What is the treatment for post-infectious glomerulonephritis?

Treatment of Post-Infectious Glomerulonephritis

The treatment of post-infectious glomerulonephritis centers on antibiotic therapy to reduce antigenic load combined with supportive management of the nephritic syndrome, with immunosuppression reserved only for severe crescentic disease. 1

Antibiotic Therapy

Administer penicillin (or erythromycin if penicillin-allergic) even when active infection is no longer present to decrease the streptococcal antigenic load. 1, 2 This recommendation applies to classic post-streptococcal glomerulonephritis occurring 1-3 weeks after pharyngitis or impetigo. 1, 2

• First-generation cephalosporins (e.g., cephalexin) are appropriate alternatives for non-anaphylactic penicillin allergies or when beta-lactamase producing organisms are suspected. 2
• Third-generation cephalosporins (e.g., ceftriaxone) should be used for severe infections or in areas with high prevalence of resistant organisms. 2
• During outbreaks, systemic antimicrobials help eliminate nephritogenic strains of Streptococcus pyogenes from the community. 2

Supportive Management of Nephritic Syndrome

The cornerstone of treatment involves managing the clinical manifestations of acute glomerulonephritis. 1, 3

Fluid and Blood Pressure Management

• Restrict dietary sodium to <2.0 g/day to control hypertension and fluid retention. 2
• Use diuretics as first-line agents for managing fluid overload and hypertension. 1, 2
• Target blood pressure <130/80 mmHg (or <125/75 mmHg if proteinuria >1 g/day). 1
• Monitor closely for diuretic-related complications including hyponatremia, hypokalemia, GFR reduction, and volume depletion. 2

ACE Inhibitors/ARBs

While the guidelines focus primarily on IgA nephropathy for ACE inhibitor recommendations 1, these agents provide additional benefit in post-infectious glomerulonephritis when proteinuria persists or hypertension requires additional control beyond diuretics. 2

Renal Replacement Therapy

Provide dialysis when necessary for severe acute kidney injury, life-threatening hyperkalemia, severe metabolic acidosis, or refractory fluid overload. 1, 2

Immunosuppressive Therapy

Corticosteroids should be considered ONLY for severe crescentic glomerulonephritis with rapidly progressive renal failure, and this recommendation is based solely on anecdotal evidence. 1 The evidence quality is weak, with one study showing no advantage of combined immunosuppressants over supportive therapy alone in crescentic disease. 4

Critical Caveat: IgA-Dominant Variant

Do NOT use corticosteroids for IgA-dominant post-infectious glomerulonephritis, which typically occurs with staphylococcal infections (including MRSA), particularly in elderly and diabetic patients. 1 This variant must be distinguished from idiopathic IgA nephropathy and Henoch-Schönlein purpura to avoid inappropriate immunosuppression. 1

Monitoring and Follow-Up

• Assess C3 complement levels at diagnosis and follow serially—C3 should normalize within 8-12 weeks in uncomplicated cases. 2
• If C3 remains low beyond 12 weeks, perform kidney biopsy to exclude complement C3 glomerulonephritis (C3GN). 2
• Monitor kidney function, blood pressure, proteinuria, and hematuria regularly throughout the disease course. 2
• Treat metabolic acidosis if serum bicarbonate <22 mmol/L. 2

Special Considerations for Non-Streptococcal Infections

For endocarditis-related glomerulonephritis (increasingly caused by staphylococcal species), antibiotic treatment must continue for 4-6 weeks, though hematuria, proteinuria, and azotemia may persist for months after infection eradication. 1

Prognosis Considerations

The majority of children and epidemic cases have excellent prognosis with supportive care alone. 3, 5, 4 However, sporadic adult cases, particularly those caused by non-streptococcal pathogens, carry significantly worse long-term outcomes with higher risk of progression to ESRD. 5, 6 This prognostic difference reinforces the importance of supportive care as the primary treatment modality, as aggressive immunosuppression has not demonstrated benefit even in higher-risk populations. 4