Résumé
Sepsis is one of the leading causes of acute kidney injury [AKI] and increases risk of death. Bused on the hemodynamic effects and anti-inflammatory properties of the hydrogen sulfide [H[2]S], this study aimed to examine its effects on renal damage using a rat model of lipopolysaccharide [LPS]-induced AKI where LPS promotes inflammation-mediated kidney damage. A total of forty adult male Wistar albino rats were included in the study. The rats were randomly divided into 4 groups: [I] control group was treated with saline. [2] H[2]S group received a single intravenous [i.v.] bolus of sodium hydrosulfide [NaHS] as H[2]S donor in ci dose of 0.2 mg/kg. [3] LPS group in which endoloxemic shock was induced through the intraperitoneal [i.p.] injection of 20 mg/kg LPS. [4] LPS H[2]S group received LPS with the same dose as the previous group, then 5 minutes later NaHS, in a single dose [0.2 mg/kg] was injected. Administration of NaHS as H[2]S donor in LPS + H[2]S group significantly abrogated kidney inflammation as evident by significant decrease of renal intercellular adhesion molecule- 1 [ICAM- 1], myeloperoxidase [MPO] and attenuated kidney cellular damage as observed by the increase of the Na -K- ATPase activity as compared with LPS group. These renoprotective effects were accompanied by improvement of hemodynamic with increase of the mean arterial blood pressure [MAP] via reduction of nitric oxide [NO] level. Kidney functions were also effectively enhanced where glomerular filtration rate [GFR], renal blood flow [RBF], filtration fraction [FF.], renal vascular resistance [RVR], urine flow rate and urinary sodium excretion [U[Na]V] were significantly increased while proteinuria, serum urea and serum creatnine were significantly decreased. Urinary kidney injury molecule-1 [KIM-1] which is a specific tubular biomarker was greatly attenuated. Consistent with these observations, H[2]S treatment significantly alleviated renal hitopatholgical changes of LPS-induced AKI. Taken together, our results indicated the enhanced renal inflamination during LPS-induced AKI and the improvement of renal hemodynamic and functions as well as suppression of both renal cellular damage and inflammation by H[2]S which may signify its renoprotective effects in septic AKI