Description
Glomerulonephritis remains one of the most complex kidney disorders, often presenting with subtle signs that challenge early diagnosis. This session will unravel the key clinical and laboratory clues that help identify the condition at its earliest stages. We will explore the latest advances in understanding its pathogenesis, diagnostic tools, and evolving treatment approaches. By bridging science with practice, the discussion aims to equip clinicians with practical strategies to improve patient outcomes.
Summary Listen
- Glomerulonephritis (GN) involves inflammation of the glomeruli, the kidney's filtering units. Early identification, investigation, and treatment are crucial to prevent serious complications. GN is a leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD). The speaker aimed to cover the classification, clinical presentations, investigations, and treatment approaches for GN, including recent advances.
- GN can be caused by immune-mediated injuries, infections, systemic diseases, and malignancies. IgA nephropathy is the most common GN worldwide, while post-infectious GN is more prevalent in developing countries. Understanding GN pathology has evolved from histopathological classification to molecular, genetic insights, and now precision medicine, focusing on personalized treatment.
- Glomeruli consist of various cells, including mesangial cells, endothelial cells, podocytes, and parietal epithelial cells. Each cell type contributes to glomerular function, and injury to these cells results in different GN types. The classification of GN has shifted from histology-based to etiology-based. A common classification system categorizes GN into immune complex-mediated, pauci-immune, anti-GBM, complement-mediated, and monoclonal immunoglobulin-associated GN.
- GN presents with distinct syndromes: nephritic (hematuria, hypertension, oliguria, edema), nephrotic (massive proteinuria, hypoalbuminemia, edema, hyperlipidemia), rapidly progressive GN (RPGN, rapid GFR decline), and chronic GN (slowly progressive kidney dysfunction). Nephrotic syndrome requires proteinuria > 3.5g/day, hypoalbuminemia, edema, and hyperlipidemia. RPGN involves a rapid decline in GFR and crescent formation, often requiring immediate treatment.
- Diagnosis involves history taking, physical examination, and laboratory investigations. Crucial lab tests include urine analysis (proteinuria, hematuria, RBC casts), metabolic panel (creatinine, urea, electrolytes), complete blood count, and lipid profile. Urinary protein estimation, preferably a 24-hour urine sample, is essential. Specialized investigations target specific diseases: complement levels, ANA, anti-dsDNA, ANCA, anti-GBM antibodies, and hepatitis serology.
- Renal biopsy remains the gold standard for diagnosing GN. Indications include unexplained kidney injury with glomerular findings, nephrotic syndrome in adults, persistent hematuria with proteinuria, RPGN, systemic diseases with renal involvement, and family history of hereditary nephritis. Biopsy techniques include percutaneous approach with ultrasound or CT guidance, and pathological examination includes light microscopy, immunofluorescence, and electron microscopy.
- Treatment principles encompass supportive care (ACE inhibitors/ARBs for proteinuria and BP control, diuretics for edema, statins for hyperlipidemia), and disease-specific therapies. Corticosteroids are used for their anti-inflammatory and immunosuppressive effects. Cytotoxic agents like cyclophosphamide, azathioprine, and mycophenolate are used in severe cases, with careful monitoring for side effects.
- Newer treatment options include targeted therapies. Budesonide is used in IgA nephropathy, while atrasentan is an endothelin receptor antagonist for nephroprotection in IgA nephropathy. Iptacopan, a complement inhibitor, can reduce proteinuria. Loopus nephritis can be managed with belimumab, a B cell-targeted therapy. Pexetacoplane, a C3 complement inhibitor, has shown promise in C3 glomerulopathy. Avacopan is a C5A receptor antagonist used in ANCA-associated vasculitis.
- Emerging biomarkers like Gd-IgA1 in IgA nephropathy and anti-PLA2R antibodies in membranous nephropathy are being studied. Urinary biomarkers (MCP1, KIM1, NGAL) also show potential. Artificial intelligence has applications in lesion detection and diagnosis but requires further refinement. Precision medicine aims to personalize treatment based on individual genetic characteristics and phenotypes.
- Special populations, such as the elderly, children, and pregnant women, require careful consideration of treatment options and potential complications. Management of complications includes addressing hypertension, hypercholesterolemia, thromboembolism, and infection risk. Prognosis depends on age, early treatment, and preserved kidney function at presentation. Future directions include newer target molecules, biomarkers, regenerative medicine, and gene therapy.
Sample Certificate
About the Speakers
Dr. Amitabh Kulkarni
Head of Department, Nephrology, NMC Speciality Hospital, Dubai
Financial Disclosure
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