Membranoproliferative GN

Causes

Glomerulonephritis is inflammation of the glomeruli. These structures of the kidney help filter wastes and fluids from the blood to form urine.

Membranoproliferative GN is a form of glomerulonephritis caused by an abnormal immune response. Deposits of antibodies build up in a part of the kidneys called the glomerular basement membrane. This membrane helps filter wastes and extra fluid from the blood.

Damage to this membrane affects the body's ability to create urine normally. It may allow blood and protein to leak into the urine. Fluid may leak out of the blood vessels into body tissues, leading to swelling (edema). Nitrogen waste products may also build up in the blood (azotemia).

There are two forms of membranoproliferative GN:

• Membranoproliferative GN I
• Membranoproliferative GN II

Most people with the disease have type I. Membranoproliferative GN II is much less common. It also tends to get worse faster than membranoproliferative GN I.

Many cases of membranoproliferative GN are due to causes such as:

• Autoimmune diseases (systemic lupus erythematosus, scleroderma, Sjogren syndrome, sarcoidosis)
• Cancer (leukemia, lymphoma)
• Infections (hepatitis B, hepatitis C, endocarditis, malaria)

The conditions mostly affect people ages 8 to 16.

Symptoms

• Blood in the urine
• Changes in mental status such as decreased alertness or decreased concentration
• Cloudy urine
• Dark urine (smoke, cola, or tea colored)
• Decrease in urine volume
• Swelling of any part of the body

Exams and Tests

The results of a physical examination depend on the symptoms. There may be swelling (usually in the legs), along with other signs of fluid overload, such as abnormal sounds when listening to the heart and lungs with a stethoscope.

Blood pressure is often high because of increased water and sodium (salt) retention and increased production of renin, a hormone that controls blood pressure.

Membranoproliferative GN may be seen as:

• Abnormal urinalysis without symptoms
• Acute nephritic syndrome
• Nephrotic syndrome

The following tests help confirm the diagnosis:

• BUN and creatinine
• Serum complement C3 nephritic factor
• Serum complement levels
• Urinalysis
• Urine protein

A kidney biopsy confirms the diagnosis of membranoproliferative GN I or II.

Treatment

Treatment depends on the symptoms. The goals of treatment are to reduce symptoms, prevent complications, and slow the progression of the disorder.

You may need a change in diet. This may include limiting salt, fluids, or protein to help control high blood pressure, swelling, and the buildup of waste products in the blood.

Medicines that may be prescribed include:

• Blood pressure medications
• Dipyridamole, with or without aspirin
• Diuretics
• Medications to suppress the immune system, such as cyclophosphamide
• Steroids

Treatment is more effective in children than in adults. Dialysis or kidney transplant may eventually be needed to manage kidney failure.

Outlook (Prognosis)

The disorder often slowly gets worse and eventually results in chronic kidney failure. Fifty percent of patients with this condition develop chronic kidney failure within 10 years.

Possible Complications

• Acute nephritic syndrome
• Acute renal failure
• Chronic kidney disease
• End-stage kidney disease
• Nephrotic syndrome

When to Contact a Medical Professional

Call for an appointment with your health care provider if:

• You have symptoms of this condition
• Your symptoms get worse or do not go away
• You develop new symptoms, including decreased urine output

Prevention

Prevention is often not possible.

Alternative Names

Membranoproliferative GN I; Membranoproliferative GN II; Mesangiocapillary glomerulonephritis; Membranoproliferative glomerulonephritis; Lobular GN; Glomerulonephritis - membranoproliferative; MPGN type I; MPGN type II

References

Appel GB. Glomerular disorders and nephrotic syndromes. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 122.

Nachman PH, Jennette JC, Falk RJ. Primary glomerular disease. In: Brenner BM, ed. Brenner and Rector's the Kidney. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 30.

Update Date: 9/19/2011

Updated by: David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine; and Herbert Y Lin, MD, PhD, Nephrologist, Massachusetts General Hospital; Associate Professor of Medicine, Harvard Medical School. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.