What is the initial treatment approach for acute glomerulonephritis?

Initial Treatment Approach for Acute Glomerulonephritis

The initial treatment of acute glomerulonephritis prioritizes supportive care targeting the immediate complications—hypertension, edema, and fluid overload—while the specific immunosuppressive approach depends entirely on the underlying etiology identified through kidney biopsy and serologic testing. 1

Immediate Supportive Management

Edema and Fluid Management

• Start loop diuretics as first-line therapy for edema, using twice-daily dosing rather than once daily 1
• Escalate the loop diuretic dose until achieving clinically significant diuresis or reaching the maximally effective dose 1
• Restrict dietary sodium to <2.0 g/day (<90 mmol/day) as essential adjunctive therapy 1
• If diuretic response is insufficient, add mechanistically different diuretics (thiazides, amiloride, or spironolactone) for synergistic effect 1
• Monitor closely for hyponatremia, hypokalemia, GFR reduction, and volume depletion—particularly in pediatric and elderly patients 1

Blood Pressure Control

• Target systolic blood pressure <120 mm Hg in adults using standardized office measurement 1
• In children, target 24-hour mean arterial pressure at the 50th percentile for age, sex, and height by ambulatory monitoring 1
• Use ACE inhibitors or ARBs at maximally tolerated doses as first-line agents when both hypertension and proteinuria are present 1
• Critical caveat: Do NOT start ACE inhibitors or ARBs in patients presenting with abrupt-onset nephrotic syndrome, as these can cause acute kidney injury, especially in minimal change disease 1
• Discontinue ACE inhibitors/ARBs if serum creatinine rises >30% or if refractory hyperkalemia develops 1

Etiology-Specific Treatment

Post-Infectious Glomerulonephritis (Most Common in Children)

• Treat with appropriate antibiotics even if active infection is not evident to decrease antigenic load—use penicillin or erythromycin if penicillin-allergic 1
• Continue antibiotics for 4-6 weeks in endocarditis-associated cases 1
• Supportive care alone is usually sufficient, as 95% of patients become afebrile within 48 hours and nearly 100% within 72 hours 2
• Reserve corticosteroids only for severe crescentic disease, based on anecdotal evidence 1
• Do NOT use corticosteroids for IgA-dominant post-infectious glomerulonephritis (typically staphylococcal, common in elderly/diabetics), as this must be distinguished from idiopathic IgA nephropathy 1

Rapidly Progressive or Crescentic Glomerulonephritis

• Intensity of immunosuppressive induction therapy is predicated on disease severity and GFR level 1
• Patients with normal eGFR and non-nephrotic-range proteinuria may be managed conservatively with supportive measures alone 1
• Do NOT treat patients with advanced CKD, severe tubulointerstitial fibrosis, small kidneys, or chronic inactive disease with immunosuppression 1
• Immunosuppressive regimens require kidney biopsy confirmation and vary by specific diagnosis (ANCA-vasculitis, anti-GBM disease, lupus nephritis, etc.) 3, 4

HCV-Associated Glomerulonephritis

• For CKD stages 1-2: use combined pegylated interferon and ribavirin 1
• For CKD stages 3-5 not on dialysis: use pegylated interferon monotherapy with dose adjustment 1

Monitoring and Escalation

• Expect clinical improvement within 48-72 hours; if not improving, obtain imaging (preferably CT scan) to evaluate for complications such as abscess or obstruction 2
• Obtain kidney biopsy if diagnostic uncertainty exists, disease progression is atypical, or rapidly progressive glomerulonephritis develops 1, 2
• Screen for latent infections before initiating immunosuppression protocols 1
• Monitor therapeutic drug levels where indicated and prescribe prophylaxis for specific immunosuppressive side effects 1

Common Pitfalls to Avoid

• Never delay supportive treatment while awaiting biopsy results—hypertension and fluid overload require immediate management 3
• Avoid starting ACE inhibitors/ARBs in acute nephrotic syndrome presentations, particularly suspected minimal change disease, due to AKI risk 1
• Do not use immunosuppression empirically without tissue diagnosis, as treatment varies dramatically by etiology and inappropriate therapy can cause harm 3, 4
• Recognize that up to 50% of diabetic patients may not present with typical flank tenderness, making clinical diagnosis more challenging 5
• Proteinuria reduction is a surrogate endpoint—complete clinical remission may not be achievable in all chronic forms 1