Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

mild disease

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treatment of underlying cause + supportive therapy

Patients with mild glomerulonephritis are typically asymptomatic with isolated hematuria, minimal to no proteinuria, and/or a normal estimated glomerular filtration rate (eGFR).[1] 

Treatment is patient-specific and directed toward the underlying cause (e.g., antivirals or antibiotics for infections, withdrawal of causative drugs).

Supportive therapy to manage complications is also important. This may include an ACE inhibitor (e.g., enalapril, lisinopril, ramipril) or an angiotensin-II receptor antagonist (e.g., candesartan, irbesartan, losartan) to reduce proteinuria and/or control hypertension. ACE inhibitor/angiotensin-II receptor antagonist combination therapy should be avoided due to risk of acute kidney injury and hyperkalemia, as well as a lack of safety and efficacy data.[1] Generally, patients are started at a low dose, and the dose is gradually adjusted based on clinical response (e.g., blood pressure, potassium level, eGFR) to a maximally tolerated dose.

Lifestyle measures such as increasing physical activity, adhering to a low-salt diet, and smoking cessation are also beneficial to improve morbidity.[1]

Frequent follow-up for proteinuria, renal function, lipid profile, and blood pressure is required to effectively slow or prevent chronic kidney disease.

Nephrotoxins such as nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided.

Primary options

enalapril: 2.5 to 5 mg orally once daily initially, increase gradually according to response, maximum 40 mg/day

OR

lisinopril: 5-10 mg orally once daily initially, increase gradually according to response, maximum 80 mg/day

OR

ramipril: 1.25 to 2.5 mg orally once daily initially, increase gradually according to response, maximum 20 mg/day

OR

candesartan cilexetil: 8-16 mg orally once daily initially, increase gradually according to response, maximum 32 mg/day

OR

irbesartan: 75-150 mg orally once daily initially, increase gradually according to response, maximum 300 mg/day

OR

losartan: 25-50 mg orally once daily initially, increase gradually according to response, maximum 100 mg/day given in 1-2 divided doses

moderate-severe disease

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treatment of underlying cause + supportive therapy

Patients with moderate-to-severe glomerulonephritis are usually symptomatic with hematuria, proteinuria, and/or reduced estimated glomerular filtration rate (eGFR).[1] 

Treatment is patient-specific and directed toward the underlying cause (e.g., antivirals or antibiotics for infections, withdrawal of causative drugs).

Supportive therapy to manage complications is also important. This may include an ACE inhibitor or angiotensin-II receptor antagonist to reduce proteinuria and/or control hypertension. ACE inhibitor/angiotensin-II receptor antagonist combination therapy should be avoided due to risk of acute kidney injury and hyperkalemia, as well as a lack of safety and efficacy data.[1] Generally, patients are started at a low dose, and the dose is gradually adjusted based on clinical response (e.g., blood pressure, potassium level, eGFR) to a maximally tolerated dose. There are many different drugs available in these classes and you should consult your local drug formulary. 

Lifestyle measures such as increasing physical activity, adhering to a low-salt diet, and smoking cessation are also beneficial to improve morbidity.[1]

Frequent follow-up for proteinuria, renal function, lipid profile, and blood pressure is required to effectively slow or prevent chronic kidney disease.

Nephrotoxins such as nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided.

Primary options

enalapril: 2.5 to 5 mg orally once daily initially, increase gradually according to response, maximum 40 mg/day

OR

lisinopril: 5-10 mg orally once daily initially, increase gradually according to response, maximum 80 mg/day

OR

ramipril: 1.25 to 2.5 mg orally once daily initially, increase gradually according to response, maximum 20 mg/day

OR

candesartan cilexetil: 8-16 mg orally once daily initially, increase gradually according to response, maximum 32 mg/day

OR

irbesartan: 75-150 mg orally once daily initially, increase gradually according to response, maximum 300 mg/day

OR

losartan: 25-50 mg orally once daily initially, increase gradually according to response, maximum 100 mg/day given in 1-2 divided doses

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diuretic ± statin ± anticoagulation

Treatment recommended for ALL patients in selected patient group

Patients with severe disease may present with nephrotic syndrome, which is characterized by proteinuria ≥3.5 g per 24 hours (or protein:creatinine ratio ≥3000 mg/g [≥300 mg/mmol]) in the presence of hypoalbuminemia, edema, and hyperlipidemia.[1] 

Management of nephrotic syndrome may include a loop diuretic (e.g., furosemide) for edema, statin therapy for hyperlipidemia, and anticoagulant prophylaxis if there is a high risk of thromboembolism.[1] Consult your local protocols for guidance on anticoagulation and statin therapy.

Primary options

furosemide: 40-120 mg/day orally given in 1-2 divided doses, adjust dose according to response, maximum 600 mg/day; 20-40 mg intravenously/intramuscularly as a single dose initially, increase by 20 mg/dose every 2 hours according to response, individually determined dose should be administered once or twice daily

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immunosuppressive therapy

Treatment recommended for SOME patients in selected patient group

Patients presenting with nephrotic syndrome are frequently treated with an immunosuppressant such as a corticosteroid (e.g., prednisone) and/or a corticosteroid-sparing agent (e.g., cyclophosphamide, rituximab, a calcineurin inhibitor, mycophenolate). Choice of immunosuppressive therapy depends on the cause of nephrotic syndrome and requires specialist consultation. Many patients will need maintenance immunosuppression depending on the underlying etiology. The precise details vary with each disease and maintenance treatment should be individualized.

Prophylaxis for complications of immunosuppressive therapy may be required.

For information on some of the most common causes of nephrotic syndrome (e.g., minimal change disease), see Evaluation of nephrotic syndrome (Differentials).

rapidly progressive

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immunosuppressive therapy + plasmapheresis

Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterized by a rapid decline in renal function and requires urgent treatment to avoid kidney failure.

Treatment for RPGN caused by antiglomerular basement membrane (anti-GBM; also known as Goodpasture disease) involves an aggressive strategy combining corticosteroids, cyclophosphamide, and plasmapheresis.[1]

See Goodpasture disease.

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immunosuppressive therapy

Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterized by a rapid decline in renal function and requires urgent treatment to avoid kidney failure.

RPGN may be immune complex-mediated: for example, in autoimmune disorders (e.g., systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis), in immunoglobulin A (IgA) nephropathy, or following infection.[1][41]

Patients presenting with immune complex-mediated RPGN are frequently treated with an immunosuppressant such as a corticosteroid (e.g., prednisone) and/or a corticosteroid-sparing agent (e.g., cyclophosphamide, rituximab, a calcineurin inhibitor, mycophenolate).[41] Choice of immunosuppressive therapy depends on the cause of RPGN and requires specialist consultation. Many patients will need maintenance immunosuppression depending on the underlying etiology. The precise details vary with each disease and maintenance treatment should be individualized.

Prophylaxis for complications of immunosuppressive therapy may be required.

See IgA nephropathy.

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immunosuppressive therapy

Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterized by a rapid decline in renal function and requires urgent treatment to avoid kidney failure.

Pauci-immune RPGN may be diagnosed in the absence of antiglomerular basement membrane (anti-GBM) antibodies or immune complex deposition. Causes include granulomatosis with polyangiitis and microscopic polyangiitis.[1][40]

Treatment of pauci-immune RPGN frequently involves an immunosuppressant such as a corticosteroid (e.g., prednisone) and cyclophosphamide or rituximab.[40] Choice of immunosuppressive therapy depends on the cause of RPGN and requires specialist consultation. Many patients will need maintenance immunosuppression depending on the underlying etiology. The precise details vary with each disease and maintenance treatment should be individualized.

See Granulomatosis with polyangiitis.

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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