Membranous glomerulonephritis is characterized by the formation of immune complexes in the basement membrane of the glomeruli. These immune complexes lead to thickening of the basement membrane, which in turn leads to proteinuria (loss of protein in the urine) and decreased kidney function. It typically produces a nephrotic syndrome clinical picture.
Membranous glomerulonephritis accounts for 25% of nephropathies in adults and 5% in children. It can occur at any age, but is most commonly diagnosed in people between the ages of 50 and 70. Men are slightly more likely to be affected than women.
In most cases, the cause of membranous glomerulonephritis is not known. However, it is thought to be an autoimmune disorder, in which the immune system mistakenly attacks the kidneys. In some cases, membranous glomerulonephritis is caused by a secondary condition, such as a viral or bacterial infection, or a cancer.
Risk factors include:
- Hepatitis B virus
- Autoimmune diseases
In membranous glomerulonephritis , immune complexes form in the basement membrane of the glomeruli. These immune complexes are composed of antibodies (proteins produced by the immune system) and antigens (substances that the immune system recognizes as foreign). The immune complexes lead to inflammation and thickening of the basement membrane, which in turn leads to proteinuria and decreased kidney function.
The most common clinical features of membranous glomerulonephritis are consistent with nephrotic syndrome, including proteinuria, hypoalbuminaemia and oedema. Other clinical features may include hypertension and hyperlipidaemia. In some cases, there may be no symptoms at all.
The diagnosis of membranous glomerulonephritis is typically made based on the presence of proteinuria (on urine tests) and a characteristic pattern of immune complexes on a kidney biopsy. Other tests that may be used to diagnose membranous glomerulonephritis include blood tests to measure kidney function and urine tests to measure protein levels.
Light microscopy shows a thickened glomerular basement membrane but normal mesangium. Electron microscopy typically demonstrates immune complex deposition described as “spike and dome” appearance. Immunofluorescence shows IgG and C3 subepithelial deposition.
The main goal of treatment for membranous glomerulonephritis is to reduce proteinuria and preserve kidney function. Patients should be advised to follow a low-salt and low-protein diet. Patients with a medium-term risk of progression to ESRD should be offered immunosuppression with a combination of corticosteroid and cyclophosphamide. Additionally, most patients are offered ACEi to reduce proteinuria and blood pressure.
If left untreated, membranous glomerulonephritis can lead to progressive kidney damage and end-stage kidney disease. In untreated cases, a third of patients have spontaneous remission, a third develop partial remission and a third progress to end-stage renal failure. In some cases, it can also lead to hypertension and heart disease.