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Opinion Article - Archives of General Internal Medicine (2024) Volume 8, Issue 2

Glomerular Diseases: Insights into the Pathogenesis and Treatment Approaches in Nephrology

Fan Bhang *

Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan

*Corresponding Author:
Fan Bhang
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
E-mail: fcbhang23@ntuh.gov.tw

Received: 10-Apr-2024, Manuscript No. AAAGIM-24-136855; Editor assigned: 12-Apr-2024, PreQC No. AAAGIM-24-136855(PQ); Reviewed: 20-Apr-2024, QC No. AAAGIM-24-136855; Revised: 25-Apr-2024, Manuscript No. AAAGIM-24-136855(R); Published: 29-Apr-2024, DOI:10.35841/aaagim-8.2.226

Citation: : Bhang F. Glomerular diseases: Insights into the pathogenesis and treatment approaches in nephrology. Arch Gen Intern Med. 2024;8(2):226.

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Introduction

Glomerular diseases encompass a diverse group of conditions affecting the glomeruli, the tiny filtering units in the kidneys responsible for removing waste and excess fluid from the blood. These diseases can lead to proteinuria, hematuria, decreased Glomerular Filtration Rate (GFR), and ultimately, Chronic Kidney Disease (CKD) if left untreated. Understanding the pathogenesis and treatment approaches for glomerular diseases is essential for improving patient outcomes and preventing progression to end-stage renal disease [1].

Many glomerular diseases, such as IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis, involve the deposition of immune complexes in the glomeruli. These immune complexes activate complement pathways and trigger inflammatory responses, leading to glomerular damage. Podocytes are specialized cells that line the outer surface of the glomerular basement membrane and play a crucial role in maintaining the integrity of the filtration barrier. Podocyte injury, caused by various factors such as genetic mutations, immune-mediated mechanisms, and metabolic abnormalities, contributes to proteinuria and glomerulosclerosis [2, 3].

Chronic inflammation and fibrosis are common features of progressive glomerular diseases. Inflammatory cytokines and growth factors promote the recruitment of immune cells and the proliferation of mesangial cells and myofibroblasts, leading to glomerular scarring and impaired kidney function. Genetic predisposition plays a significant role in certain glomerular diseases, such as Alport syndrome, Focal Segmental Glomerulosclerosis (FSGS), and thin basement membrane disease. Mutations in genes encoding structural components of the glomerular basement membrane or podocyte proteins can disrupt glomerular function and lead to kidney dysfunction [4, 5].

The management of glomerular diseases aims to reduce proteinuria, preserve kidney function, and alleviate symptoms. Treatment strategies may include: In glomerular diseases with an immune-mediated pathogenesis, such as lupus nephritis and membranous nephropathy, immunosuppressive agents are often used to suppress inflammation and modulate the immune response. Commonly prescribed medications include corticosteroids, calcineurin inhibitors (e.g., cyclosporine, tacrolimus), and cytotoxic agents (e.g., cyclophosphamide, mycophenolate mofetil) [6, 7].

Angiotensin-Converting Enzyme Inhibitors (ACEIs) and Angiotensin Ii Receptor Blockers (ARBs) are first-line agents for reducing proteinuria and delaying the progression of glomerular diseases. These medications block the RAAS, leading to vasodilation of the efferent arteriole, decreased intraglomerular pressure, and attenuation of proteinuria [8].

Patients with glomerular diseases may benefit from supportive measures to manage complications and improve overall health. This may include dietary modifications (e.g., sodium restriction for hypertension and fluid retention), control of hypertension and dyslipidemia, and treatment of complications such as edema and hyperkalemia [9].

Plasma exchange, also known as plasmapheresis, is a therapeutic procedure used in certain glomerular diseases characterized by circulating immune complexes, such as Anti-Glomerular Basement Membrane (anti-GBM) disease and some forms of rapidly progressive glomerulonephritis. Plasma exchange removes pathogenic antibodies and inflammatory mediators from the circulation, leading to rapid reduction of disease activity. In advanced stages of glomerular diseases, when kidney function is severely impaired, renal replacement therapy may be necessary to sustain life. This includes hemodialysis, peritoneal dialysis, and kidney transplantation. Kidney transplantation offers the best long-term outcomes for eligible patients with ESRD [10].

Conclusion

Glomerular diseases represent a significant burden on public health, contributing to morbidity and mortality worldwide. The pathogenesis of these diseases is complex and involves a combination of immune-mediated, genetic, and environmental factors. Treatment approaches aim to attenuate inflammation, reduce proteinuria, and preserve kidney function through a combination of immunosuppressive therapy, RAAS inhibition, supportive care, and, in severe cases, renal replacement therapy.

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