CALL FOR PAPERS Comparative Genomics Nephron deficit is not required for progressive proteinuria development in the Munich Wistar Frömter rat
نویسندگان
چکیده
Angela Schulz, Jonna Hänsch, Kristina Kuhn, Maria Schlesener, Peter Kossmehl, Jens R. Nyengaard, Norbert Wendt, Matthias Huber, and Reinhold Kreutz Department of Clinical Pharmacology and Toxicology, CharitéCentrum für Therapieforschung, Charité Universitätsmedizin Berlin, Berlin, Germany; and Stereology and Electron Microscopy Research Laboratory and MIND Center, University of Aarhus, Aarhus, Denmark
منابع مشابه
Nephron deficit is not required for progressive proteinuria development in the Munich Wistar Frömter rat.
The Munich Wistar Frömter (MWF) rat represents a genetic model with an inherited nephron deficit and exhibits mild hypertension and progressive albuminuria, which is more pronounced in males than females. Previously, we demonstrated in a consomic strain that replacement of a quantitative trait locus on chromosome 6 normalized the nephron deficit and suppressed albuminuria development, suggestin...
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Munich Wistar Frömter (MWF) rats develop spontaneous albuminuria that is linked to autosomal genetic loci and inherit a nephron deficit in both female and male animals, respectively. However, albuminuria and kidney damage are clearly more pronounced in males. Here we tested whether androgens and the androgen receptor influence albuminuria in male MWF. We first demonstrated in a pilot study that...
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The inherited nephron deficit and progressive albuminuria development observed in hypertensive Munich Wistar Frömter (MWF) rats are influenced by quantitative trait loci on rat chromosome (RNO) 6 and RNO8. Previous studies in young MWF rats suggested that the nephron deficit represents a cause for glomerular hypertrophy preceding onset of albuminuria at 8 weeks and demonstrated a simultaneous i...
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Micropuncture and morphologic studies were performed in six groups of male Munich-Wistar rats after removal of the right kidney and segmental infarction of two-thirds of the left kidney. Groups 1 and 4 received no specific therapy. Groups 2 and 5 were treated with the angiotensin I-converting enzyme inhibitor, enalapril, 50 mg/liter, in the drinking water. Groups 3 and 6 were treated with reser...
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