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
An 8-week-old infant with hypertension, hyperkalemia, and hyperchloremic acidosis, presumably due to chloride shunt type of distal renal tubular acidosis, is described. The patient's renin-aldosterone axis was intact. The infant was also found to have an obstructed solitary kidney. Despite correction of the obstruction and improvement in the glomerular filtration rate accompanied by normal development, hyperkalemia and renal tubular acidosis persisted. The defect was still demonstrable 9 months following relief of the obstruction. We conclude that neonatal obstructive uropathy can result in renal tubular acidosis of the chloride shunt type. The reversibility of this defect is, as yet, unknown.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1159/000167258 | DOI Listing |
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