Artikel
Congenital oligonephropathy deteriorates development of hypertension and albuminuria due to renal mass reduction
Kongenitale Oligonephronie erhöht den arteriellen Blutdruck und die Albuminurie nach Nierenteilresektion
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Autoren
Veröffentlicht: | 11. November 2004 |
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Gliederung
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Background
Deficit of congenital nephron number determines development of arterial hypertension in adult life. We investigated the role of congenital oligonephropathy for development of hypertension and renal function due to renal mass reduction.
Methods and Results
Munich Wistar Fömter (MWF) rats with a genetic reduction of nephron number were compared to Wistar rats with normal nephron number. At 8 weeks of age animals underwent sham-operation (sham), renal mass reduction (Nx), or Nx and treatment with the angiotensin-converting enzyme inhibitor ramipril (ACE) for 4 weeks.
Systolic blood pressure (SBP), and albuminuria (UAE), were elevated, and creatinine clearance (Ccrea) was decreased in both MWF-Nx and Wistar-Nx groups compared to their sham-operated controls (p<0.05, respectively). Dependent on nephron number, SBP, UAE, were increased, whereas Ccrea was not altered in MWF-Nx compared to Wistar-Nx (p<0.05, respectively). Treatment with ramipril in MWF-Nx-ACE and Wistar-Nx-ACE did lower SBP, UAE, and increased Ccrea compared to MWF-Nx and Wistar-Nx (p<0.05, respectively).
Conclusion
Reduced inborn nephron number deterioretes manifestation of hypertension and albuminuria due to renal mass reduction. ACE inhibition exerts antihypertensive and renoprotective effects after renal mass reduction in congenital oligonephropathy.