RGD Reference Report - Genetic linkage of albuminuria and renal injury in Dahl salt-sensitive rats on a high-salt diet: Comparison with spontaneously hypertensive rats. - Rat Genome Database

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Genetic linkage of albuminuria and renal injury in Dahl salt-sensitive rats on a high-salt diet: Comparison with spontaneously hypertensive rats.

Authors: Siegel, AK  Kossmehl, P  Planert, M  Schulz, A  Wehland, M  Stoll, M  Bruijn, JA  De Heer, E  Kreutz, R 
Citation: Siegel AK, etal., Physiol Genomics 2004 Jul 8;18(2):218-25. Epub 2004 May 25.
RGD ID: 1300043
Pubmed: (View Article at PubMed) PMID:15161966
DOI: Full-text: DOI:10.1152/physiolgenomics.00068.2004

Our aim was to study the effects of high-salt diet on the genetics of albuminuria and renal injury in the Dahl salt-sensitive (SS) rat. We compared SS with salt-resistant spontaneously hypertensive rats (SHR) and with genetically related salt-sensitive stroke-prone SHR (SHRSP). Moreover, we performed genome-wide linkage analysis to identify quantitative trait loci (QTL) contributing to salt-induced renal injury in an F2-population derived from SS and SHR (n=230). In response to high-salt diet SS and SHRSP developed a striking increase in systolic blood pressure, urinary albumin excretion (UAE), and renal damage indices compared to SHR. Both SHRSP and SS developed severe glomerulosclerosis, while microangiopathy, tubulointerstitial fibrosis and inflammation were more pronounced in SHRSP. We detected two QTL with significant linkage to UAE on rat chromosomes (RNO) 6 and 19. Comparison with the recently identified salt-independent UAE QTL in young animals revealed that the UAE QTL on RNO6 is unique to high-salt conditions, while RNO19 plays a significant role during both low- and high-salt conditions. Some F2-animals demonstrated severe microangiopathy and tubulointerstitial injury, that exceeded the degree observed in the parental SS strain. Three loci demonstrated suggestive linkage to these phenotypes on RNO3, RNO5, and RNO20, while no linkage to glomerular damage was found. Further analyses at these loci indicated, that the severity of renal injury was attributable to the SHR-allele. Our data suggest, that the SHR genetic background confers greater susceptibility for the development of microangiopathy and tubulointerstitial injury in salt-sensitive hypertension than the SS background.

Annotation

Disease Annotations    
Albuminuria  (IAGP)
proteinuria  (IAGP)

Phenotype Annotations    

Mammalian Phenotype
Objects Annotated

QTLs
Uae28  (Urinary albumin excretion QTL 28)
Uae29  (Urinary albumin excretion QTL 29)

Objects referenced in this article
Strain SHR/FubRkb null Rattus norvegicus
Strain SS/JrRkb null Rattus norvegicus

Additional Information