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10.1007/s00467-020-04843-6 http://scihub22266oqcxt.onion/10.1007/s00467-020-04843-6 33230698!7682775!33230698     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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33230698.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Pediatr+Nephrol 2021 ; 36 (10): 3007-3022 Nephropedia Template TP {{tp|p=33230698|t=2021. Fibroblast growth factor 23-Klotho and hypertension: experimental and clinical mechanisms |pdf=|usr=}}{{33230698}} gab.com Text Fibroblast growth factor 23-Klotho and hypertension: experimental and clinical mechanisms JO: Pediatr Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=33230698 #FOAvip Hypertension (HTN) and chronic kidney disease (CKD) are increasingly recognized in pediatric patients and represent risk factors for cardiovascular morbidity and mortality later in life. In CKD, enhanced tubular sodium reabsorption is a leading cause of HTN due to augmented extracellular fluid volume expansion. The renin-angiotensin-aldosterone system (RAAS) upregulates various tubular sodium cotransporters that are also targets of the hormone fibroblast growth factor 23 (FGF23) and its co-receptor Klotho. FGF23 inhibits the activation of 1,25-dihydroxyvitamin D that is a potent suppressor of renin biosynthesis. Here we review the complex interactions and disturbances of the FGF23-Klotho axis, vitamin D, and the RAAS relevant to blood pressure regulation and discuss the therapeutic strategies aimed at mitigating their pathophysiologic contributions to HTN. Twit Text FOAVip Fibroblast growth factor 23-Klotho and hypertension: experimental and clinical mechanisms ????Pediatr Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=33230698 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33230698 #FOAvip English Wikipedia <ref>{{Cite pmid|33230698}}</ref> Fibroblast growth factor 23-Klotho and hypertension: experimental and clinical mechanisms #MMPMID33230698 Freundlich M; Gamba G; Rodriguez-Iturbe B Pediatr Nephrol 2021[Oct]; 36 (10): 3007-3022 PMID33230698show ga Hypertension (HTN) and chronic kidney disease (CKD) are increasingly recognized in pediatric patients and represent risk factors for cardiovascular morbidity and mortality later in life. In CKD, enhanced tubular sodium reabsorption is a leading cause of HTN due to augmented extracellular fluid volume expansion. The renin-angiotensin-aldosterone system (RAAS) upregulates various tubular sodium cotransporters that are also targets of the hormone fibroblast growth factor 23 (FGF23) and its co-receptor Klotho. FGF23 inhibits the activation of 1,25-dihydroxyvitamin D that is a potent suppressor of renin biosynthesis. Here we review the complex interactions and disturbances of the FGF23-Klotho axis, vitamin D, and the RAAS relevant to blood pressure regulation and discuss the therapeutic strategies aimed at mitigating their pathophysiologic contributions to HTN. |*Hypertension[MESH] |*Renal Insufficiency, Chronic/metabolism[MESH] |Child[MESH] |Fibroblast Growth Factor-23[MESH] |Fibroblast Growth Factors/metabolism[MESH] |Glucuronidase[MESH] |Humans[MESH] |Klotho Proteins[MESH]Fibroblast growth factor 23-Klotho and hypertension: experimental and (epmc).pdf DeepDyve Pubget Overpricing