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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
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Immunosuppressive agents for treating IgA nephropathy.

Patrizia Natale1,2, Suetonia C Palmer3, Marinella Ruospo1,2

  • 1University of Bari, Department of Emergency and Organ Transplantation, Bari, Italy.

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|March 13, 2020
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Summary
This summary is machine-generated.

Corticosteroid therapy likely prevents kidney function decline in IgA nephropathy patients with proteinuria. However, evidence for other immunosuppressants is limited, and steroid therapy

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Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • IgA nephropathy is the most prevalent glomerulonephritis worldwide.
  • It leads to end-stage kidney disease (ESKD) in a significant proportion of patients.
  • This review is an update of previous Cochrane reviews from 2003 and 2015.

Purpose of the Study:

  • To evaluate the efficacy and safety of immunosuppression strategies for IgA nephropathy.
  • To determine the benefits and harms of various immunosuppressive treatments.

Main Methods:

  • Systematic review and meta-analysis of randomized controlled trials (RCTs) and quasi-RCTs.
  • Included studies compared immunosuppressants with placebo, no treatment, or other agents.
  • Data extraction and risk of bias assessment were performed independently by two authors.

Main Results:

  • Corticosteroid therapy (2-4 months) probably prevents ESKD progression in patients with IgA nephropathy and proteinuria > 1 g/day (moderate certainty).
  • Steroids may improve remission rates, prevent serum creatinine doubling, and reduce proteinuria, but evidence quality is low.
  • Other immunosuppressants like cytotoxic agents (AZA, CPA), MMF, calcineurin inhibitors, mizoribine, and leflunomide showed uncertain effects on clinical outcomes due to limited or low-quality evidence.

Conclusions:

  • Corticosteroids likely preserve kidney function in IgA nephropathy patients with proteinuria.
  • Evidence for other immunosuppressive agents is sparse and of low quality, with no clear benefit shown for AZA, CPA, or MMF.
  • Further research is needed to clarify the adverse effects of steroid therapy and identify patient subgroups that may benefit from specific treatments.