gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Genetic nephron number deficit is associated with reduced renal IGF2/IGF2 receptor ratio during fetal development

Angeborenes Nephron-Defizit ist mit erniedrigter renaler IGF2/IGF2 Rezeptor Ratio in der Fetalentwicklung assoziiert

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker L. Rothermund - Berlin, D
  • O. Fialkowski - Berlin, D
  • F. Freese - Berlin, D
  • R. Ibscher - Berlin, D
  • M. Wehland - Berlin, D
  • M. Paul - Berlin, D
  • W. Zidek - Berlin, D
  • R. Kreutz - Berlin, D

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochV26

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Rothermund et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




The pathogenesis of primary hypertension remains enigmatic. Recent studies support the concept that a reduced number of nephrons, determined during ontogenesis, is an important determinant of primary hypertension and cardiovascular disease in adult life. Oligonephropathy has to be due to changes in renal development. This study investigated the expression of the insulin like growth factor (IGF)system during nephrogenesis in a rat strain with genetic oligonephropathy, hypertension and cardiovascular damage in adult life.

Methods and Results

We compared rats with inborn oligonephropathy (MWF) and Wistar control rats with normal nephron number at day 19 of fetal development (F19). Quantitative mRNA expression was determined by Real-Time PCR. Histomorphometric analysis of fetal kidneys revealed a reduction in glomerular number of 31% in MWF compared to Wistar (p<0.05). Renal IGF2 mRNA expression was unchanged in both strains, whereas IGF2 receptor expression was increased by 34% in MWF compared to Wistar (p<0.05). IGF2/IGF2 receptor ratio was lowered by 57% in MWF compared to Wistar in fetal kidneys (p<0.05). In contrast, no difference in F19 heptatic mRNA expression of IGF2, IGF2 receptor, or IGF2/IGF2 receptor ratio was observed between both strains.


These data clearly demonstrate a reduction of nephron number already present at day 19 of fetal MWF development, and an organ specific regulation of the fetal IGF system in the MWF rat model. Finally, the results point to a possible role of the renal IGF system in mediating fetal manifestation of nephron number deficit in genetic oligonephropathy.