Comprehensive Management Strategies for Chronic Glomerulonephritis: Evidence-Based Approaches to Preserve Kidney Function and Improve Quality of Life

Chronic glomerulonephritis (CGN) is a progressive, long-term kidney disorder characterized by persistent inflammation and scarring of the glomeruli—the tiny filtering units in the kidneys. Unlike acute kidney conditions, CGN develops gradually over months or years, often without obvious early symptoms. Effective management focuses not only on symptom relief but—more critically—on slowing disease progression, preserving renal function, reducing proteinuria, preventing cardiovascular complications, and enhancing overall patient well-being. Treatment must be highly individualized, grounded in the underlying cause (e.g., IgA nephropathy, membranous nephropathy, lupus nephritis), histopathological findings, clinical presentation, and risk stratification.

Core Pillars of Integrated Care

A multidimensional, patient-centered approach is essential. This includes pharmacologic interventions, lifestyle modifications, nutritional optimization, regular monitoring, and timely referral to nephrology specialists. The ultimate goal is to delay or prevent the onset of end-stage kidney disease (ESKD) and reduce mortality—particularly from cardiovascular events, which remain the leading cause of death in CGN patients.

Aggressive Blood Pressure Control: A Renal Protective Priority

Hypertension coexists in up to 70–80% of individuals with chronic glomerulonephritis—and uncontrolled high blood pressure significantly accelerates glomerular injury and tubulointerstitial fibrosis. Therefore, rigorous yet safe blood pressure management is non-negotiable. Target goals are proteinuria-driven:

For patients with urinary protein excretion < 1 g/day, the recommended target is <130/80 mmHg.
For those with proteinuria ≥1 g/day and no established cardiovascular disease, a stricter target of <125/75 mmHg is advised to maximize renoprotection.

Crucially, blood pressure reduction must be gradual and sustained—not abrupt—to avoid renal hypoperfusion or ischemic injury. If monotherapy fails to achieve targets, combination antihypertensive regimens are strongly recommended. First-line agents should include renin-angiotensin-aldosterone system (RAAS) inhibitors—such as ACE inhibitors (e.g., lisinopril) or ARBs (e.g., losartan)—which offer dual benefits: lowering systemic pressure and reducing intraglomerular hypertension and protein leakage. In select cases, newer agents like nonsteroidal MRAs (e.g., finerenone) may be added for additional antifibrotic and anti-inflammatory effects.

Nutrition & Lifestyle Optimization: Foundational Non-Pharmacologic Interventions

Dietary and behavioral strategies form the bedrock of conservative management:

Sodium restriction: Limit intake to <2 g/day (≈5 g salt). Excess sodium blunts RAAS inhibitor efficacy, promotes volume expansion, and worsens hypertension and proteinuria.
Protein moderation: Aim for 0.8 g/kg/day of high-biological-value protein—sufficient to maintain nutrition while minimizing glomerular hyperfiltration.
Weight management & physical activity: Maintain BMI within 18.5–24.9 kg/m²; engage in ≥150 minutes/week of moderate-intensity aerobic exercise (e.g., brisk walking, cycling) to improve insulin sensitivity, endothelial function, and BP control.
Smoking cessation & alcohol moderation: Smoking independently accelerates CKD progression; alcohol should be limited to ≤1 drink/day for women and ≤2 for men.

Targeted Pharmacotherapy Beyond Hypertension

Depending on etiology and severity, additional evidence-based therapies may include:

Immunosuppression for immune-mediated forms (e.g., corticosteroids ± cyclophosphamide or mycophenolate mofetil in lupus nephritis or vasculitis).
SGLT2 inhibitors (e.g., dapagliflozin, empagliflozin)—now recommended across CKD stages regardless of diabetes status—for their proven ability to reduce albuminuria, slow eGFR decline, and lower heart failure hospitalization risk.
Statins for lipid management in patients with elevated cardiovascular risk.
Phosphate binders or vitamin D analogs if mineral bone disorder emerges in advanced stages.

Regular follow-up—including serial measurements of serum creatinine, eGFR, urinary albumin-to-creatinine ratio (UACR), electrolytes, and hemoglobin—is vital to assess treatment response and adjust therapy proactively. Early involvement of dietitians, pharmacists, and renal educators further improves adherence and outcomes.

In summary, managing chronic glomerulonephritis successfully demands a proactive, holistic strategy rooted in current guidelines—from precision BP targets and RAAS blockade to SGLT2 inhibition and sustainable lifestyle change. With early diagnosis, consistent monitoring, and integrated care, many patients can enjoy prolonged kidney health and significantly improved longevity.