Ischemic Preconditioning to Prevent Acute Kidney Injury
Overview
- Phase
- Not Applicable
- Intervention
- Not specified
- Conditions
- Acute Kidney Injury
- Sponsor
- University of Kansas Medical Center
- Enrollment
- 115
- Locations
- 1
- Primary Endpoint
- Acute Kidney Injury
- Status
- Completed
- Last Updated
- 8 years ago
Overview
Brief Summary
The purpose of this study is to learn about the impact of ischemic preconditioning in reducing contrast induced kidney damage in people with pre-existing kidney problems who are undergoing cardiac catheterization procedures.
Detailed Description
Ischemic preconditioning is thought to work by down-regulating pro-inflammatory gene expression and up-regulating anti-inflammatory gene expression in leukocytes. There is a local release of vasodilators, including adenosine and nitric oxide that are thought to have renal protective effects \[16\]. More is known regarding ischemic preconditioning in the heart, where it has been shown to decrease the adenine nucleotide pool, increase creatine phosphate and intracellular glucose, decrease ATP depletion, and lactate and H+ accumulation. This leads to sodium maintenance of the transmembrane sodium gradient that prevents intracellular edema. Ischemic preconditioning is thought to yield protection in the first minutes of reperfusion. Activation of the adenosine A1, bradykinin, and opioid receptors is thought to trigger protection. This is supported by the interference with protection if an adenosine receptor antagonist is administered. The role of reactive oxygen species as part of the protective mechanism has also been described via mitochondrial mKATP channels which lead to increased production of protective superoxide. Protein kinase C may also be involved in the protective mechanism of ischemic preconditioning, however the exact mechanism is unknown and controversial.
Investigators
Eligibility Criteria
Inclusion Criteria
- •Stage III-IV chronic kidney disease (with serum creatinine at or above 1.4 mg/dl and eGFR 15-55 ml/min/1.73m2 calculated by the Modification of Diet in Renal Disease formula)
- •Undergoing planned coronary angiography (including both cardiac and peripheral vascular) and/or intervention at KUMC
Exclusion Criteria
- •Patients with normal renal function (stage 0 to 2 chronic kidney disease and/or serum creatinine less than 1.4 mg/dl)
- •Inability or unwillingness to provide consent
- •Patients undergoing hemodialysis or peritoneal dialysis therapy
- •Patients with renal artery stenting
- •Hemodynamically unstable patients
- •Patients with acute or acute on chronic heart failure
- •Patients who are unable to undergo the study procedure due to any upper extremity problems such as prior amputation, prior radical mastectomy, etc
- •Patients who have not been hydrated prior to procedure using the standard protocols
Outcomes
Primary Outcomes
Acute Kidney Injury
Time Frame: 1 year
Defined as an absolute increase in serum creatinine greater than or equal to 0.5 mg/dl or a relative increase of greater than or equal to 25% compared with pre-procedural baseline as compared to 48-72 hours post-angiography.
Secondary Outcomes
- Progression of kidney disease(1 year)