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Abstract: TH-PO078

The Impact of Iodinated Contrast Media on Renal Outcomes in Diabetes and CKD

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Fernandes, Sheila Marques, Universidade de São Paulo, São Paulo, SP, Brazil
  • Brandi, Beatriz De almeida, Universidade de São Paulo, São Paulo, SP, Brazil
  • Peres, Karina Batista, Universidade de São Paulo, São Paulo, SP, Brazil
  • da Fonseca, Cassiane Dezoti, Federal University of Sao Paulo, Sao Paulo, SP, Brazil
  • Santos, Luciana soares Costa, Universidade de São Paulo, São Paulo, SP, Brazil
  • Watanabe, Miriam M., Faculdades Metrpolitana Unidas, São Paulo, Brazil
  • Vattimo, Maria De Fatima, Universidade de São Paulo, São Paulo, SP, Brazil

Group or Team Name

  • Group of Studies on Acute Kidney Injury (GERA)
Background

Iodinated radiocontrast media induced nephropaty (CI-AKI) is a major clinical problem accounting for 12% of all hospital-acquired cases of acute kidney injury (AKI), especially in patients with Chronic Kidney Disease (CKD) and Diabetes Mellitus (DM).
Aim of this study was to estimate the influence of DM and CKD regarding the incidence of CI-AKI in rats. Renal function, global and renal hemodynamics were measured and the discriminating value of NGAL for assessing early renal injury was evaluated.

Methods

Wistar, adult, male rats were randomized into four groups: Sham (control); Citrate (citrate buffer, streptozotocin vehicle); CKD (5/6 nefrectomy); DM (streptozotocin, 65 mg/kg, iv); CKD+IC (CKD that received iodinated contrast-IC, 6ml/kg); DM+IC (DM animals that received IC, 4 weeks after DM, 6 ml/kg, ip). Renal function (inulin clearance), urinary neutrophil gelatinase (uNGAL), global and renal hemodynamics (systemic blood pressure, renal blood flow, renal vascular resistance) were evaluated.

Results

Renal hemodynamics showed an increase in renal vascular resistance in CKD and DM, while IC enhanced this damage. Also, CKD and DM rats presented lower inulin clearance and higher uNGAL levels. These paramethers were worsened when IC was associated.

Conclusion

Our results indicated that CKD and DM improves renal vulnerability to the toxicity of IC, once association between CKD or DM with CI predisposes to severe kidney injury by modulating renal hemodynamics in rats. NGAL showed to be a sensitive marker for CI-AKI when comorbidities are involved.

Renal hemodynamics, renal function
Groups (n)Blood pressure (mmHg)Renal blood flow (mL/min)Renal vascular resistence (mmHg/mL/min)Inulin Clearance (mL/min)Urinary neutrophil gelatinase (ng/mL)
Sham (5)87±69.5±1.69.4±2.40.66±0.1047.9±19.1
Citrate (5)93±69.2±1.311.2±2.10.96±0.1837.9±0.8
CKD (5)132±13 *8.7±2.316.1±4.8 *0.28±0.04 *76.7±31.3 *
DM (5)96±45.3±1.7 &23.9±8.3 &0.55±0.08 &53.8±17.8 &
CKD+IC122±6 *3.2±1.3 *#37.9±15.0 *#0.10±0.03 *#153.5±70.0 *#
DM+IC106±19 §3.3±1.2 &§38.4±9.3 &§0.17±0.02 &§99.8±18.7 &§

* p<0,05 versus Sham; # p<0,05 versus CKD; & p<0,05 versus Citrate; § p<0,05 versus DM

Funding

  • Government Support - Non-U.S.