|
Membranous nephropathy Causes and Risks:
The glomeruli are the inner structures of the kidney that include small capillaries surrounded by membranes through which the blood is filtered to form urine. Membranous nephropathy is caused by thickening of the capillary wall of the glomerular basement membrane (the deepest membrane) by immune complexes. The cause is not known.
It is one of the most common causes of nephrotic syndrome , which is the most common presentation of the disease. It may also appear as asymptomatic excretion of protein in the urine . Glomerular filtration rate (the "speed" of blood purification) is usually nearly normal, and examination of sediment in the urine may be unremarkable or may show oval fat bodies, and hyaline, granular, and fatty casts .
Membranous nephropathy may be a primary renal disease of uncertain origin, or it may be associated with other conditions. Risks include systemic disorders such as hepatitis B , malaria , malignant solid tumors, non-Hodgkin's lymphoma , systemic lupus erythematosus , syphilis , and others. Risks also include exposure to substances or medications, including gold, mercury , penicillamine, trimethadione, skin-lightening creams, and others.
The disorder occurs in approximately 2 out of 10,000 people. It may occur at any age but is more common after age 40.
Prevention:
Prompt treatment of associated disorders, and avoidance of associated substances, may reduce risk.
Symptoms:
Note: Symptoms vary and no symptoms may be present in many cases.
Signs and Tests:
An examination may be nonspecific except for edema . A urinalysis may reveal protein in the urine and/or blood in the urine ( hematuria ). Serum albumin may be low. Blood lipid levels may increase. Kidney biopsy confirms the diagnosis of membranous nephropathy.
Treatment:
The goal of treatment is to minimize symptoms and slow the progression of the disease. Symptoms should be treated as appropriate. Medications vary. Often, corticosteroids or immunosuppressive medications may be used to attempt to reduce symptoms and progression of the disorder, with variable results. Medications to treat symptoms may include antihypertensive and diuretic medications. Antibiotics may be needed to control infections.
Treatment of high blood cholesterol and triglyceride levels is recommended to reduce the development of atherosclerosis secondary to nephrotic syndrome . Dietary limitation of cholesterol and saturated fats may be of only limited benefit as the high levels of cholesterol and triglyceride seem to be caused by overproduction by the liver rather than excessive intake of fats. Medications to reduce cholesterol and triglycerides may be recommended.
High-protein diets are of debatable value. In many patients, reducing the amount of protein in the diet produces decrease in urine protein . In most cases, a moderate protein diet (1 gram of protein per kilogram of body weight per day) is usually recommended. Sodium in diet (salt) may be restricted to help control edema . Vitamin D may need to be replaced if nephrotic syndrome is chronic and unresponsive to therapy.
Prognosis:
Remissions and exacerbations may occur with or without therapy. The course of the disorder is highly variable. Spontaneous remission is possible, as is a variable course of remissions (symptom-free periods) and acute symptomatic episodes. 70 to 90% will have some degree of irreversible kidney damage within 2 to 20 years, with about 20% progressing to end-stage renal disease .
Complications:
Call Your Healthcare Provider:
Call for an appointment with your health care provider if symptoms indicate membranous nephropathy may be present. Call for an appointment with your health care provider if symptoms worsen or persist, if you experience a decreased urine output or other new symptom develops.
The kidneys are responsible for removing wastes from the body, regulating electrolyte balance and blood pressure, and the stimulation of red blood cell production. The gross anatomical structure of the kidney is illustrated.
|
