Glomerulonephritis
- Overview
- Theory
- Diagnosis
- Management
- Follow up
- Resources
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
mild disease
treatment of underlying cause + supportive therapy
Patients with mild glomerulonephritis are typically asymptomatic with isolated haematuria, minimal to no proteinuria, and/or a normal estimated glomerular filtration rate (eGFR).[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com
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 hyperkalaemia, as well as a lack of safety and efficacy data.[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com 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]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com
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 non-steroidal 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: 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
treatment of underlying cause + supportive therapy
Patients with moderate-to-severe glomerulonephritis are usually symptomatic with haematuria, proteinuria, and/or reduced estimated glomerular filtration rate (eGFR).[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com
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 hyperkalaemia, as well as a lack of safety and efficacy data.[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com 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]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com
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 non-steroidal 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: 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
diuretic ± statin ± anticoagulation
Treatment recommended for ALL patients in selected patient group
Patients with severe disease may present with nephrotic syndrome, which is characterised by proteinuria ≥3.5 g per 24 hours (or protein:creatinine ratio ≥300 mg/mmol [≥3000 mg/g]) in the presence of hypoalbuminaemia, oedema, and hyperlipidaemia.[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com
Management of nephrotic syndrome may include a loop diuretic (e.g., furosemide) for oedema, statin therapy for hyperlipidaemia, and anticoagulant prophylaxis if there is a high risk of thromboembolism.[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com 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
immunosuppressive therapy
Additional 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., prednisolone) 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 aetiology. The precise details vary with each disease and maintenance treatment should be individualised.
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 Assessment of nephrotic syndrome (Differentials).
rapidly progressive
immunosuppressive therapy + plasmapheresis
Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterised by a rapid decline in renal function and requires urgent treatment to avoid kidney failure.
Treatment for RPGN caused by anti-glomerular basement membrane (anti-GBM; also known as Goodpasture's disease) involves an aggressive strategy combining corticosteroids, cyclophosphamide, and plasmapheresis.[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com
immunosuppressive therapy
Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterised 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]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com [41]Kidney Disease: Improving Global Outcomes (KDIGO) Lupus Nephritis Work Group. KDIGO 2024 clinical practice guideline for the management of lupus nephritis. Kidney Int. 2024 Jan;105(1s):S1-69. https://www.kidney-international.org/article/S0085-2538(23)00627-0/fulltext http://www.ncbi.nlm.nih.gov/pubmed/38182286?tool=bestpractice.com
Patients presenting with immune complex-mediated RPGN are frequently treated with an immunosuppressant such as a corticosteroid (e.g., prednisolone) and/or a corticosteroid-sparing agent (e.g., cyclophosphamide, rituximab, a calcineurin inhibitor, mycophenolate).[41]Kidney Disease: Improving Global Outcomes (KDIGO) Lupus Nephritis Work Group. KDIGO 2024 clinical practice guideline for the management of lupus nephritis. Kidney Int. 2024 Jan;105(1s):S1-69. https://www.kidney-international.org/article/S0085-2538(23)00627-0/fulltext http://www.ncbi.nlm.nih.gov/pubmed/38182286?tool=bestpractice.com Choice of immunosuppressive therapy depends on the cause of RPGN and requires specialist consultation. Many patients will need maintenance immunosuppression depending on the underlying aetiology. The precise details vary with each disease and maintenance treatment should be individualised.
Prophylaxis for complications of immunosuppressive therapy may be required.
See IgA nephropathy.
immunosuppressive therapy
Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome characterised 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 anti-glomerular basement membrane (anti-GBM) antibodies or immune complex deposition. Causes include granulomatosis with polyangiitis and microscopic polyangiitis.[1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021 Oct;100(4s):S1-276. https://www.kidney-international.org/article/S0085-2538(21)00562-7/fulltext http://www.ncbi.nlm.nih.gov/pubmed/34556256?tool=bestpractice.com [40]Kidney Disease: Improving Global Outcomes (KDIGO) ANCA Vasculitis Work Group. KDIGO 2024 clinical practice guideline for the management of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Kidney Int. 2024 Mar;105(3s):S71-116. https://www.kidney-international.org/article/S0085-2538(23)00744-5/fulltext http://www.ncbi.nlm.nih.gov/pubmed/38388102?tool=bestpractice.com
Treatment of pauci-immune RPGN frequently involves an immunosuppressant such as a corticosteroid (e.g., prednisolone) and cyclophosphamide or rituximab.[40]Kidney Disease: Improving Global Outcomes (KDIGO) ANCA Vasculitis Work Group. KDIGO 2024 clinical practice guideline for the management of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Kidney Int. 2024 Mar;105(3s):S71-116. https://www.kidney-international.org/article/S0085-2538(23)00744-5/fulltext http://www.ncbi.nlm.nih.gov/pubmed/38388102?tool=bestpractice.com Choice of immunosuppressive therapy depends on the cause of RPGN and requires specialist consultation. Many patients will need maintenance immunosuppression depending on the underlying aetiology. The precise details vary with each disease and maintenance treatment should be individualised.
Choose a patient group to see our recommendations
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
Use of this content is subject to our disclaimer