azilsartan

Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.

Yagasaki Motohiro M, Yamada Koshi K, Koshida Takeo T, Takagi Miyuki M et al.

IgA nephropathy (IgAN) has been reported in association with several biologic agents; however, renal events related to selective interleukin (IL)-23p19 inhibition remain poorly characterized. We report a case of biopsy-proven IgAN that became clinically apparent after initiation of risankizumab for psoriatic arthritis. A 37-year-old man with psoriatic arthritis achieved marked improvement in joint and skin manifestations after starting risankizumab in October 2022. Thereafter, kidney function gradually declined, with the estimated glomerular filtration rate decreasing from approximately 90-100 to 69.9 mL/min/1.73 m2 by August 2023, accompanied by proteinuria and microscopic hematuria. Despite supportive therapy with azilsartan and dapagliflozin, kidney function continued to worsen and proteinuria persisted, prompting a percutaneous kidney biopsy in February 2025. Light microscopy showed mesangial and focal endocapillary hypercellularity without crescents. Immunofluorescence demonstrated granular mesangial deposits of IgA and C3, and KM-55 staining was positive, indicating glomerular deposition of galactose-deficient IgA1; electron microscopy revealed para-mesangial electron-dense deposits. The biopsy was consistent with primary IgAN (Oxford classification M0E1S0T0C0). We administered steroid pulse therapy according to the Pozzi protocol (methylprednisolone 500 mg/day for 3 consecutive days), achieving remission of urinary abnormalities with modest improvement in kidney function, while risankizumab was continued. This case highlights the need for periodic urinalysis and kidney function monitoring during IL-23-targeted therapy and suggests that IgAN-directed treatment may be effective even when continuation of the biologic agent is clinically necessary.

Paraxanthine and azilsartan attenuate gentamicin-induced renal fibrosis via modulation of TGF-β1/Smad3/7 signaling and miRNA-21/miRNA-200b expression.

Rizk El-Adwy Nany Saad NS, El-Ashmawy Nahla E NE, Al-Ashmawy Ghada M GM, Khedr Naglaa F NF

Renal fibrosis is a key contributor to chronic kidney disease progression. The TGF-β1/Smad signaling pathway, particularly Smad2 and Smad3 mediate pro-fibrotic responses, while Smad7 exerts inhibitory effects. The study aimed to evaluate the therapeutic potential of paraxanthine (Para), an active caffeine metabolite, and azilsartan (Azil), an angiotensin II receptor blocker, in attenuating gentamicin (GM)-induced renal fibrosis through targeting Smad pathway and miRNA-21/200b. Seventy male albino mice were randomized into seven groups (n = 10): Control, GM, SIS3 + GM, Para + GM, Azil + GM, Para + SIS3 + GM, and Azil + SIS3 + GM. GM (40 mg/kg, I.P.) was administered daily for 7 days. Subsequently, Para (20.5 mg/kg) and Azil (5 mg/kg) were given orally, while SIS3 (2 mg/kg, I.P.) was administered for 7 days. Serum and urine renal function markers were measured. Renal histopathology, protein expression of TGF-β1, CTGF, Smad3, Smad2 and Smad7, and gene expression of miRNA-21 and miRNA-200b were evaluated. GM caused significant (p < 0.001) nephrotoxicity with elevated BUN, serum creatinine, urinary albumin/creatinine ratio, and KIM-1 and increased fibrosis and marked type I collagen deposition compared to normal control. However, treatments with Para & Azil resulted in significant (p < 0.05) improvement in renal functions. Pro-fibrotic markers TGF-β1, connective tissue growth factor (CTGF), Type I Collagen, Smad 2 and Smad3 were reduced, while Smad7 was increased in treated groups versus GM group. Additionally, miRNA-21 was downregulated and miRNA-200b was upregulated following treatments. Paraxanthine and azilsartan demonstrated significantl restoring of kidney function and suppressing fibrotic progression. Their actions were mediated through regulation of Smad3/7 signaling and modulation of miRNA-21 and miRNA-200b expression, highlighting these pathways as promising therapeutic targets for the treatment of renal fibrosis.

Retraction notice to "Nephroprotective effect of AT-MSCs against cisplatin-induced EMT is improved by azilsartan via attenuating oxidative stress and TGF-β/Smad signaling" [Biomedicine & Pharmacotherapy 158 (2023) 114097].

Fawzy Michael A MA, Beshay Olivia N ON, Bekhit Amany Abdlrehim AA, Abdel-Hafez Sara Mohamed Naguib SMN et al.

Cytokine Toxicity and Bacterial Dysbiosis in Chemotherapy- and/or Radiotherapy-Induced Oral Mucositis: Pathophysiological Mechanisms and Therapeutic Interventions.

Abdolmohammadi Pouria P, Aali Maral M, Lehmann Christian C

Chemotherapy- and/or radiotherapy-induced oral mucositis (CRIOM) is a common complication in patients with head and neck cancer, driven largely by excessive proinflammatory cytokine signalling and treatment-associated bacterial dysbiosis. This narrative review synthesizes current mechanistic evidence and summarizes emerging therapeutic strategies targeting these pathways. Research indicates that elevated levels of IL-1β, IL-6, TNF, iNOS, and nitric oxide amplify tissue injury and ulceration, while disruption of oral and gut microbial communities, characterized by loss of beneficial commensals and enrichment of pathogenic taxa, further exacerbates mucosal inflammation. Anti-inflammatory agents, including pentoxifylline, atorvastatin, trans-caryophyllene, azilsartan, recombinant human IL-11, and low-level laser therapy have been shown in preclinical models to reduce cytokine levels and promote mucosal healing. Similarly, microbiome-targeted approaches, such as oral microbiota transplantation and multi-strain probiotic formulations, have demonstrated potential in restoring microbial balance and attenuating CRIOM severity, with current evidence including both preclinical and clinical studies. Overall, current findings highlight cytokine toxicity and dysbiosis as synergistic drivers of CRIOM and support anti-inflammatory and microbiome-modulating strategies as promising adjunctive approaches; however, further well-designed clinical studies are required to validate their efficacy and guide clinical translation.