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• W4240216101 abstract "Our paper [1.Sanchez-Lozada L.G. Tapia E. Johnson R.J. et al.Glomerular hemodynamic changes associated with arteriolar lesions and tubulointerstitial inflammation.Kidney Int. 2003; 64: S9-S14Abstract Full Text Full Text PDF Scopus (62) Google Scholar] focused primarily on the relationship of arteriolar disease and tubulointerstitial inflammation in renal progression. With renal mass reduction there is an increase in systemic blood pressure with glomerular hyperfiltration, glomerular hypertension, and proteinuria. Tubulointerstitial inflammation results and appears to mediate afferent arteriolar disease, which further impairs autoregulation, resulting in further increases in glomerular pressure and acceleration of glomerulosclerosis. Arteriolopathy in other conditions is also associated with glomerular hypertension, reduced plasma flow, ischemia, and fibrosis. Drs. Tylicki and Rukowski ask about the relationship of arteriolopathy and tubulointerstitial inflammation in essential hypertension. This is an area of special interest to us because we have proposed that these changes are responsible for the development of salt-sensitive hypertension [2.Johnson R.J. Herrera-Acosta J. Schreiner G. Rodriguez-Iturbe B. Subtle acquired renal injury as a mechanism of salt-sensitive hypertension.N Engl J Med. 2002; 346: 913-923Crossref PubMed Scopus (372) Google Scholar, 3.Kanellis J. Nakagawa T. Herrera-Acosta J. et al.A single pathway for the development of essential hypertension.Cardiol Rev. 2003; 11: 180-196Crossref PubMed Scopus (14) Google Scholar]. As we have proposed, renal injury is initiated by vasoconstriction and glomerular hypertension induced by sympathetic nervous system overactivity, endothelial dysfunction, hyperuricemia, or activation of the renin-angiotensin system; this leads to tubulointerstitial inflammation, intrarenal oxidant and angiotensin II generation, and afferent arteriolar disease [4.Franco M. Tapia E. Santamaria J. et al.Renal cortical vasoconstriction contributes to development of salt-sensitive hypertension after angiotensin II exposure.J Am Soc Nephrol. 2001; 12: 2263-2271PubMed Google Scholar]. The arteriolopathy results in impaired autoregulation and worsens glomerular hypertension, and also decreases renal plasma flow, causing ischemia, thus perpetuating tubulointerstitial inflammation [2.Johnson R.J. Herrera-Acosta J. Schreiner G. Rodriguez-Iturbe B. Subtle acquired renal injury as a mechanism of salt-sensitive hypertension.N Engl J Med. 2002; 346: 913-923Crossref PubMed Scopus (372) Google Scholar]. The observation by Drs. Tylicki and Rutkowski of urinary excretion of tubular markers in untreated hypertension [4.Franco M. Tapia E. Santamaria J. et al.Renal cortical vasoconstriction contributes to development of salt-sensitive hypertension after angiotensin II exposure.J Am Soc Nephrol. 2001; 12: 2263-2271PubMed Google Scholar] is consistent with our pathway. Thus, salt-sensitive hypertension may be considered a type of subtle acquired renal disease, which targeted therapies could possibly reverse and/or cure." @default.
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• W4240216101 date "2004-05-01" @default.
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• W4240216101 title "Reply from the Authors" @default.
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• W4240216101 doi "https://doi.org/10.1111/j.1523-1755.2004.607_6.x" @default.
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