Comprehensive, Personalized Treatment Strategies for Chronic Glomerulonephritis

Chronic glomerulonephritis (CGN) is not a single disease—but rather a group of progressive kidney disorders with diverse underlying causes and pathological patterns. Effective management begins with precise diagnosis: renal biopsy remains the gold standard for identifying the specific histological subtype—whether it's focal segmental glomerulosclerosis (FSGS), membranous nephropathy, IgA nephropathy, lupus nephritis, or another variant. This critical step determines whether the disease is currently active (showing ongoing inflammation or cellular proliferation) or in a quiescent, non-inflammatory phase.

Tailored Conservative Management for Stable or Non-Active Disease

When biopsy results reveal minimal or no active inflammation—such as in chronic scarring or fibrotic stages—aggressive immunosuppression is typically unnecessary. Instead, the focus shifts to slowing disease progression and protecting remaining kidney function. Key pillars include:

1. Rigorous Blood Pressure Control

Hypertension accelerates kidney damage in CGN. Target blood pressure is generally < 130/80 mmHg, often achieved with ACE inhibitors (e.g., lisinopril) or ARBs (e.g., losartan)—which offer dual benefits: lowering systemic pressure and reducing intraglomerular hypertension and proteinuria.

2. Proteinuria Reduction & Renal Protection

Even modest levels of proteinuria (>0.5 g/day) signal increased risk of long-term decline. ACEi/ARB therapy is first-line; if proteinuria persists, clinicians may add SGLT2 inhibitors (e.g., dapagliflozin)—recently FDA-approved for chronic kidney disease regardless of diabetes status—due to their proven renoprotective and cardio-protective effects.

3. Lifestyle & Comorbidity Optimization

Dietary sodium restriction (< 2 g/day), smoking cessation, weight management, and tight control of dyslipidemia and glucose (if diabetic) are evidence-based, non-pharmacologic interventions that significantly improve outcomes and delay progression to end-stage renal disease (ESRD).

Immunomodulatory Therapy for Active or Proliferative Disease

When biopsy confirms active inflammation—such as endocapillary hypercellularity, crescent formation, or significant immune complex deposition—immunosuppressive therapy becomes essential to halt immune-mediated injury. Treatment is highly individualized based on histopathology, severity, rate of decline, and patient-specific factors (age, comorbidities, infection risk).

Corticosteroids: Dosing & Duration Matter

Oral corticosteroids (e.g., prednisone) are foundational—but dosing varies widely: low-dose regimens may suffice for mild IgA nephropathy, while high-dose pulse methylprednisolone followed by tapering is common in rapidly progressive glomerulonephritis. Duration must be carefully balanced—longer courses increase risks of osteoporosis, diabetes, and infections without always improving renal survival.

Combination Therapy for High-Risk Cases

In aggressive forms like ANCA-associated vasculitis or severe lupus nephritis, combining steroids with cytotoxic agents (e.g., cyclophosphamide) or newer biologics (e.g., rituximab, voclosporin) significantly improves remission rates and preserves kidney function. For patients intolerant to traditional agents, calcineurin inhibitors (e.g., tacrolimus) or mycophenolate mofetil (MMF) offer effective alternatives backed by robust clinical trial data.

Emerging Approaches & Long-Term Monitoring

Research is rapidly evolving—from complement-targeted therapies (e.g., eculizumab for C3 glomerulopathy) to B-cell depletion strategies and novel antifibrotic agents. Meanwhile, consistent monitoring—including serial eGFR tracking, urine albumin-to-creatinine ratio (UACR), and periodic imaging—is vital to assess treatment response and adjust strategy early. Shared decision-making between patient and nephrologist ensures goals align with quality-of-life priorities and personal values—making care not just effective, but truly patient-centered.