Kidney is crucial to preserve salt and mineral homeostasis and excretion of toxic metabolites in body. It is more inclined to toxicity due to high blood flow and its ability to contemplate the tubular fluid. Kidneys may have several renal dysfunctions if not taken care properly. It has been reported that generation of reactive oxygen species, by oxidation of polyunsaturated fatty acids in renal membrane lipids, with help of NADPH oxidase, contributes to renal damage1.
Thioacetamide (TAA) is a toxic compound used to encourage hepato-toxicity of different types including; liver fibrosis, cirrhosis and neoplasm. The TAA has also been accounted for inducing a nephro-toxic model imitating proximal tubule injury2. It may be the reason for injury by free radical mediated lipid peroxidation and/or through its nephrotoxic metabolites. In addition, TAA metabolizes to acetate that is excreted through urine3.
Angiotensin II receptor blockers (ARBs), also known as angiotensin II receptor antagonists, are a group of pharmaceuticals. Their main uses are in the treatment of hypertension (high blood pressure), diabetic nephropathy (kidney damage due to diabetes) and congestive heart failure.
Candesartan and Losartan are the two Angiotensin II receptor blockers (ARBs) scientists studied. It was previously reported that long term high dose of candesartan significantly reduced inflammation in rats with hypertensive renal damage mainly through nuclear factor (NF)-κB suppression4. Moreover, Losartan has shown to protect against non-diabetic and non-hypertensive chronic kidney damage5.
Previous studies have demonstrated their effects over high and low renal damage but researchers in a new study investigated the role of 2 ARBs (losartan and candesartan) in low dose TAA-induced mild renal damage which may mimic early diabetic or early hypertensive kidney disease6.
Researchers induced the low grade renal dysfunction by in rats. Rats were treated once daily by gastric gavages as follows: Positive control (vehicle), two losartan and two candesartan groups with different concentrations and normal control group. At end of treatment, blood urea and keratinize were measured in addition to the histo-pathological examination of renal tissues.
Only the losartan revealed significant decrease in blood urea and creatinine compared to the positive control group. Thioacetamide caused a decrease in glomerular cellularity, widening of capsular space and dilatation of tubular lumina.
Conclusively authors said that:
“Losartan in high doses protected against the mild renal damage induced by low dose thioacetamide while candesartan did not offer any benefit. Limitations of the study are non-measurement of other inflammatory, oxidative and renal injury markers and non-inclusion of other members of ARBs. Further studies can be planned to generate a more scientific hypothesis.”
Written by: Rabeeia
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18 February, 2019