Sepsis-induced acute kidney injury: kidney protection effects by antioxidants

The study used 20 Wistar adult male rats divided into the following groups: control (laparotomy with no induction of abdominal sepsis), sepsis (experimental model of sepsis with cecal ligation and puncture), N-acetylcysteine + sepsis and diosmin-hesperidin + sepsis. The evaluation contemplated physiological parameters (temperature, glycemia, and average blood pressure), kidney function (creatinine clearance), oxidative stress (urinary peroxides) and kidney histology.

Results:

The animals submitted to cecal ligation and puncture (sepsis) presented lower body temperature, lower average blood pressure, reduced creatinine clearance and increased urinary hydrogen peroxide levels. Treatment with diosmin-hesperidin improved kidney function and led to a reduction in the excretion of oxidative metabolites.

Conclusion:

The present study highlighted the protective antioxidant action of diosmin-hesperidin in the experimental model of sepsis-induced acute kidney injury.

Descriptors:
Acute Kidney Injury; Sepsis; Diosmin; Hesperidin; Oxidative Stress

Groups (n)	Rectal temperature (°C)	AAP (mmHg)	Capillary glycemia (mg/dL)	Urinary volume (mL/min)
Control (5)	36.1 ± 0.34	85.8 ± 5.89	114.2 ± 50.1	0.067 ± 0.001
Sepsis (5)	34.2 ± 0.32^a a p < 0.05 versus control;	58.8 ± 5.60^a a p < 0.05 versus control;	232.0 ± 47.6^a a p < 0.05 versus control;	0.010 ± 0.006^a a p < 0.05 versus control;
NAC+sepsis (5)	35.8 ± 0.32	78.8 ± 5.62	194.4 ± 47.8	0.009 ± 0.003^a a p < 0.05 versus control;
DH+sepsis (5)	36.0 ± 0.10^b b p < 0.05 versus sepsis. AAP – average arterial pressure, NAC – N-acetylcysteine, DH –diosmin-hesperidin.	92.0 ± 0.60^b b p < 0.05 versus sepsis. AAP – average arterial pressure, NAC – N-acetylcysteine, DH –diosmin-hesperidin.	221.0 ± 51.0^a a p < 0.05 versus control;	0.008 ± 0.002^a a p < 0.05 versus control;

Groups (n)	Urinary creatinine (mg/dL)	Serum creatinine (mg/dL)	Creatinine clearance/100 g (mL/min)	Urinary peroxides (nmol/mg creatinine)
Control (5)	104.9 ± 8.3	0.49 ± 0.19	0.64 ± 0.05	2.1 ± 2.2
Sepsis (5)	41.3 ± 7.8^a a p < 0.001 versus control,	0.74 ± 0.18	0.20 ± 0.04^a a p < 0.001 versus control,	12.4 ± 2.1^a a p < 0.001 versus control,
NAC+sepsis (5)	38.1 ± 7.9^a a p < 0.001 versus control,	0.69 ± 0.18	0.18 ± 0.04^a a p < 0.001 versus control,	11.4 ± 2.1^a a p < 0.001 versus control,
DH+sepsis (5)	94.0 ± 8.0^b b p < 0.001 versus sepsis, cp < 0.001 versus NAC + sepsis; NAC – N-acetylcysteine. ^c c p < 0.001 versus NAC + sepsis; NAC – N-acetylcysteine.	0.80 ± 0.11^a a p < 0.001 versus control,	0.49 ± 0.05^a a p < 0.001 versus control, ^b b p < 0.001 versus sepsis, cp < 0.001 versus NAC + sepsis; NAC – N-acetylcysteine. ^c c p < 0.001 versus NAC + sepsis; NAC – N-acetylcysteine.	3.4 ± 1.1^b b p < 0.001 versus sepsis, cp < 0.001 versus NAC + sepsis; NAC – N-acetylcysteine. ^c c p < 0.001 versus NAC + sepsis; NAC – N-acetylcysteine.

Histopathological alterations	Groups (n)
Histopathological alterations	Control (5)	Sepsis (5)	NAC + sepsis (5)	DH + sepsis (5)
Loss of microvilli in proximal tubules	-	+	+	+
Tubular cell swelling	-	+++	+++	+++
Inflammation, necrosis and tubular regeneration	-	-	-	-
Ischemic glomeruli	-	++	+	+
Congestion	-	+++	++	++
Amorphous corticomedullary	-	+	+++	++

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[1] CORRESPONDING AUTHOR: Carolina Ferreira Vasco. E-mail: carolfvasco@gmail.com