesis is hypertension, which further amplifies the risk of onset and progression of kidney disease. Hypertension is associated with low nephron numbers in white individuals, but the association is not universal and is not seen in individuals of African origin. The derangement of intrauterine kidney development is an example of a more general principle that illustrates the paradigm of plasticity during development—that is, that transcription of the genetic code is modified by epigenetic factors (as has increasingly been documented). This Review outlines the concept of prenatal programming and, in particular, describes its role in kidney disease and hypertension.

Key Points

  • Intrauterine growth restriction with reduced renal organogenesis is a powerful predictor of adult renal disease (such as albuminuria, reduced glomerular filtration rate and progressive kidney disease) and cardiovascular disease (such as hypertension and coronary heart disease)

  • Impaired kidney development in an adverse intrauterine environment results in a low nephron number, which predisposes individuals to hypertension and kidney disease in adulthood

  • The main factors that predispose individuals to reduced renal development are protein and calorie malnutrition, placental malfunction and maternal hyperglycemia

  • Low birthweight can be used as a surrogate marker of some, but not all, disturbances of intrauterine growth, thereby enabling the identification of at-risk children who might benefit from regular surveillance

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Figure 1: Prenatal programming and renal malfunction.
Figure 2: Theoretical model for how disturbed nephrogenesis contributes to progressive kidney disease.

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N. Koleganova and K. Benz researched data for the article. E. Ritz, K. Amann and K. Benz provided substantial contributions to discussion of the content and contributed equally to writing the article. K. Amann and K. Benz contributed equally to reviewing and editing the article.

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Correspondence to Eberhard Ritz.

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Ritz, E., Amann, K., Koleganova, N. et al. Prenatal programming—effects on blood pressure and renal function. Nat Rev Nephrol 7, 137–144 (2011). https://doi.org/10.1038/nrneph.2011.1

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