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Hemolytic anemia (HA) is a serious health condition resulting from reduced erythrocytes' average life span. Echinochrome (Ech) is a dark-red pigment found in shells and spines of sea urchins. Studying the potential therapeutic effect of Ech on phenylhydrazine (PHZ)-induced HA in rats. Eighteen rats were divided into three groups ( = 6): the control group, the phenylhydrazine-induced HA group and the Ech group, injected intraperitoneally with PHZ and supplemented with oral Ech daily for 6 days. Ech resulted in a considerable increase in RBCs, WBCs, and platelets counts, hemoglobin, reduced glutathione, catalase, and glutathione-S-transferase levels, and a significant decrease in aspartate & alanine aminotransferases, alkaline phosphatase, gamma-glutamyl transferase, bilirubin, creatinine, urea, urate, malondialdehyde & nitric oxide levels in anemic rats. Histopathological examination of liver and kidney tissue samples showed marked improvement. Ech ameliorated phenylhydrazine-induced HA with a hepatorenal protective effect owing to its anti-inflammatory and antioxidant properties.

Background: Cerebral venous sinus thrombosis (CVST) secondary to nephrotic syndrome (NS) is rarely reported. Additionally, treating steroid-sensitive nephrotic syndrome (SSNS) that changes to steroid resistance (SRNS) is difficult, with many relapses and side effects. Case presentation: A 32-month-old SSNS male child turned into SRNS and developed cerebral venous sinus thrombosis (CVST), a rare complication of NS. As a result of the administration of combined pulse methylprednisolone and IV Rituximab (RTX) therapy, the patient showed marked improvement, the results of urine analysis were remarkably improved, and the child started to respond to treatment. Conclusions: Successful treatment of a rare case of juvenile SSNS behaving as SRNS with the development of CVST could be established using combined steroid pulse therapy, Enoxaparin, and the B lymphocytes monoclonal antibodies RTX.

Diabetes mellitus is an oxidative stress-related disease characterized by hyperglycemia and a variety of complications, including nephropathy. Vitamin D has variable functions extending beyond the calcium metabolism to prevent oxidative tissue damage. We aimed to investigate whether vitamin D supplements could enhance Glibenclamide's effectiveness in treating diabetes and minimize the risk of associated pathology. Wistar rats were divided into normal control (n = 10) and diabetic (n = 30), where animals received two low doses of Streptozotocin 30 mg/kg/BW intraperitoneally to develop diabetes. The diabetic rats were then randomly divided into three equal groups: untreated, treated with Glibenclamide (0.6 mg/kg), and treated with Glibenclamide and Vitamin D3 (500 IU/kg). After eight weeks, the animals were sacrificed, and blood samples and kidney tissues were collected to evaluate biochemical, anti-oxidant, and pro-inflammatory cytokine levels and histological and immunohistochemical changes. Diabetic animals had significantly increased fasting blood glucose, lipid profile, blood urea, serum creatinine, and Malondialdehyde levels, whereas serum insulin, albumin, and the anti-oxidant enzymes superoxide dismutase and catalase were significantly decreased compared to normal control (p < 0.01). Furthermore, some renal histological changes were observed together with significantly increased immunoreactivity of anti-p53, anti-TNF-α, and anti-IL-6 antibodies when compared to the normal control. All abnormal parameters improved significantly with Glibenclamide therapy (p < 0.01), but combination therapy with vitamin D produced a much better result. In conclusion, vitamin D supplementation along with anti-diabetic medication can help prevent or reduce the severity of diabetic nephropathy due to its potent antioxidant, anti-inflammatory, and anti-apoptotic properties.

Urinary tract infections (UTIs), predominantly caused by , constitute a major global health issue due to the escalating antimicrobial resistance. This study was designed to assess the in vitro susceptibility of fosfomycin among clinical uropathogenic (UPEC) isolates and to detect plasmid-mediated and genes in those exhibiting fosfomycin resistance. A total of 158 non-duplicated UPEC strains were collected from urine samples of patients with UTIs. Antimicrobial susceptibility of these isolates was evaluated. Phenotypic detection of extended-spectrum β-lactamases (ESBL) and carbapenemase producers in UPEC was assessed. Identification of plasmid mediated and genes in those exhibiting fosfomycin resistance was carried out by PCR. A total of 72% of the isolates demonstrated multidrug resistance (MDR). Extensively drug-resistant (XDR) isolates represented 15%, while PDR isolates were rare (0.6%, 1/158). ESBLs were detected in 40% of the isolates, and 31% exhibited carbapenemase production. Fosfomycin resistance was detected in 9.5% of UPEC isolates, with the gene identified in 33% of these resistant strains, whereas gene was not identified in any isolate. Fosfomycin demonstrated considerable in vitro activity against carbapenemase-producing, ESBL-producing, and MDR isolates with susceptibility rates of 78%, 84%, and 97%, respectively. Fosfomycin resistance among UPEC isolates is emerging but still at a relatively low level of resistance. Continuous surveillance and antimicrobial stewardship are essential to preserve fosfomycin efficacy.