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ABSTRACT
In a clinical setting, kidney illnesses can be roughly classified as either chronic kidney disease (CKD) or acute kidney injury (AKI), and these two conditions are intimately related to one another. AKI is characterized by a sudden drop in glomerular filtration rates (GFRs), and it has a complicated etiology that includes trauma, ischemia, sepsis, and medication toxicity. The pathogenic mechanisms of kidney disease have been explained by means of a variety of animal models. The aim of this study is to induce renal injury using aspartame as a model. Twenty (20) female Sprague Dawley rats were obtained and separated into 4 groups consisting of 5 rats each. The rats were acclimatized for two weeks before commencement of administration. The rats were randomly grouped into Group 0 (control group) - received just feed and water, Group 1- received 50mg/kg of Aspartame per body weight, Group 2 - received 75 mg/kg of Aspartame per body weight and Group 3 - received 100mg/kg of Aspartame per body weight. Urine samples were collected at 2 weeks of administration and at 4 weeks of administration using a metabolic cage. Data was analyzed using GraphPad statistical software version 9.5 and comparisons between groups were performed using T TEST and data were presented mean + standard error of mean (SEM). Statistically significant levels were at (P≤0.05, *P≤0.005, *** P≤0.0001). There was no significant increase in urinary protein levels when compared with control after 2 weeks of administration. However, there was a significant increase in urinary protein concentration after 4 weeks of administration. There was a significant increase in serum creatinine concentrations in group that was administered 100mg/kg. There was no significant increase in urea concentrations in all the treated groups when compared with control.
