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
We studied 15 renal transplant recipients for evidence of tubular dysfunction. Eight patients were hypophosphatemic, and two had systemic acidosis with a urinary acidification defect. Mild aminoaciduria and bicarbonaturia were present in four and 14 patients, respectively. Elevated parathyroid hormone level was found in only one patient. Tubular reabsorption of phosphorus was depressed in all eight hypophosphatemic patients, while no such abnormalities were observed in 14 control subjects. Defective tubular reabsorption of phosphorus was the most striking abnormality. None of the parameters studied, including immunosuppressant therapy, parathyroid hormone levels, creatinine clearance, or acid-base balance, clearly account for the pathogenesis of this abnormality.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1097/00007611-197905000-00009 | DOI Listing |
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