A cohort study of membranous nephropathy, primary or secondary

Arghiani, Maryam; Zamani, B; Nazemian, Fatemeh; Samadi, Sara; Afsharian, Malihe Saber; Habibzadeh, Mahmoud; Eslami, Saeid; Sabbagh, Mahin Ghorban

doi:10.1186/s12882-021-02338-6

Cited by 7 publications

(2 citation statements)

References 31 publications

(34 reference statements)

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“…Clinical manifestations of MN include proteinuria, edema, hypoalbuminemia and hyperlipidemia [ 53 ]. In diabetic rats, crocin reduces serum creatinine levels, BUN, proteinuria, triglycerides and total cholesterol with concomitant increase in urinary creatinine clearance, improving kidney functions [ 28 , 54–56 ].…”

Section: Discussionmentioning

confidence: 99%

Crocin improves the renal autophagy in rat experimental membranous nephropathy via regulating the SIRT1/Nrf2/HO-1 signaling pathway

Liu,

Cheng,

Wang

et al. 2023

Renal Failure

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Membranous nephropathy (MN) is a glomerular disease. Crocin is isolated from saffron and gardenia. Its antioxidant, anti-inflammatory, anti-hyperlipidemic, anti-atherosclerotic, anti-tumor, free-radical scavenging and neuroprotective activities have been well established. We investigated the biological functions of crocin and its related mechanisms in MN. We established an experimental passive Heymann nephritis (PHN) rat model induced by anti-Fx1A antiserum. The rats were divided into sham, sham + crocin, PHN, PHN + crocin, and PHN + enalapril groups. Blood samples and kidneys of rats were collected for estimation of biochemical parameters in serum and oxidative stress indicators in kidney tissues. Histopathological changes of renal tissues were evaluated by hematoxylin and eosin, periodic acid-Schiff (PAS) and Masson staining. The podocyte number was estimated by immunohistochemistry staining of Wilms tumor type 1 (WT1). The deposition of rat anti-rabbit IgG antibodies, complement C3 and C5b-9 was detected by immunofluorescence staining. Western blotting was performed to measure the levels of Sirtuin 1 (Sirt1), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and apoptosis-related proteins. The total cholesterol, triglycerides, creatinine, blood urea nitrogen, urine volume and urine albumin of PMN rats were significantly reduced by crocin. Additionally, crocin attenuated the renal histopathological changes. Moreover, the oxidative stress damage and podocyte loss and immune injury were relieved by crocin in PHN rats. Mechanistically, crocin administration activated the Sirt1/Nrf2/HO-1 pathways. The results provide a scientific basis that crocin could alleviate MN by inhibiting immune injury and podocyte damage through activating the Sirt1/Nrf2/HO-1 pathways.

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Section: Discussionmentioning

confidence: 99%

Crocin improves the renal autophagy in rat experimental membranous nephropathy via regulating the SIRT1/Nrf2/HO-1 signaling pathway

Liu,

Cheng,

Wang

et al. 2023

Renal Failure

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“…Secondary MN accounts for almost 25% of MN. It includes forms of disease caused by infections, malignancies, autoimmune diseases and drugs [81]. Recognition of secondary forms is critical because treatment of these forms depends on treatment of the underlying disease and, furthermore, immunosuppressive therapy can be dangerous in malignant or infectious secondary forms.…”

Section: Treatment Of Secondary Membranous Nephropathymentioning

confidence: 99%

How to Choose the Right Treatment for Membranous Nephropathy

Peritore,

Labbozzetta,

Maressa

et al. 2023

Medicina

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Membranous nephropathy is an autoimmune disease affecting the glomeruli and is one of the most common causes of nephrotic syndrome. In the absence of any therapy, 35% of patients develop end-stage renal disease. The discovery of autoantibodies such as phospholipase A2 receptor 1, antithrombospondin and neural epidermal growth factor-like 1 protein has greatly helped us to understand the pathogenesis and enable the diagnosis of this disease and to guide its treatment. Depending on the complications of nephrotic syndrome, patients with this disease receive supportive treatment with diuretics, ACE inhibitors or angiotensin-receptor blockers, lipid-lowering agents and anticoagulants. After assessing the risk of progression of end-stage renal disease, patients receive immunosuppressive therapy with various drugs such as cyclophosphamide, steroids, calcineurin inhibitors or rituximab. Since immunosuppressive drugs can cause life-threatening side effects and up to 30% of patients do not respond to therapy, new therapeutic approaches with drugs such as adrenocorticotropic hormone, belimumab, anti-plasma cell antibodies or complement-guided drugs are currently being tested. However, special attention needs to be paid to the choice of therapy in secondary forms or in specific clinical contexts such as membranous disease in children, pregnant women and patients undergoing kidney transplantation.

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