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Abstract: TH-OR03

Associations of Blood Mitochondrial DNA Copy Number With Risk of AKI After Cardiac Surgery

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology‚ Risk Factors‚ and Prevention


  • Jotwani, Vasantha, University of California San Francisco, San Francisco, California, United States
  • Thiessen Philbrook, Heather, Johns Hopkins University, Baltimore, Maryland, United States
  • Katz, Ronit, University of Washington, Seattle, Washington, United States
  • Arking, Dan, Johns Hopkins University, Baltimore, Maryland, United States
  • Ix, Joachim H., University of California San Diego, La Jolla, California, United States
  • Tranah, Gregory J., California Pacific Medical Center, San Francisco, California, United States
  • Waikar, Sushrut S., Boston University, Boston, Massachusetts, United States
  • Parikh, Samir M., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Sarnak, Mark J., Tufts University, Medford, Massachusetts, United States
  • Shlipak, Michael, University of California San Francisco, San Francisco, California, United States
  • Parikh, Chirag R., Johns Hopkins University, Baltimore, Maryland, United States

Mitochondria are necessary for recovery from ischemia-reperfusion injury due to their critical roles in oxidative phosphorylation. Mitochondrial DNA copy number (mtDNA-CN) is an indirect marker of mitochondrial abundance that has been used to quantify the number of mitochondrial genomes per cell. Prior epidemiologic studies have associated higher blood mtDNA-CN with reduced risks of chronic kidney disease and mortality, but to our knowledge no study has examined risk of acute kidney injury (AKI).


Among 628 adults undergoing cardiac surgery, mtDNA-CN was quantified in pre-operative blood buffy coat specimens using multiplexed SYBR Green-based qPCR. AKI was defined as >50% increase in serum creatinine or need for dialysis following surgery. Subclinical AKI was defined by the highest quintiles of urine interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), monocyte chemoattractant protein-1 (MCP-1), and chitinase-3-like-protein-1 (YKL-40) on the first post-operative day among those without clinical AKI. Multivariable logistic regression models were used to evaluate associations of mtDNA-CN with clinical and subclinical AKI.


The mean age was 73±9 years and mean pre-operative eGFR was 72±18 ml/min/1.73m2. Each SD higher mtDNA-CN was associated with about a 38% lower risk of AKI (Table) in both unadjusted and multivariable adjusted models. There were no significant associations of mtDNA-CN with subclinical AKI, as defined by urinary levels of IL-18, KIM-1, MCP-1, or YKL-40.


Among adults undergoing cardiac surgery, higher pre-operative mtDNA-CN was associated with reduced risk of AKI but not with urinary biomarkers of tubular injury. MtDNA-CN may reflect kidney energetic reserve that promotes defense against acute ischemic stress.


  • NIDDK Support