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Kidney Week

Abstract: PO2616

Obesity Has Opposing Effects on Acute vs. Chronic Kidney Disease

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention


  • Rousselle, Thomas V., UTHSC, Memphis, Tennessee, United States
  • Eason, James D., UTHSC, Memphis, Tennessee, United States
  • Maluf, Daniel, UTHSC, Memphis, Tennessee, United States
  • Mas, Valeria R., UTHSC, Memphis, Tennessee, United States
  • Bajwa, Amandeep, UTHSC, Memphis, Tennessee, United States

With an accumulation of lipid droplets, mitochondria become incapable of upregulating the glucose-dependent response to ischemia and the cell becomes dependent upon glycolysis to satisfy metabolic need. This dysregulation has contributed to the exacerbation of ischemic injury in various tissues in diet-induced obese (DIO) mice. However, very little is known in how DIO can contribute to ischemic kidney disease. We hypothesized that obesity may dampen the response to acute kidney injury (AKI) and further exacerbate the development of dysfunction in chronic kidney disease.


Fat content and lean muscle mass of 20-wk old B6 lean and DIO mice were analyzed via EchoMRI (calculate fat %) and data used to randomize mice between either acute (AKI, 26 mins of bilateral ischemia with 24 hrs of reperfusion) or chronic (CKD, 26 mins of unilateral ischemia with 14 days of reperfusion) models of kidney injury. Kidney injury was assessed by plasma creatinine (PlCr; mg/dL), blood urea nitrogen (BUN; mg/dL), and histological analysis (H&E or MT).


Fat % significantly differed between lean and DIO mice (4.18±0.4 vs 17.49±1.2; p<0.001) along with blood glucose levels (384±27.8 vs 522±16.1; p<0.01). In AKI, DIO mice had worsened kidney function when compared to lean mice as shown by the significant increase in PlCr (1.43±0.23 vs 2.32±0.14; <0.05). However, the degree of injury was not reflected in BUN or acute tubular necrosis (ATN). Interestingly, there was no significant changes in either PlCr or BUN between DIO and lean mice at 14 days.


When compared to lean controls, mice fed HFD and then subjected to IRI expressed significant exacerbation of injury by a heightened expression of clinical chemistry markers. Though this dysregulation has been associated in other tissues with an accumulation of dysfunctional mitochondria secondary to the increased accrual of lipid-droplets, this does not seem to be the case in the kidney as no lipid-deposits were observed in the histological analysis. In addition, no significance existed between DIO and lean mice having undergone unilateral ischemia. With the increasing prevalence of obesity and obesity-related co-morbidities, more studies are warranted to explicitly unravel the effects of DIO in relation to acute and CKD.


  • NIDDK Support