Treatment for glomerulonephritis is targeted at the underlying cause and often involves supportive care and immunosuppression, such as corticosteroids.
Nephritic syndrome refers to a group of features that occur with nephritis: Haematuria (blood in the urine), which can be microscopic (not visible) or macroscopic (visible); Oliguria (significantly reduced urine output); Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome); Fluid retention.
Nephrotic syndrome involves: Proteinuria (more than 3g per 24 hours); Low serum albumin (less than 25g per litre); Peripheral oedema; Hypercholesterolaemia.
Goodpasture syndrome, also known as anti-glomerular basement membrane (anti-GBM) disease, involves anti-GBM (glomerular basement membrane) antibodies attacking the glomerulus and pulmonary basement membranes, causing glomerulonephritis and pulmonary haemorrhage, typically presenting in a patient in their 20s or 60s with acute kidney failure and haemoptysis.
Membranoproliferative glomerulonephritis typically affects patients under 30, involves immune complex deposits and mesangial proliferation, and can be secondary to malignancy, systemic lupus erythematosus or drugs (e.g., NSAIDs).
The top causes of nephrotic syndrome in adults are Membranous nephropathy, Focal segmental glomerulosclerosis, and other causes such as Membranoproliferative glomerulonephritis, Henoch-Schönlein purpura (HSP), Diabetes, and Infection (e.g., HIV).
Diagnosis of glomerulonephritis may require a renal biopsy for histology, and treatment depends on the underlying cause, which may involve supportive care, immunosuppression, or a combination of both.
IgA nephropathy (or Berger’s disease) is the most common cause of primary glomerulonephritis, with an unclear cause, typically presenting in their 20s with haematuria, and histology showing IgA deposits and mesangial proliferation.
Post-streptococcal glomerulonephritis tends to affect patients under 30, presenting 1-3 weeks after a streptococcal infection (e.g., tonsillitis or impetigo), and usually making a full recovery.
Systemic diseases that can cause glomerulonephritis include Henoch-Schönlein purpura (HSP), Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis), Lupus nephritis (associated with systemic lupus erythematosus), and others.
Rapidly progressive glomerulonephritis presents with an acute severe illness but tends to respond well to treatment, with histology showing glomerular crescents.
Membranous nephropathy involves deposits of immune complexes in the glomerular basement membrane, causing thickening and malfunctioning of the membrane and proteinuria, with histology showing IgG and complement deposits on the basement membrane.