Approach

The goal of specific therapy for GN is to reverse the renal damage or to preserve the renal function; this is monitored by checking renal function and the degree of proteinuria. Treatment is patient-specific and directed toward the underlying aetiology. Complications such as hypertension and hyperlipidaemia should be managed appropriately to counteract cardiovascular events, as well as to delay progression of renal pathology. Choice of treatment, particularly immunosuppression, requires specialist consultation. In larger centres in high-income countries, patients with glomerulonephritis are often managed by a multi-professional subspeciality team. Prophylaxis for complications of immunosuppressive therapy may be required. Many patients will need maintenance immunosuppression; the precise details vary with each disease and maintenance treatment should be individualised.

See:

Mild disease

Patients with mild glomerulonephritis are typically asymptomatic with isolated haematuria, 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 or an 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] 

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 non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided.

Moderate-to-severe disease

Patients with moderate-to-severe glomerulonephritis are usually symptomatic with haematuria, proteinuria, and/or reduced eGFR.[1]

The principles of supportive therapy are the same as for mild disease.

Some patients with severe disease may present with nephrotic syndrome. This 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] Management of nephrotic syndrome may include a loop diuretic for oedema, statin therapy for hyperlipidaemia, and anticoagulant prophylaxis if there is a high risk of thromboembolism.[1] Immunosuppressive therapy with a corticosteroid (e.g., prednisolone) and/or a corticosteroid-sparing agent (e.g., cyclophosphamide, rituximab, a calcineurin inhibitor, mycophenolate) may also 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 glomerulonephritis

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 categorised into the following:[1]

  • Anti-glomerular basement membrane (linear type)

  • Immune complex-mediated: causes include post-infectious causes, autoimmune disorders (e.g., systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis), immunoglobulin A nephropathy, and membranoproliferative pattern of glomerular injury

  • Pauci-immune: causes include granulomatosis with polyangiitis and microscopic polyangiitis.

Immunosuppressant therapy with or without plasmapheresis (depending on the aetiology) is the mainstay of treatment for RPGN.[1][40][41]​[44][45][46]​​​​ As for other forms of glomerulonephritis, choice of treatment depends on the underlying cause of RPGN and requires specialist consultation. 

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