|Other names: Mesangiocapillary glomerulonephritis|
|Micrograph of glomerulus in membranoproliferative glomerulonephritis with increased mesangial matrix and increased mesangial cellularity. Kidney biopsy. PAS stain.|
|Symptoms||Foamy urine, blood in the urine, swelling|
|Complications||High blood pressure, low red blood cells, kidney failure|
|Usual onset||Children and young adults|
|Types||Primary (type I, II, III), secondary|
|Causes||Unknown, infections, autoimmune disorders, cancer, liver disease, certain drugs|
|Diagnostic method||Kidney biopsy|
|Differential diagnosis||Minimal change disease, lupus nephritis, diabetic nephropathy, focal segmental glomerulonephritis|
|Treatment||Steroids, cyclophosphamide, ASA, kidney transplant, plasma exchange|
Membranoproliferative glomerulonephritis (MPGN) is a pattern of injury of the glomeruli of the kidneys. Symptoms may include foamy urine, blood in the urine, or swelling. Generally it gradually worsens over time. Complications often include high blood pressure, low red blood cells, and kidney failure.
The cause can be unknown or it can occur as a result of infections, autoimmune disorders, cancer, liver disease, or certain drugs. The underlying mechanism is believed to involve immune complexes building up in the kidneys and activating the complement system. This results in mesangial cell growth with thickening of the walls of the small blood vessels. Diagnosis is by kidney biopsy.
The best method of management is unclear. Treatment may include the use of steroids, cyclophosphamide, or aspirin. Plasma exchange has been tried. While a kidney transplant may be carried out, the disease may reoccur afterwards. It is uncommon for the disease to resolve without treatment. Outcomes are generally poor.
MPGN is uncommon. It most commonly occurs in children and young adults. Males and females are affected equally frequently. It makes up about 4% of primary kidney causes of nephrotic syndrome in children and 7% in adults. MPGN was first described in 1965 by Gotoff and West.
Signs and sympoms
Symptoms may include foamy urine, blood in the urine, or swelling. Generally it gradually worsens over time. Complications often include high blood pressure, low red blood cells, and kidney failure.
Membranoproliferative glomerulonephritis involves deposits at the intraglomerular mesangium.
It is also the main hepatitis C associated nephropathy.
It also is related to a number of autoimmune diseases, prominently systemic lupus erythematosus (SLE). Also found with Sjögren syndrome, rheumatoid arthritis, inherited complement deficiencies (esp C2 deficiency), scleroderma, Celiac disease.
There are three types of MPGN, but this classification is becoming obsolete as the causes of this pattern are becoming understood.
Type I, the most common by far, is caused by immune complexes depositing in the kidney. It is characterised by subendothelial and mesangial immune deposits.
The preferred name is "dense deposit disease." Most cases of dense deposit disease do not show a membranoproliferative pattern. A 2012 review considers DDD to be in a continuum with C3 glomerulonephritis, one reason the use of the type I to type III classification system is falling out of favour.
DDD is associated with deposition of complement C3 within the glomeruli with little or no staining for immunoglobulin. The presence of C3 without significant immunoglobulin suggested to early investigators that DDD was due to abnormal activation of the complement alternative pathway (AP). There is now strong evidence that DDD is caused by uncontrolled AP activation.
In many cases, people with MPGN II can develop drusen caused by deposits within Bruch's membrane beneath the retinal pigment epithelium of the eye. Over time, vision can deteriorate, and subretinal neovascular membranes, macular detachment, and central serous retinopathy can develop.
Type III is very rare, it is characterized by a mixture of subepithelial and subendothelial immune and/or complement deposits. These deposits elicit an immune response, causing damage to cells and structures within their vicinity. Has similar pathological findings of Type I disease.
Primary MPGN is treated with steroids, plasma exchange and other immunosuppressive drugs. Secondary MPGN is treated by treating the associated infection, autoimmune disease or neoplasms. Pegylated interferon and ribavirin are useful in reducing viral load. 
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