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10.1097/MNH.0b013e32835b36c1 http://scihub22266oqcxt.onion/10.1097/MNH.0b013e32835b36c1 23132368!3942995!23132368     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Opin+Nephrol+Hypertens 2013 ; 22 (1): 1-9 Nephropedia Template TP {{tp|p=23132368|t=2013. Renal microvascular dysfunction, hypertension and CKD progression |pdf=|usr=}}{{23132368}} gab.com Text Renal microvascular dysfunction, hypertension and CKD progression JO: Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=23132368 #FOAvip 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. Twit Text FOAVip Renal microvascular dysfunction, hypertension and CKD progression ????Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=23132368 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23132368 #FOAvip English Wikipedia <ref>{{Cite pmid|23132368}}</ref> Renal microvascular dysfunction, hypertension and CKD progression #MMPMID23132368 Bidani AK; Polichnowski AJ; Loutzenhiser R; Griffin KA Curr Opin Nephrol Hypertens 2013[Jan]; 22 (1): 1-9 PMID23132368show ga 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. |*Homeostasis[MESH] |Angiotensin II/metabolism[MESH] |Blood Pressure[MESH] |Disease Progression[MESH] |Humans[MESH] |Hypertension, Renal/complications/*drug therapy/*physiopathology[MESH] |Kidney Glomerulus/*blood supply[MESH] |Microvessels/*physiopathology[MESH] |Nitric Oxide/metabolism[MESH]Renal microvascular dysfunction, hypertension and CKD progression (epmc).pdf DeepDyve Pubget Overpricing