Membranous nephropathy is a kidney disorder that leads to changes and inflammation of the structures inside the kidney that help filter wastes and fluids. The inflammation may lead to problems with kidney function. It is also known as Membranous glomerulonephritis.
It occurs when a thin layer in the filtering unit of the kidneys (the glomerulus) becomes inflamed and then appears thickened. This inflammation causes the kidneys to leak protein which can lead to nephritic syndrome which causes the body to retain excess fluid. The fluid appears as swelling which usually starts in the ankles and feet. Membranous nephropathy leads to long term kidney damage.
Causes
About two thirds of membranous nephropathy is what is called ‘idiopathic’. This means that no cause can be identified. However the remaining one third of cases are associated with other conditions, usually diseases which are caused by a disturbance of the immune system. The problem is caused by an autoimmune attack on the cell within the glomerulus that make the glomerular basement membrane, known as podocytes. “Autoimmune” means that the damage is caused by the body’s own immune system.
The thicker glomerular membrane does not work normally. Large amounts of protein are lost in the urine as a result. This condition is one of the most common causes of nephrotic syndrome. It may be a primary kidney disease, or it may be associated with other conditions.
Risk Factors
Factors that can increase your risk of membranous nephropathy include –
- Having a medical condition that can damage the kidneys – Certain diseases and conditions increase the risk of developing membranous nephropathy, such as lupus and other autoimmune diseases.
- Use of certain medications – Examples of medications that can cause membranous nephropathy include nonsteroidal anti-inflammatory drugs and gold salts.
- Exposure to certain infections – Examples of infections that increase the risk of membranous nephropathy include hepatitis B, hepatitis C and syphilis.
- Genetic background – Certain genetic factors make it more likely that people will develop membranous nephropathy.
- Toxins – Exposure to toxins, including gold and mercury
Symptoms
The symptoms of MGN are different for each person. Patients may have no symptoms at all. If symptoms develop, they typically include the following –
- swelling (edema) in the hands, feet, or face
- fatigue
- foamy urine
- excessive need to urinate at night
- weight gain
- poor appetite
MGN causes damage to the kidney, and that results in protein being filtered from the blood and into the urine. Because protein is needed by the body, a lack of protein leads to water retention and swelling. All these symptoms are associated and known as nephrotic syndrome.
Complications
Complications associated with membranous nephropathy include –
- High cholesterol – Levels of cholesterol and triglycerides are often high in people with membranous nephropathy, which greatly increases the risk of heart disease.
- Blood clots – With proteinuria, some may lose proteins that help prevent clotting from the blood into the urine. This makes the person more prone to having blood clots develop in deep veins or blood clots that travel to the lungs.
- High blood pressure – Waste buildup in your blood (uremia) and salt retention can raise blood pressure.
- Infections – Patients are more susceptible to infections when proteinuria causes them to lose immune system proteins (antibodies) that protect people from infection.
- Nephrotic syndrome – High protein levels in the urine, low protein levels in the blood, high blood cholesterol, and swelling (edema) of the eyelids, feet and abdomen can lead to nephrotic syndrome — a cluster of signs and symptoms that affect the kidneys’ filtering ability.
- Acute kidney failure – In cases of severe damage to the kidneys’ filtering units (glomeruli), waste products may build up quickly in the blood. Patient may need emergency dialysis to remove extra fluids and waste from the blood.
- Chronic kidney disease – The kidneys may gradually lose function over time to the point where affected person may need dialysis or a kidney transplant.
Treatment
The goal of treatment is to reduce symptoms and slow the progression of the disease.
Controlling blood pressure is the most important way to delay kidney damage. The goal is to keep blood pressure at or below 130/80 mmHg. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are the medicines most often used to lower blood pressure.
Corticosteroids and other drugs that suppress the immune system may be used.
High blood cholesterol and triglyceride levels should be treated to reduce the risk of atherosclerosis. However, a low-fat, low-cholesterol diet is usually not as helpful for people with membranous nephropathy. Medications to reduce cholesterol and triglyceride levels (most often statins) may be recommended.
A low-salt diet may help with swelling in the hands and legs. Water pills or diuretics may also help with this problem.
Low-protein diets may be helpful. A moderate-protein diet (1 gram of protein per kilogram of body weight per day) may be suggested.
This disease increases the risk for blood clots in the lungs and legs. Patients are occasionally prescribed blood thinners to prevent these complications.
Screening for age-appropriate malignancies is warranted, if not already done.
Alternative Treatment
Zinc – An essential trace element, zinc is a metal that is necessary for human health. Its immune boosting capabilities treat the bacteria that is often associated with membranous glomerulonephritis. In turn, the amount of protein in the body is also reduced.
Magnesium – A key mineral in the human metabolism, magnesium is also an effective treatment option for MGN. Magnesium functions in a number of ways to treat the condition including reducing inflammation, attacking the bacteria in the kidney, balancing immune function and eliminating protein in the kidney.
Vitamin D supplementation may be required for patients with chronic membranous nephritis that is not responsive to treatment. Vitamin D is converted to its active form, 1,25-dihydroxyvitamin D, in the kidney. In chronic kidney disease, the ability of the kidney to synthesize this vitamin is reduced, therefore supplementation is sometimes warranted.
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