ArticlePhysiological genomics2012
Increased susceptibility to kidney injury by transfer of genomic segment from SHR onto Dahl S genetic background.
Article in Physiological genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Genome-wide association study of kidney function decline in individuals of European descent.Kidney international · 2015Pooled it
- Understanding hypertensive renal injury: a well-structured approach.Physiological genomics · 2026Article
- Systemic and proximal tubule specific knockout ofPhysiological genomics · 2026Article
- Spontaneous vascular dysfunction in Dahl salt-sensitive male rats raised without a high-salt diet.Physiological reports · 2024Article
- Article
- Sept8/SEPTIN8 involvement in cellular structure and kidney damage is identified by genetic mapping and a novel human tubule hypoxic model.Scientific reports · 2021Article
- 1,3-Butanediol attenuates hypertension and suppresses kidney injury in female rats.American journal of physiology. Renal physiology · 2020Article
- Loss ofHypertension (Dallas, Tex. : 1979) · 2020Article
- Will the real Dahl S rat please stand up?American journal of physiology. Renal physiology · 2019Article
- Sodium bicarbonate loading limits tubular cast formation independent of glomerular injury and proteinuria in Dahl salt-sensitive rats.Clinical science (London, England : 1979) · 2018Article
- Genetic susceptibility and loss of Nr4a1 enhances macrophage-mediated renal injury in CKD.Journal of the American Society of Nephrology : JASN · 2014Article
- Construction of two novel reciprocal conplastic rat strains and characterization of cardiac mitochondria.American journal of physiology. Heart and circulatory physiology · 2013Article
- Genetic variants in Arhgef11 are associated with kidney injury in the Dahl salt-sensitive rat.Hypertension (Dallas, Tex. : 1979) · 2012Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The Dahl salt-sensitive (S) rat is a widely studied model of salt-sensitive hypertension and develops proteinuria, glomerulosclerosis, and renal interstitial fibrosis. An earlier genetic analysis using a population derived from the S and spontaneously hypertensive rat (SHR) identified eight genomic regions linked to renal injury in the S rat and one protective locus on chromosome 11. The "protective" locus in the S rat was replaced with the SHR genomic segment conferring "susceptibility" to kidney injury. The progression of kidney injury in the S.SHR(11) congenic strain was characterized in the present study. Groups of S and S.SHR(11) rats were followed for 12 wk on either a low-salt (0.3% NaCl) or high-salt (2% NaCl) diet. By week 12 (low-salt), S.SHR(11) demonstrated a significant decline in kidney function compared with the S. Blood pressure was significantly elevated in both strains on high salt. Despite similar blood pressure, the S.SHR(11) exhibited a more significant decline in kidney function compared with the S. The decline in S.SHR(11) kidney function was associated with more severe kidney injury including tubular loss, immune cell infiltration, and tubulointerstitial fibrosis compared with the S. Most prominently, the S.SHR(11) exhibited a high degree of medullary fibrosis and a significant increase in renal vascular medial hypertrophy. In summary, genetic modification of the S rat generated a model of accelerated renal disease that may provide a better system to study progression to renal failure as well as lead to the identification of genetic variants involved in kidney injury.
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