Perspectives on the relationship of renal disease and coronavirus disease 2019

Coronavirus disease 2019 (COVID-19) is now a pandemic and its death toll is rocketing up. Patients with acute kidney injury (AKI) and chronic kidney disease (CKD) are at high risk of developing COVID-19 complications and COVID-19 infection can also lead to renal dysfunction. Considering the importance of kidney function in COVID-19 patients, the present review is aimed to dig into the available evidence about kidney and COVID-19. We summarize the mechanisms underlying the renal injury in COVID-19 patients, and treatment strategies in dialysis and kidney transplant patients. We conclude, it is imperative to highlight the early monitoring of patients with AKI and carefully control kidney function during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection

Antioxidative and anti-inflammatory impact of valsartan against renal ischemia-reperfusion injury; role of nitric oxide signaling pathway

Introduction: Renal ischemia reperfusion injury is one of the main causes of acute renal failure, which is associated with high mortality. Tissue damage caused by ischemia-reperfusion occurs due to the release of oxygen free radicals. Type I angiotensin receptor antagonists such as valsartan can be useful in the treatment of chronic kidney disease and hypertension. Objectives: We aimed to evaluate the protective effect of valsartan against renal ischemia reperfusion via antioxidant property and nitric oxide (NO) signaling pathway. Materials and Methods: Fifty male Wistar rats (220 +/- 10 g) were randomly divided into five groups as follows: Group 1; healthy rats without ischemia-reperfusion (control group). Group 2; rats with ischemia reperfusion (IR) (IR control group). Group 3; rats with IR which received 30 mg/kg valsartan orally. Group 4; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-NAME. Group 5; rats with IR which received 30 mg/kg valsartan together with 40 mg/kg L-arginine. To induce ischemia-reperfusion, rats were anesthetized with thiopental and underwent surgery. Then, we induced ischemia with blocking blood vessels for 45 minutes by clamping. Biochemical parameters including urea and creatinine were measured using commercial kits. Oxidative stress and inflammatory parameters were measured by ELISA method. Renal tissues were stained with hematoxylin and eosin. Finally, the Kolmogorov-Smirnov test was used to determine the normal distribution of data. Results: The findings of this study indicated that treatment with valsartan and valsartan plus L-arginine leads to significant decrease in the serum levels of creatinine, urea, and albumin/creatinine, malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in contrast to IR control group which has increased level of these parameters. On the other hand, treatment with valsartan and valsartan plus L-arginine lead to increase in the serum levels of glutathione peroxidase (GPX), in contrast to ischemia reperfusion control group. Conclusion: Our data revealed that valsartan as a type I angiotensin receptor antagonist could decrease oxidative stress and inflammation due to renal ischemia reperfusion injury. Hence, valsartan could propose as a therapeutic agent for kidney diseases such as renal ischemia-reperfusion injury regarded to these renoprotective effects. Keywords Author Keywords:Valsartan; Renal ischemia reperfusion; Antioxidant property; Kidney; Acute renal failure; Reactive oxygen species KeyWords Plus:KIDNEY-DISEASE; HYPERTENSIO

Antioxidants and cisplatin nephrotoxicity; an updated review on current knowledge

Cisplatin is a first-line antitumor drug which is applied in the therapeutic field of numerous kinds of cancers. The main dose-dependent adverse effect of cisplatin is nephrotoxicity in approximately one-third of patients, who received this drug during their treatment. Oxidative stress is one of the most significant mechanisms in cisplatin nephrotoxicity. Cisplatin-induced oxidative stress stimulates apoptosis, inflammation, mitochondrial damage within cells, and endoplasmic reticulum (ER) stress. The administration of an antioxidant in this context could be a suitable approach for preventing of cisplatin nephrotoxicity. Antioxidants are categorized into four classes: dietary antioxidants, free radical scavengers, thiol-containing compounds, and iron chelators

The impact of metformin in chronic kidney disease-mineral and bone disorder

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a disorder of mineral and bone metabolism due to chronic kidney disease (CKD). Bone disease and mortality are more common in patients with CKD. In addition of antidiabetic properties of metformin (MET), it possesses anti-inflammatory, anti-fibrotic properties and increases the markers of osteogenic effects. Therefore, it improves bone quality and decreases the risk of fractures in patients with type 2 diabetes. Metformin can also inhibit arterial calcification, maintain calcium-phosphorus balance, decrease cellular infiltration, fibrosis, and inflammation in kidney. Based on evidence, the prevalence of lactic acidosis due to metformin in patients with type 2 diabetes (T2D) and renal dysfunction is lower compared to other oral antidiabetic agents. Metformin decreases all-cause mortality in patients with diabetic nephropathy. The administration of metformin showed no difference in the prevalence of lactic acidosis in patients with T2D who had normal, mild, moderate, or severe renal dysfunction. Therefore, metformin can be used in patients with significant CKD to inhibit CKD-MBD due to its osteogenic effects

Protective effect of aliskiren against renal ischemia reperfusion via antioxidant property and nitric oxide signaling pathway

Introduction: Renal ischemia reperfusion (RIR) is created following different mechanisms such as oxidative stress and inflammation. Objectives: The roles of chemical drugs, including aliskiren, have been evaluated in various kidney diseases. Hence, we assessed the effect of aliskiren on renal ischemia reperfusion. Materials and Methods: Fifty male Wistar rats (220 +/- 10 g) were grouped randomly in five groups; 1. Healthy control group, 2. Ischemia of reperfusion (IR) control group, 3. Rats with IR which received 30 mg/kg aliskiren orally, 4. Rats with IR which received 30 mg/kg aliskiren together with 40 mg/kg L-NAME, 5. Rats with IR which received 30 mg/kg aliskiren together with 40 mg/kg L-arginine. To induce ischemia-reperfusion, rats were anesthetized treated with thiopental and went under surgery. Then, we revealed the left and right kidneys, and we induced ischemia with blocking blood vessels for 45 minutes by clamping. Biochemical parameters including urea and creatinine were measured using commercial kits with auto analyzer. Oxidative stress and inflammatory parameters were evaluated using ELISA method. Renal tissues were stained with hematoxylin and eosin. Finally, Kolmogorov-Smirnov test was applied to determine the normal distribution of data. Results: Our results showed that treatment with aliskiren and aliskiren plus L-arginine causes a significant decrease in the serum levels of creatinine, urea, albumin/creatinine and malondialdehyde (MDA), in contrast with IR control group which has increased level of these parameters. On the other hand, treatment with aliskiren and aliskiren plus L-arginine leads to increase in the serum levels of glutathione peroxidase (GPX) and superoxide dismutase (SOD) in contrast with IR control group. Conclusion: The protective effect of aliskiren has been proven in different kidney diseases such as RIR and diabetic nephropathy. Our results demonstrated that aliskiren could be proposed as a therapeutic agent against renal ischemia complication