What are the treatment options for acute nephritis?

Acute glomerulonephritis is typically a self-limiting immune-mediated condition, most commonly triggered by a preceding streptococcal infection—such as pharyngitis or impetigo—leading to post-infectious glomerulonephritis. Management focuses on supportive care and close monitoring rather than specific immunosuppressive therapy, as the disease usually resolves spontaneously over weeks to months.

Initial treatment emphasizes control of hypertension and fluid overload, often requiring sodium and fluid restriction, diuretics (e.g., furosemide), and antihypertensive agents such as ACE inhibitors or calcium channel blockers if blood pressure remains elevated. Patients with significant proteinuria or nephrotic-range losses may benefit from ACE inhibitors not only for blood pressure control but also for their renoprotective effects, including reduction of intraglomerular pressure and proteinuria.

Renal function must be closely monitored via serial serum creatinine, estimated glomerular filtration rate (eGFR), electrolytes, and urinalysis. In cases of rapidly progressive glomerulonephritis—characterized by crescent formation on biopsy, rapidly declining eGFR, or pulmonary-renal syndrome—urgent evaluation for alternative etiologies (e.g., ANCA-associated vasculitis, anti-GBM disease, or lupus nephritis) is essential, and immunosuppression (e.g., corticosteroids, cyclophosphamide, or rituximab) may be indicated.

Antibiotics are prescribed only if active infection is present; routine antibiotic prophylaxis is not recommended. Patients should avoid NSAIDs due to risk of acute kidney injury and worsening hypertension. Long-term follow-up is critical—even after clinical recovery—to assess for persistent hematuria, proteinuria, or subtle declines in renal function that may signal chronic kidney disease.