Serum level of Vitamin D is associated with COVID-19 mortality rate in hospitalized patients.

BACKGROUND: Due to widespread of coronavirus disease 2019 (COVID-19) infection, identification of its risk factors and clinical characteristics are important. The aim of the present study was to assess Vitamin D levels in individuals with severe acute respiratory syndrome coronavirus-19 infection and to report on its potential as a predictive marker. MATERIALS AND METHODS: All patients, diagnosed with COVID-19 infection from February 16 to March 21, 2020, and referred to Firoozgar Hospital, Tehran, Iran, were enrolled in this study. Vitamin D analysis was undertaken on patient serum samples using a commercial kit (Pars Azmoon Co., Tehran, Iran). SPSS v. 22 was used for statistical analysis. RESULTS: Vitamin D serum concentration was analyzed in a total of 317 patients whose mean age ± standard deviation was 62.05 ± 15 years and with 62.5% being male. A significant association of Vitamin D level and death was observed. Higher levels of serum Vitamin D had protection against death (odds ratio = 0.955 [95% confidence interval = 0.923-0.988], P = 0.008). CONCLUSION: As a preliminary study in the Iranian population who suffered COVID-19 disease, we identified that Vitamin D deficiency was associated with a higher death rate and intensive care unit admission.

Antioxidative Effects of Tempol on Mitochondrial Dysfunction in Diabetic Nephropathy.

INTRODUCTION: Oxidative stress has a well-known role in diabetic nephropathy, and mitochondria are the major source of reactive oxygen species production. This study aimed to assess the effect of tempol, a superoxide dismutase mimetic agent, on mitochondrial antioxidant enzymes and cell viability in diabetic nephropathy. MATERIALS AND METHODS: Adult male Wistar rats were divided into 4 groups of 7 animals. Diabetes mellitus was induced by injection of streptozotocin in 2 groups, the rat in one of which were also treated with tempol for 4 weeks. Another group without diabetes mellitus received tempol, and the last group was the control. At the end of the treatment period, the kidney mitochondria were isolated and their antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, and catalase were assessed. Malondialdehyde, total antioxidant capacity, and kidney cells viability were studied, as well. RESULTS: The diabetic group was significantly different compared with the control group in malondialdehyde, catalase, and glutathione peroxidase activities. Superoxide dismutase and total antioxidative capacity did not show any significant differences among the four groups. Moreover, the diabetic group treated with tempol had significantly different glutathione peroxidase level and kidney cells viability, compared to the other diabetic group (P < .05) Conclusions. Diabetic nephropathy induces changes in mitochondrial antioxidative biomarkers and cells viability, some of which can be modified by tempol administration in rats.

Tempol effect on epithelial-mesenchymal transition induced by hyperglycemia.

BACKGROUND: One of common mechanisms in pathophysiology of chronic kidney diseases is epithelial-mesenchymal transition (EMT). On the other hand oxidative stress has been known to participate in kidney damage of diabetic nephropathy (DN). OBJECTIVES: We studied if tempol, a well-known antioxidant agent, can ameliorate EMT in DN induced in male rats. MATERIALS AND METHODS: Twenty-seven male rats were equally divided in to 4 groups. Group I (control or C), group II (diabetic or D), group III (T) rats which was given tempol (100 mg/kg/day) by gavages for 28 days and group IV (D&T) was diabetic rats that also received same dose of tempol. After treatment, their kidneys were studied by immunohistochemicalstaining. RESULTS: Pathological changes in the kidney were detected concurrently with increasing kidney weight and urinary albumin excretion. In addition, EMT indices, i.e. decline of E-cadherin and increase of α SMA staining were significantly emerged in the renal tubular cells of diabetic group and were partially modified in diabetic group which were simultaneously treated by tempol. CONCLUSIONS: Tempol can modify, but not significantly, EMT induced by DN.

Long-term efficacy of atorvastatin in allograft rejection following renal transplantation: A randomized clinical trial.

Statins are a class of drug that can efficiently reduce the level of low-density lipoprotein (LDL) as well as increase the LDL receptors. Several non-lipid-lowering effects of this type of drug have been described. It is reported that they have an influence in preventing graft rejection, especially of the acute type. In this study, patients with end-stage renal disease and candidates for kidney transplantation were divided into two groups. Group A (intervention group) received atorvastatin for two weeks prior to their transplant surgery while group B (control group) received placebo. The lipid profile was tested (triglycerides, cholesterol, LDL) in all patients two weeks before the transplantation. After transplantation, drug use was stopped. We also checked the LDL serum levels in patients with raised lipid levels (LDL >100) every two weeks. After this period, the serum lipid levels were checked monthly up to six months. Hyperlipidemia, when present, was controlled by fibrates. Concerning the rejection episodes, there was no significant difference between the two groups. In group A (13 men and nine women), three (14.3%) cases of rejection were observed whereas four (21.3%) cases of rejection were seen in group B (11 men and 10 women) (P = 0.5). Within group A, five (22.7%) cases of delayed graft function were found while four (19%) similar cases were observed in group B (P = 0.7). There was no statistically significant difference concerning delayed graft function between the two groups. Despite all the mechanisms attributed to the probable anti-rejection properties of statins, we found no significant correlation with the administration of these drugs before transplantation and the protection against graft rejection episodes.

Endoplasmic reticulum and its role in diabetic nephropathy.

Endoplasmic reticulum produces folds and exports proteins. There are studies showing the role of endoplasmic reticulum in pathogenesis of diabetic complications including diabetic nephropathy. This article reviews the pathophysiology associated with the role of endoplasmic reticulum in diabetic nephropathy and the therapeutic aspects of this finding.

Mitochondrion and its role in diabetic nephropathy.

Diabetic nephropathy is a major cause of end-stage renal disease throughout the world. Elevated oxidative stress in diabetic patients results from overproduction of reactive oxygen species and decreased efficiency of antioxidant defenses. Moreover, diabetes-associated metabolic disorders impair activities of enzymes of the mitochondrial respiratory chain complex. Therefore, oxidative stress is closely related to mitochondrial dysfunction. This paper reviews studies of mitochondrial dysfunction in diabetic nephropathy.

NF-E2-related factor 2 and its role in diabetic nephropathy.

Diabetic nephropathy is the leading cause of chronic kidney disease and end-stage renal disease. Oxidative stress has been recognized as a major contributor to its pathogenesis. Defensive mechanisms have also widely been studied. One of them, the NF-E2-Related Factor 2, is reviewed in this article.

The new technique of using the epigastric arteries in renal transplantation with multiple renal arteries.

The most common anatomic variant seen in the donor kidneys for renal transplantation is multiple renal arteries (MRA), which can cause an increased risk of complications. We describe the long-term outcomes of 16 years of experience in 76 kidney transplantations with MRAs. In a new reconstruction technique, we remove arterial clamps after anastomosing the donor to the recipient's main renal vessels, which cause backflow from accessory arteries to prevent thrombosis. By this technique, we reduce the ischemic times as well as the operating times. Both in live or cadaver donor kidneys, lower polar arteries were anastomosed to the inferior epigastric artery and upper polar arteries were anastomosed to the superior epigastric arteries. Injection of Papaverine and ablation of sympathic nerves of these arteries dilate and prevent them from post-operative spasm. Follow-up DTPA renal scan in all patients showed good perfusion and function of the transplanted kidney, except two cases of polar arterial thrombosis. Mean creatinine levels during at least two years of follow-up remained acceptable. Patient and graft survival were excellent. No cases of ATN, hypertension, rejection and urologic complications were found. In conclusion, this technique can be safely and successfully utilized for renal transplantation with kidneys having MRAs, and may be associated with a lower complication rate and better graft function compared with the existing techniques.

Non-Hodgkin's lymphoma in autosomal dominant polycystic kidney disease, 12 years after renal transplantation.

Autosomal dominant polycystic kidney disease (ADPKD) is a systematic disease which accounts for 10-15% of patients receiving dialysis or renal transplantation. It has a statistically significant association with malignancy in renal transplant recipients. We report a 47-year-old ADPKD female who developed a large renal tumor in the right kidney 12 years after kidney transplantation. During the follow-up, her ultrasound and laboratory tests were within normal limits. Bilateral nephrectomy of the native kidneys was performed, and followed by radiotherapy on the right side because pathology of the tumor suggested non-Hodgkin's lymphoma (NHL).