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World J Nephrol. May 6, 2015; 4(2): 235-244
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.235
Primary and secondary hyperoxaluria: Understanding the enigma
Bhavna Bhasin, Hatice Melda Ürekli, Mohamed G Atta
Bhavna Bhasin, Division of Nephrology, Medical University of South Carolina, Charleston, SC 29425, United States
Hatice Melda Ürekli, Suleyman Demirel University Faculty of Medicine, 32260 Isparta, Turkey
Mohamed G Atta, Division of Nephrology, Johns Hopkins University, Baltimore, MD 21287, United States
Author contributions: Bhasin B generated the figures and tables and wrote the manuscript; Ürekli HM contributed to the writing of the manuscript; Atta MG provided critical appraisal of the manuscript for scientific ideas and clinical relevance for publication; Atta MG also edited the manuscript in preparation for submission and publication.
Conflict-of-interest: The authors declare that they have no competing interests.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Mohamed G Atta, MD, MPH, Division of Nephrology, Johns Hopkins University, 1830 E. Monument Street, Suite 416, Baltimore, MD 21287, United States. matta1@jhmi.edu
Telephone: +1-410-9555268 Fax: +1-410-9550485
Received: July 24, 2014
Peer-review started: July 24, 2014
First decision: August 14, 2014
Revised: August 29, 2014
Accepted: February 4, 2015
Article in press: February 9, 2015
Published online: May 6, 2015
Core Tip

Core tip: Hyperoxaluria is a disorder characterized by increased urinary oxalate excretion. Primary hyperoxaluria is an inherited defect of oxalate metabolism while secondary hyperoxaluria is seen in states of increased ingestion of oxalate, its precursors or altered gut flora. These disorders can lead to recurrent renal stones, nephrocalcinosis and eventually end stage renal disease. Despite these common features, the sub types of hyperoxaluria differ in their pathogenesis, severity of clinical presentation and treatment plan. Prompt clinical recognition and distinction between these disorders is essential not only for timely intervention but also impacts prognosis in patients with hyperoxaluria.