Literature DB >> 17699327

Progression of renal disease: renoprotective specificity of renin-angiotensin system blockade.

Karen A Griffin1, Anil K Bidani.   

Abstract

Recent guidelines for management of patients with chronic kidney disease recommend both lower optimal BP targets and agents that block the renin-angiotensin system (RAS) for specific additional BP-independent renoprotection. Although there are other compelling rationales to use RAS blockade in patients with chronic kidney disease, including its antihypertensive effectiveness and ability to counteract the adverse effects of diuretics, a critical review of the available scientific evidence suggests that the specificity of renoprotection that is provided by RAS blockade has been greatly overemphasized. Little evidence of truly BP-independent renoprotection is observed in experimental animal models when ambient BP is assessed adequately by chronic continuous BP radiotelemetry. Although the clinical trial evidence is somewhat stronger, nevertheless, even when interpreted favorably, the absolute magnitude of the BP-independent component of the renoprotection that is observed with RAS blockade is much smaller than what is due to its antihypertensive effects.

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Year:  2006        PMID: 17699327     DOI: 10.2215/CJN.02231205

Source DB:  PubMed          Journal:  Clin J Am Soc Nephrol        ISSN: 1555-9041            Impact factor:   8.237


  39 in total

Review 1.  Immune and inflammatory role in renal disease.

Authors:  John D Imig; Michael J Ryan
Journal:  Compr Physiol       Date:  2013-04       Impact factor: 9.090

2.  Metabolically healthy obesity and risk of incident CKD.

Authors:  Yoshitaka Hashimoto; Muhei Tanaka; Hiroshi Okada; Takafumi Senmaru; Masahide Hamaguchi; Mai Asano; Masahiro Yamazaki; Yohei Oda; Goji Hasegawa; Hitoshi Toda; Naoto Nakamura; Michiaki Fukui
Journal:  Clin J Am Soc Nephrol       Date:  2015-01-29       Impact factor: 8.237

3.  Role of blood pressure and the renin-angiotensin system in development of diabetic nephropathy (DN) in eNOS-/- db/db mice.

Authors:  Ming-Zhi Zhang; Suwan Wang; Shilin Yang; Haichun Yang; Xiaofeng Fan; Takamune Takahashi; Raymond C Harris
Journal:  Am J Physiol Renal Physiol       Date:  2011-11-23

4.  Lymphocyte responses exacerbate angiotensin II-dependent hypertension.

Authors:  Steven D Crowley; Young-Soo Song; Eugene E Lin; Robert Griffiths; Hyung-Suk Kim; Phillip Ruiz
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2010-02-10       Impact factor: 3.619

Review 5.  Obesity and diabetic kidney disease.

Authors:  Christine Maric-Bilkan
Journal:  Med Clin North Am       Date:  2012-11-27       Impact factor: 5.456

6.  Modulation of angiotensin II-induced inflammatory cytokines by the Epac1-Rap1A-NHE3 pathway: implications in renal tubular pathobiology.

Authors:  Ping Xie; Darukeshwara Joladarashi; Pradeep Dudeja; Lin Sun; Yashpal S Kanwar
Journal:  Am J Physiol Renal Physiol       Date:  2014-02-19

Review 7.  In hypertension, the kidney breaks your heart.

Authors:  Steven D Crowley; Thomas M Coffman
Journal:  Curr Cardiol Rep       Date:  2008-11       Impact factor: 2.931

Review 8.  Potential risks of calcium channel blockers in chronic kidney disease.

Authors:  Karen A Griffin; Anil K Bidani
Journal:  Curr Cardiol Rep       Date:  2008-11       Impact factor: 2.931

Review 9.  [Hypertension and the kidney].

Authors:  Katharina Hohenstein; Bruno Watschinger
Journal:  Wien Med Wochenschr       Date:  2008

10.  Uncritical acceptance of combination treatment of angiotensin II receptor blocker and angiotensin-converting enzyme inhibitor in nondiabetic renal disease trial results.

Authors:  Karen A Griffin; Anil K Bidani
Journal:  Hypertension       Date:  2008-12-01       Impact factor: 10.190

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