Document Detail

Renal microvascular dysfunction, hypertension and CKD progression.
MedLine Citation:
PMID:  23132368     Owner:  NLM     Status:  MEDLINE    
PURPOSE OF REVIEW: Despite apparent blood pressure (BP) control and renin-angiotensin system (RAS) blockade, the chronic kidney disease (CKD) outcomes have been suboptimal. Accordingly, this review is addressed to renal microvascular and autoregulatory impairments that underlie the enhanced dynamic glomerular BP transmission in CKD progression.
RECENT FINDINGS: Clinical data suggest that failure to achieve adequate 24-h BP control is likely contributing to the suboptimal outcomes in CKD. Whereas evidence continues to accumulate regarding the importance of preglomerular autoregulatory impairment to the dynamic glomerular BP transmission, emerging data indicate that nitric oxide-mediated efferent vasodilation may play an important role in mitigating the consequences of glomerular hypertension. By contrast, the vasoconstrictor effects of angiotensin II are expected to potentially reduce glomerular barotrauma and possibly enhance ischemic injury. When adequate BP measurement methods are used, the evidence for BP-independent injury initiating mechanisms is considerably weaker and the renoprotection by RAS blockade largely parallels its antihypertensive effectiveness.
SUMMARY: Adequate 24-h BP control presently offers the most feasible intervention for reducing glomerular BP transmission and improving suboptimal outcomes in CKD. Investigations addressed to improving myogenic autoregulation and/or enhancing nitric oxide-mediated efferent dilation in addition to the more downstream mediators may provide additional future therapeutic targets.
Anil K Bidani; Aaron J Polichnowski; Rodger Loutzenhiser; Karen A Griffin
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Current opinion in nephrology and hypertension     Volume:  22     ISSN:  1473-6543     ISO Abbreviation:  Curr. Opin. Nephrol. Hypertens.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-04     Completed Date:  2013-06-03     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  9303753     Medline TA:  Curr Opin Nephrol Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  1-9     Citation Subset:  IM    
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MeSH Terms
Angiotensin II / metabolism
Blood Pressure
Disease Progression
Hypertension, Renal / complications,  drug therapy*,  physiopathology*
Kidney Glomerulus / blood supply*
Microvessels / physiopathology*
Nitric Oxide / metabolism
Renal Insufficiency, Chronic / etiology*,  metabolism
Grant Support
DK-40426/DK/NIDDK NIH HHS; DK-61653/DK/NIDDK NIH HHS; IK2 BX001285/BX/BLRD VA; R01 DK061653/DK/NIDDK NIH HHS; //Canadian Institutes of Health Research
Reg. No./Substance:
11128-99-7/Angiotensin II; 31C4KY9ESH/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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