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research:risk_of_acute_kidney_injury_between_conventional_nsaids_and_selective_cox-2_inhibitors [2018/01/08 04:04] scyou created |
research:risk_of_acute_kidney_injury_between_conventional_nsaids_and_selective_cox-2_inhibitors [2018/01/08 04:12] scyou [Risk of acute kidney injury between conventional NSAIDs and selective COX-2 inhibitors] |
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- | ====== < Risk of acute kidney injury between conventional NSAIDs and selective COX-2 inhibitors >====== | + | ====== Risk of acute kidney injury between conventional NSAIDs and selective COX-2 inhibitors ====== |
<WRAP box justify round> | <WRAP box justify round> | ||
- | **Objective:** //<To compare the risk of acute kidney injury between conventional nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors.>// | + | **Objective:** To compare the risk of acute kidney injury between conventional nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors. |
- | **Rationale:** //<NSAIDs are most commonly used class of medication worldwide. NSAIDs are often associated with adverse drug events including renal toxicity. | + | **Rationale:** NSAIDs are most commonly used class of medication worldwide. NSAIDs are often associated with adverse drug events including renal toxicity. |
In states of reduced renal blood flow, adequate glomerular filtration rate may be dependent on afferent arteriole dilatation mediated by prostaglandins. Nonspecific Inhibition of COX-mediated renal prostaglandins synthesis would then remove this compensatory mechanism and increase the risk of kidney injury. The hypothesis of COX-1-sparing COX-2 inhibition underlying development of COX-2 inhibitors is that anti-inflammatory and analgesic efficacy can be achieved without deleterious effects on gastrointestinal, platelet, and possibly renal function. | In states of reduced renal blood flow, adequate glomerular filtration rate may be dependent on afferent arteriole dilatation mediated by prostaglandins. Nonspecific Inhibition of COX-mediated renal prostaglandins synthesis would then remove this compensatory mechanism and increase the risk of kidney injury. The hypothesis of COX-1-sparing COX-2 inhibition underlying development of COX-2 inhibitors is that anti-inflammatory and analgesic efficacy can be achieved without deleterious effects on gastrointestinal, platelet, and possibly renal function. | ||
Early studies suggested that selective COX-2 inhibitors caused fewer renal adverse effects including reduction in glomerular filtration rate, increased serum creatinine and hypertension. However, other studies have shown no significant differences in renal risk between selective COX-2- inhibitors and conventional NSAIDs. Therefore, the aim of this study is to compare the risk of acute kidney injury between selective COX-2 inhibitor and conventional NSAIDs in the large population. | Early studies suggested that selective COX-2 inhibitors caused fewer renal adverse effects including reduction in glomerular filtration rate, increased serum creatinine and hypertension. However, other studies have shown no significant differences in renal risk between selective COX-2- inhibitors and conventional NSAIDs. Therefore, the aim of this study is to compare the risk of acute kidney injury between selective COX-2 inhibitor and conventional NSAIDs in the large population. | ||
- | >// | ||
- | **Project Lead(s):** //<Ji In Park, MD, Kangwon National University Hospital, Korea | + | **Project Lead(s):** Ji In Park, MD, Kangwon National University Hospital, Korea; |
- | Seng Chan You, MD, Ajou University, Korea>// | + | Seng Chan You, MD, Ajou University, Korea |
- | **Coordinating Institution(s):** //<Ajou University>// | + | **Coordinating Institution(s):** Ajou University; Kangwon National University Hospital |
- | ** Additional Participants:** //< | + | ** Additional Participants:** |
- | Gacheon Gil hospital | + | |
- | Samsung Medical Center>// | + | |
- | **Full Protocol:** //<if available, a link to protocol. not necessary for initial planning>// | + | **Full Protocol:** |
**Initial Proposal Date:** | **Initial Proposal Date:** | ||
- | **Launch Date:** //<8th Jan 2018>// | + | **Launch Date:** 8th Jan 2018 |
- | **Study Closure Date: //<>//** | + | **Study Closure Date: ** |
- | **Results Submission:** //<applegna@gmail.com>// | + | **Results Submission:** applegna@gmail.com |
</WRAP> | </WRAP> | ||
===== Requirements ===== | ===== Requirements ===== | ||
- | **CDM:** //<V4 or V5 or both>// | + | **CDM:** V5 |
- | **Table Accessed:** //<e.g., person, drug_exposure, observations>// | + | **Table Accessed:** person, condition, drug, procedure, measurement |
- | **Database Dialects:** SQL Server, Postgres, Oracle | + | **Database Dialects:** Any that SqlRender provides |
- | **Software:** //<<e.g., R>// | + | **Software:** R |
===== Code ===== | ===== Code ===== | ||
- | [[https://github.com/OHDSI/StudyProtocolSandbox]] | + | [[]] |
===== Discussion ===== | ===== Discussion ===== | ||
- | //Post a thread letting everyone know about this new proposed study at [[http://forums.ohdsi.org/c/researchers]]// | + | //Post a thread letting everyone know about this new proposed study at [[]]// |
===== Datasets Run ===== | ===== Datasets Run ===== | ||
- | * <list your own datasets or leave blank> | + | * AUSOM |
+ | * NHIS-CDM | ||
~~NOTOC~~ | ~~NOTOC~~ |