how do you get minimal change disease

The cause of minimal change disease is unknown, but if you have secondary causes for minimal change disease, the disease may occur or be related to:

• Allergic reactions
• Use of nonsteroidal anti-inflammatory drugs (NSAIDs)
• Tumors
• Vaccinations (flu and pneumococcal, though rare)
• Viral infections

Full Answer

What causes minimal change disease?

What causes minimal change disease? In adults, the disease is usually secondary (it is caused by another disease or drug). In children, MCD is usually primary (or idiopathic, which means the exact cause is not known).

How is minimal change disease treated in adults?

These two drugs control high blood pressure and reduce the amount of protein in the urine. How is minimal change disease treated in adults? The treatment for nephrotic syndrome in adults with MCD is usually with a type of drug called a corticosteroid, often called steroids.

What is minimal change nephrotic syndrome?

Those with MCD experience the signs and symptoms of nephrotic syndrome much quicker than they would with other glomerular diseases. What causes minimal change disease? In adults, the disease is usually secondary (it is caused by another disease or drug). In children, MCD is usually primary (or idiopathic, which means the exact cause is not known).

What is minimally change disease (MCD)?

Minimal change disease (MCD) is a major cause of idiopathic nephrotic syndrome (NS), characterized by intense proteinuria leading to edema and intravascular volume depletion.

What Is Minimal Change Disease?

Many diseases can affect your kidney function by attacking and damaging the glomeruli, the tiny filtering units inside your kidney where blood is c...

What Causes Minimal Change Disease?

In adults, the disease is usually secondary (it is caused by another disease or drug). In children, MCD is usually primary (or idiopathic, which me...

What Are The Signs and Symptoms of Minimal Change Disease?

You may notice the following signs and symptoms of MCD: 1. Foamy urine due to large amounts of protein leaking into your urine, called proteinuria...

How Is Minimal Change Disease Diagnosed?

The first clues are the signs and symptoms. Your healthcare provider may run tests to help understand the cause of your symptoms and find the prope...

How Is Minimal Change Disease Treated in Children?

MCD is usually easier to treat than other glomerular diseases. The treatment plan for nephrotic syndrome in children with MCD is usually with a typ...

How Is Minimal Change Disease Treated in Adults?

The treatment for nephrotic syndrome in adults with MCD is usually with a type of drug called a corticosteroid, often called steroids. You may noti...

Will Minimal Change Disease Cause Kidney Failure?

Kidney failure is rare if you have minimal change disease. Almost all children and adults recover from MCD and avoid relapses over the long term. H...

What is Minimal Change Disease?

Minimal Change Disease (MCD for short) is a kidney disease in which large amounts of protein is lost in the urine. It is one of the most common causes of the Nephrotic Syndrome (see below) worldwide. The kidneys normally work to clean the blood of the natural waste products that build up over time. To do this they have to filter all of the blood in the body many times each day. That is in fact what urine is- filtered blood. Normally, the kidneys can filter this blood without losing any of the proteins that are supposed to remain in circulation. When the kidney filters are damaged, however, protein sometimes “slips through” into the urine. This is called proteinuria.

What is the treatment?

Minimal Change Disease is one of the more treatable kidney diseases, especially in children. Therapy almost always consists of a course of oral steroids (prednisone), which is generally effective within weeks. A complete remission is not uncommon, though the disease can come back later in life. Patients with recurrent MCD, or with MCD that does not completely resolve with steroids, may require other forms of chemotherapy.

What are the symptoms?

The most noticeable symptom of MCD is often edema, or swelling, which can be profound. This typically starts in the feet and legs, but can move into the hips and abdomen as well. In contrast to many of the other diseases that can cause the Nephrotic Syndrome, the proteinura and edema of MCD can develop very rapidly- almost overnight. Other symptoms include high blood pressure, high cholesterol, and a tendency to form blood clots. Unlike the majority of other kidney diseases, especially those that cause the Nephrotic Syndrome, the ability of the kidney to clean the blood is often unaffected in MCD. This is especially true in children and young adults.

Can a child have MCD?

This is especially true in children and young adults. None of the above symptoms, or even all of them together, is specific for MCD. If you or your doctor are concerned about MCD, the only way to know for sure is to have a kidney biopsy. However, because of how common this disease is in children, when a child is diagnosed with ...

What is Minimal Change Disease (MCD)?

MCD is a condition that damages the tiny blood vessels in your kidneys (glomeruli) that clean your blood. MCD is called "minimal change" disease because the damage to the blood vessels is too small (minimal) for doctors to see under a regular microscope — so they must use a powerful device called an electron microscope.

What causes MCD?

Doctors do not know exactly what causes MCD. In children, MCD often happens without any known cause or reason. In adults, MCD may be related to:

How can I prevent MCD?

There is no known way to prevent MCD because doctors do not know exactly what causes it.

What is minimal change disease?

Listen. Minimal change disease is a kidney disease in which there is damage to the filtering units of the kidney (glomeruli). It is the most common cause of nephrotic syndrome in children. [1] [2] Nephrotic syndrome is comprised of a group of symptoms including protein in the urine ( proteinuria ), low protein levels in the blood, ...

What is the first line of treatment for minimal change disease?

Listen. Corticosteroids are typically the first line of treatment for minimal change disease. The fluid retention and high blood pressure that often accompanies minimal change disease may be treated with the use of water pills (diuretics) in combination with a low sodium diet and blood pressure medications (such as angiotensin-converting enzyme ...

How long does it take for MCD to recur?

MCD may recur or relapse in about half of all adults. This usually occurs within one year of treatment. [4] Despite the potential for the disease to recur, the occurrence of kidney failure and end stage renal disease is rare. [4] [5] Last updated: 1/12/2018.

Can you get a blood clot with minimal change?

There is an increased risk for the formation of blood clots ( thromboembolic events) and infection in individuals with minimal change disease. It is recommended that individuals with minimal change disease stay active and should a blood clot occur, they may be treated with blood thinners. Infections, such as cellulitis , peritonitis, ...

What is minimal change disease?

Minimal change disease (MCD) is a major cause of idiopathic nephrotic syndrome (NS), characterized by intense proteinuria leading to edema and intravascular volume depletion. In adults, it accounts for approximately 15% of patients with idiopathic NS, reaching a much higher percentage at younger ages, up to 70%–90% in children >1 year of age. In the pediatric setting, a renal biopsy is usually not performed if presentation is typical and the patient responds to therapy with oral prednisone at conventional doses. Therefore, in this setting steroid-sensitive NS can be considered synonymous with MCD. The pathologic hallmark of disease is absence of visible alterations by light microscopy and effacement of foot processes by electron microscopy. Although the cause is unknown and it is likely that different subgroups of disease recognize a different pathogenesis, immunologic dysregulation and modifications of the podocyte are thought to synergize in altering the integrity of the glomerular basement membrane and therefore determining proteinuria. The mainstay of therapy is prednisone, but steroid-sensitive forms frequently relapse and this leads to a percentage of patients requiring second-line steroid-sparing immunosuppression. The outcome is variable, but forms of MCD that respond to steroids usually do not lead to chronic renal damage, whereas forms that are unresponsive to steroids may subsequently reveal themselves as FSGS. However, in a substantial number of patients the disease is recurrent and requires long-term immunosuppression, with significant morbidity because of side effects. Recent therapeutic advances, such as the use of anti-CD20 antibodies, have provided long-term remission off-therapy and suggest new hypotheses for disease pathogenesis.

What is the pathogenesis of minimal change disease?

Pathogenesis of minimal change disease: hypotheses. In the presence of a normal glomerular basement membrane (shown at the center), with healthy podocyte foot processes (light blue), serum proteins, mainly albumin, remain within the glomerular capillary lumen. Mechanisms, that are as yet not fully elucidated but are partly intrinsic to the podocyte and partly due to the presence of soluble mediators released by a disregulated immune system (see top of the figure and text), modify this integrity. Therefore (red arrow), the actin cytoskeleton of the podocyte and the glomerular basement membrane are disrupted, and albumin and other serum proteins filter out of the bloodstream and into the urinary space. This leads to the intense proteinuria seen in nephrotic syndrome.

What is MCD in nephropathy?

In adults, minimal change disease (MCD) represents approximately 10%–15% of patients with idiopathic nephrotic syndrome ( Figure 1) ( 1, 2 ). In children >1 year of age, MCD is the most common cause of nephrotic syndrome, accounting for 70%–90% of patients; around puberty, this proportion decreases significantly as other glomerular diseases, such as membranous nephropathy, become more frequent ( Figure 1) ( 3, 4 ). The histologic picture of MCD is identical in adults and children. Because most children respond to steroid treatment, the disease is termed “steroid-sensitive nephrotic syndrome” (steroid-sensitive NS) on the basis of clinical features, and renal biopsy is not performed unless steroid resistance is observed. If performed, it usually shows the absence of significant changes by light microscopy (LM), a finding that has puzzled physicians for decades. When ultrastructural analyses were first performed in the 1950s, extensive fusion of podocyte foot processes was observed ( 5 ). Soon after, the term “lipoid nephrosis,” introduced in the early 1900s to describe the presence of microscopic lipid droplets in urine and tubular cells, was replaced by MCD, to highlight the existence of minimal alterations of the glomerulus by LM. However, a minority of patients that have FSGS lesions on their renal biopsy do respond to steroids and, conversely, patients with steroid-resistant nephrotic syndrome (steroid-resistant NS) may have MCD at disease onset, before developing FSGS lesions later in the course of their disease ( 6 ).

How many cases of MCD in children?

The reported incidence of MCD in children varies between two and seven new cases per 100,000 children ( 3, 7 ). The exact prevalence is not known, but on the basis of disease evolution and average age of onset, it can be estimated at approximately 10–50 cases per 100,000 children. The disease is slightly more common in Asia and has a male predominance (approximately 2:1) in young children that disappears in adolescents and adults ( 3, 8 ). MCD is much less frequent in adults, but the exact incidence in this population is less well documented.

Is MCD a NS?

The histologic picture of MCD is identical in adults and children. Because most children respond to steroid treatment, the disease is termed “steroid- sensitive nephrotic syndrome” (steroid-sensitive NS) on the basis of clinical features, and renal biopsy is not performed unless steroid resistance is observed.

Is MCD a disease continuum?

It is as yet debated whether MCD and FSGS represent a disease continuum with a common pathogenesis or two separate disease entities. Excluding secondary forms of MCD ( Table 2 ), the vast majority of cases arise in otherwise healthy individuals. Because the main histologic feature is foot process effacement, visible by electron microscopy, studies have concentrated on finding what disrupts the integrity of the glomerular filtration barrier. Figure 3 shows a sketch of this disruption and of some of the mechanisms that may contribute to determining it. The existence of one or more circulating factors capable of increasing its permeability, thus resulting in proteinuria, was first hypothesized on the basis of observations of the capability of plasma taken from nephrotic subjects to induce proteinuria in previously non-nephrotic subjects, and a vast body of literature in both human and mouse models has been accrued regarding FSGS ( 19 ). In MCD there is less clinical evidence of this, but the existence of a circulating mediator produced by abnormal T cells was postulated as far back as 1974 by Shalhoub, on the basis of the following observations: ( 1) remission may follow measles infection, which causes cell-mediated immunosuppression; ( 2) MCD may occur in Hodgkin disease, a lymphoid neoplasia; ( 3) MCD responds to drugs that suppress cell-mediated immunity; and ( 4) unlike other glomerular disorders, there is an absence of humoral (Ig and complement) deposition in glomeruli ( 16, 20 ). This hypothesis was strengthened by studies showing that supernatants of T cell hybridoma lines produced from patients with MCD were able to induce foot process effacement and proteinuria in rats ( 21 ). Subsequently, a vast body of evidence has emerged implicating different aspects of T cell regulation and function in driving podocyte injury in MCD ( 20 ). These are reinforced by the therapeutic effectiveness of immunosuppression, both with prednisone and second-line steroid-sparing agents, as will be discussed below. In summary, these results ( 22, 23) have shown an imbalance in T cell subpopulations during active phase of disease, with a prevalence of circulating CD8+ T suppressor cells that aggravate renal damage in mouse models of nephrotic syndrome ( 24) and a prevalence of a type 2 T helper cell (Th2; IL4, IL5, IL9, IL10, and IL13) cytokine profile in patients ( 25 ), which is mirrored by the spontaneous model of idiopathic nephrotic syndrome in the Buffalo/Mna rat ( 26 ). These observations fit with the clinical observation of an association between MCD and atopy, as allergies are driven by Th2 responses. Of all Th2 cytokines, IL13 overexpression has been shown to induce foot process effacement and proteinuria in rats ( 27 ). Certainly, no single cytokine can be considered pathogenic per se in MCD, but rather may play a role in the context of a complex network with multiple cellular and circulating players ( 28 ). Moreover, different lines of evidence suggest a reduced function of regulatory T cells in MCD in adult patients ( 29 ). Confirming this, MCD has been observed in immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome, a congenital immunodeficiency with severe T regulatory cell hypofunction ( 30 ).

What are the symptoms of minimal change?

Symptoms and Signs of Minimal Change Disease. Minimal change disease causes nephrotic syndrome, usually without hypertension or azotemia; microscopic hematuria occurs in about 20% of patients, mainly adults. Azotemia can occur in secondary cases and in patients > 60 years.

What is the treatment for nephrotic syndrome?

Treatment is with corticosteroids or, in patients who do not respond, cyclophosphamide or cyclosporine. (See also Overview of Nephrotic Syndrome .) Minimal change disease is the most common cause of nephrotic syndrome in children 4 to 8 years (80 to 90% of childhood nephrotic syndrome), but it also occurs in adults ...

Is minimal change disease idiopathic?

Minimal change disease accounts for most cases of nephrotic syndrome in children and is usually idiopathic.

What is minimal change disease?

Minimal change disease is responsible for idiopathic nephrotic syndrome in >75% of children and up to 30% of adults ( 1 – 5 ). Although secondary causes of minimal change disease ( i.e., nonsteroidal anti-inflammatory drugs, lithium, and lymphoproliferative disorders) are uncommon in children, they account for up to 15% ...

How often do you relapse with minimal change?

Relapses occur in 65%–80% of adults with minimal change disease, with the majority of relapses being seen within the first 3–6 months after a remission ( 3, 4, 6 ). However, younger adults (<45 years of age) tend to relapse more frequently (88% versus 57%) ( 4 ). Most adults with minimal change disease have only an occasional relapse ( i.e., less than or equal to one per year). In this situation, a second course of treatment with steroids is often used, typically resulting in another remission. Patients who relapse two or more times within 6 months or four or more times within 12 months are “frequent relapsers,” and those patients having two relapses with steroid taper or within 1 month of ending therapy are “steroid dependent” ( 7 ).

What is the treatment for nephrotic syndrome?

Although initial treatment of the nephrotic syndrome includes a low sodium diet and loop diuretics, the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for their antiproteinuric effects or lipid-lowering agents, such as statins, is generally not advocated ( 7 ).

How many people are in remission for ESKD?

The long-term prognosis for adults with minimal change disease is excellent, because 75%–90% of treated patients remain in remission ( 1, 3, 4, 6 ). Progression to ESKD occurs in <5% of adults and is often due to an alternative diagnosis of FSGS.