This Article Full Text Full Text (PDF) All Versions of this Article: 46/2/e4    most recent 01.HYP.0000171477.63859.b2e4v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by McMullen, S. Articles by Herrera-Acosta, J. Search for Related Content PubMed PubMed Citation Articles by McMullen, S. Articles by Herrera-Acosta, J. Pubmed/NCBI databases Medline Plus Health Information High Blood Pressure Seniors' Health Related Collections Clinical Studies

(Hypertension. 2005;46:e4.)
© 2005 American Heart Association, Inc.

Hypertension Electronic Pages

Essential Hypertension: Defending the Contribution of a Congenital Nephron Deficit

Division of Nutritional Sciences, University of Nottingham, Sutton Bonington Campus, Loughborough, United Kingdom

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read the recent review by Johnson et al in the March 2005 edition of Hypertension¹ with great interest. The authors scrutinized the various hypotheses put forward to explain the mechanism responsible for the defect in sodium handling generally accepted to underlie the renal origins of hypertension. This was a timely and thorough review of the literature, but we write to defend one of the potential mechanisms we feel was undervalued: a congenital reduction in nephron number.

It has become apparent that the timing of partial renal ablation is critical in determining its long-term effects. As stated by Johnson et al, uninephrectomy in adult life (ie, once nephrogenesis is complete) does not necessarily lead to the development of hypertension. However, interruption of nephron formation during nephrogenesis, either surgically or pharmacologically in animal models or in the case of unilateral renal agenesis in humans, clearly does result in the onset of hypertension in later life.² While nephron number, per se, may not program hypertension, a maladaptation to the nephron deficit limited to the period of nephrogenesis may play a critical role. The absence of increased frequency of hypertension in renal transplant donors does not mitigate against a role for congenital nephron insufficiency in promoting hypertension but instead may highlight a critical window in determining risk.

The absence of hypertension in the 1900s in populations exposed to suboptimal maternal nutrition is easily reconciled with respect to the theory of predictive adaptive response.³ Adaptations made by the fetus in response . . . [Full Text of this Article]

Richard J. Johnson

Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville

Bernardo Rodriguez-Iturbe

Hospital Universitario and Universidad del Zulia, Maracaibo, Venezuela

Takahiko Nakagawa

Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville

Duk-Hee Kang

Division of Nephrology, Ewha University College of Medicine, Seoul, Korea

Dan I. Feig

Division of Pediatric Nephrology, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas

Jaime Herrera-Acosta

Department of Nephrology, Instituto Nacional de Cardiologia I, Mexico City, Mexico