Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Background: The incidence of cardiovascular disease (CVD) is increased in patients with diabetic kidney disease (DKD).
Summary: Aortic stiffness is a well-accepted biomarker for cardiovascular (CV) events in all stages of CKD. The worldwide prevalence of diabetes continues to grow, as does the prevalence of DKD. Insulin resistance, hyperglycaemia, hypertension, and the metabolic abnormalities of type-2 diabetes are all involved in the pathogenesis of CVD. The effect of these toxins on cardiac and vascular function is amplified by the worsening of renal function and the parallel rise of uraemic toxins.
Key Messages: In this narrative review, we analysed why arterial stiffening can be considered a vascular mediator between diabetes and cardiac dysfunction, and we discussed the strong CV and nephroprotective effects of sodium-glucose cotransporter type-2 inhibitors.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1159/000527274 | DOI Listing |
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