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Nephron Number and Renal Risk in Hypertension and Diabetes

Marie-Luise Gro^*, Kerstin Amann and Eberhard Ritz

^* Pathology and Internal Medicine, Ruprecht-Karl University, Heidelberg; and Department Pathology, Friedrich-Alexander University, Erlangen, Germany

Address correspondence to: Prof. Eberhard Ritz, Department Internal Medicine, Bergheimer Strasse 56a, D-69115 Heidelberg, Germany. Phone: 0049-6221-601705; Fax: 0049-6221-603302; E-mail: Prof.E.Ritz{at}t-online.de

It has been proposed that "nephron underdosing," i.e., a low number of nephrons at the time of birth, is linked to essential hypertension and a greater propensity to develop progressive loss of renal function after renal injury. This hypothesis was confirmed recently by examining the number of glomeruli in patients with essential hypertension. The mechanisms through which a low number of nephrons causes hypertension have not been clarified, but it is likely that functional changes in postglomerular segments of the nephron, e.g., handling of sodium, play an important role. Neonatal uninephrectomy increases BP, renders BP salt sensitive, and renders the kidney more susceptible to damage. Apart from genetic factors, fetal/maternal malnutrition during pregnancy seems to play an important role in the pathogenesis of nephron underdosing. Furthermore, intrauterine programming during organogenesis, e.g., by hyperglycemia, seems to be important: In animal experiments, offspring of either hyperglycemic or diabetic mothers have fewer nephrons.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673