Membranous nephropathy (MN), a significant cause of nephrotic syndrome, has gained widespread attention in recent years as a result of its increasing frequency among the general public. With primary glomerulonephritis, it is the second or third main cause of end-stage renal disease (ESRD). It is also the most common glomerulopathy that reappears after kidney transplantation.
Membranous Nephropathy: A Brief Overview
Membranous nephropathy (MEM-bruh-nus nuh-FROP-uh-thee) is a condition in which the tiny blood arteries of the kidney (glomeruli) become damaged and swollen, allowing wastes to pass through. As a result, proteins leak into the urine from the wounded blood vessels as a result of the injury (proteinuria). Nephrotic syndrome, which is characterised by signs and symptoms, is caused by the loss of these proteins in a large proportion of the population.
Membranous nephropathy (MN) is a significant cause of nondiabetic nephrotic syndrome in adults. It is the second or third main cause of end-stage renal disease (ESRD) in individuals with primary glomerulonephritis and the most often recurrent glomerulopathy after kidney transplantation. MN may affect persons of various ages, but is more prevalent in adults.
MN is characterised by edoema, severe proteinuria, hypoalbuminemia, and hyperlipidemia. Its distinctive pathological manifestations include diffuse homogeneous thickening of the glomerular basement membrane (GBM) and the formation of spikes under a light microscope; granular deposition of immunoglobulin G (IgG) and C3 in glomerular capillary loops under immunofluorescence; extensive fusion of podocyte foot processes under an electron microscope; and subepithelial electron dense deposits.
MN is categorised into two subtypes based on its aetiology: idiopathic membranous nephropathy (IMN) and secondary membranous nephropathy (SMN). SMN is primarily caused by autoÂimmune diseases (systemic lupus erythematosus [SLE], rheumatoid arthritis, Sjögren’s syndrome, mixed connective tissue disease, and thyroiditis), tumours (thyroid tumours, solid tumours such as lung and colon cancer, leukaemia, lymphoma, and other malignant blood tumours), chronic infection (hepatitis B and C, syphilis, These secondary causes should be ruled out before to making an IMN diagnosis.
To date, the majority of scholars believe that IMN is an autoimmune disease caused by antigen-antibody complexes; the antigens include neutral endopeptidase (NEP), M-type phospholipase A2 receptor (PLA2R), and thrombospondin type-1 domain-containing 7A (THSD7A), as well as other endogenous podocyte antigens that bind to autoantibodies, forming subepithelial deposits in the Additionally, environmental contamination and genetic variables have been linked to the prevalence of IMN.
In the normal course of IMN, about 1/3 of patients obtain spontaneous remission, another 1/3 achieve remission with immunosuppressive therapy, and the other 1/3 develop to renal failure with uncontrolled proteinuria and recurring episodes. Due to the disease’s high incidence and recurrence, it is critical to understand the pathophysiology of IMN in order to provide appropriate therapy, prognosis assessment, and treatment modification. This article focuses on the pathogenesis of IMN at the molecular and genetic level, establishing a link between IMN molecular indicators and clinical treatment.
Causes of Membranous Nephropathy:
An extracellular layer, or membrane, exists between the glomeruli and assists in the filtration of waste and fluid from your blood. Membranous nephropathy is caused by a thickening of the membrane around the kidney. ‌
It is not clear why this thickness arises, however it is assumed to be caused by immune cells producing antibodies. Membranous nephropathy is a disorder in which your body creates antibodies, or protective proteins, against proteins in your kidneys, resulting in kidney damage.
An increase of immune cells in your kidney filters leads in inflammation and thickening of the filter membranes. Because of the thickness, your kidneys are unable to perform their functions properly, resulting in a large loss of protein via your urine.
Secondary membranous nephropathy is a disorder that develops as a result of other kidney-related health issues or treatments. There are a variety of them, including the following:
- Diabetes
- Rheumatoid arthritis
- Lupus
- Sjorgen syndrome
- Heavy metal poisoning
- Nonsteroidal anti-inflammatory drugs
- Probenecid
- Penicillamine
- Hepatitis B
- Hepatitis C
- Syphilis
- HIV
- Malaria
Membranous nephropathy may affect anybody, however it is more common in older Caucasian men than in any other group. Children are seldom affected by this kidney ailment, which is also less common in women.
Which tests are performed to identify whether or not I have MN?
Urine test: A pee test may be used to determine whether or not there is protein or blood present in your urine.
Blood test: In certain cases, it may be used to determine the quantities of protein, cholesterol, and waste in your blood.
Glomerular filtration rate (GFR): A blood test will be done to evaluate the efficiency with which your kidneys eliminate wastes from your body. Glomerular filtration rate is a measure of how efficiently your kidneys remove wastes from your body.
The kidney biopsy is performed with the use of a particular needle and is viewed under a microscope during this process to determine the condition of your kidney. A kidney biopsy may indicate whether or not you have a certain kind of protein known as an antibody, which assists your body in fighting disease. When you have MN, your body normally creates this antibody in response to the infection.
Symptoms of Membranous nephropathy:
Membranous nephropathy develops slowly, and you may be unaware that anything is amiss. As you lose protein from your blood, you may experience swelling in your legs and ankles, as well as weight gain due to excess fluid. While many patients have significant edoema from the start of the illness, others may not exhibit severe symptoms until they have advanced renal impairment.
The following are the signs and symptoms of membranous nephropathy:
- Legs and ankles swollen.
- Gain in weight.
- Fatigue.
- Appetite deficit.
- Urine that seems to be frothy.
- Cholesterol levels are elevated.
- Increased protein concentration in the urine (proteinuria).
- Protein levels in the blood, notably albumin, are decreased.
When to consult a physician:
Make an appointment with your physician if you have any of the following:
- Your pee contains blood.
- Legs and ankles that continue to swell.
- Blood pressure is elevated.
- Sudden discomfort between your upper abdomen and midback.
- Sudden shortness of breath, which might be a consequence of a blood clot.
