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Glomerulonephritis (Nephritic Syndrome)
Glomerulonephritis (nephritic syndrome) is a disorder of glomeruli (clusters of microscopic blood vessels in the kidneys with small pores through which blood is filtered). It is characterized by body tissue swelling (edema), high blood pressure, and the presence of red blood cells in the urine.
Glomerulonephritis can be caused by various disorders, such as infections, an inherited genetic disorder, or autoimmune disorders.
Diagnosis is based on tests of blood and urine and sometimes imaging tests, a biopsy of the kidneys, or both.
People often need to restrict salt and protein intake and take diuretics or antibiotics until kidney function improves.
Glomerulonephritis can develop over a short time period (acute glomerulonephritis) or develop and progress slowly (chronic glomerulonephritis). In 1% of children and 10% of adults who have acute glomerulonephritis, it evolves into rapidly progressive glomerulonephritis, in which most of the glomeruli are destroyed, resulting in kidney failure.
Glomerulonephritis can be primary, originating in the kidneys, or secondary, caused by a vast array of disorders. Those disorders may affect other parts of the body.
Acute glomerulonephritis most often occurs as a complication of a throat or skin infection with streptococcus, a type of bacteria. Acute glomerulonephritis that occurs after a streptococcal infection (poststreptococcal glomerulonephritis) typically develops in children between the ages of 2 and 10 after recovery from the infection. Infections with other types of bacteria, such as staphylococcus and pneumococcus, viral infections, such as chickenpox, and parasitic infections, such as malaria, can also result in acute glomerulonephritis. Acute glomerulonephritis that results from any of these infections is called postinfectious glomerulonephritis.
Acute glomerulonephritis may also be caused by noninfectious disorders, including membranoproliferative glomerulonephritis, immunoglobulin A (IgA) nephropathy, immunoglobulin A–associated vasculitis (formerly, Henoch-Schönlein purpura), systemic lupus erythematosus (lupus), cryoglobulinemia, Goodpasture syndrome, and granulomatosis with polyangiitis (formerly, Wegener granulomatosis). Acute glomerulonephritis that develops into rapidly progressive glomerulonephritis most often results from conditions that involve an abnormal immune reaction.
Often, chronic glomerulonephritis seems to result from some of the same conditions that cause acute glomerulonephritis, such as IgA nephropathy or membranoproliferative glomerulonephritis. Sometimes, acute glomerulonephritis does not resolve and instead becomes long lasting (chronic). Occasionally, chronic glomerulonephritis is caused by hereditary nephritis, an inherited genetic disorder. In many people, the cause of chronic glomerulonephritis cannot be identified.
About half of the people with acute glomerulonephritis have no symptoms. If symptoms do occur, the first to appear are tissue swelling (edema) due to fluid retention, low urine volume, and production of urine that is dark because it contains blood. Edema may first appear as puffiness of the face and eyelids but later is prominent in the legs. Blood pressure increases as kidney function becomes impaired. Some people become drowsy or confused. In older people, nonspecific symptoms, such as nausea and a general feeling of illness (malaise), are more common.
When rapidly progressive glomerulonephritis develops, weakness, fatigue, and fever are the most frequent early symptoms. Loss of appetite, nausea, vomiting, abdominal pain, and joint pain are also common. About 50% of people have a flu-like illness in the month before kidney failure develops. These people have edema and usually produce very little urine. High blood pressure is uncommon and rarely severe when it does occur.
Because chronic glomerulonephritis usually causes only very mild or subtle symptoms, it goes undetected for a long time in most people. Edema may occur. High blood pressure is common. The disease may progress to kidney failure, which can cause itchiness, decreased appetite, nausea, vomiting, fatigue, and difficulty breathing.
Doctors investigate the possibility of acute glomerulonephritis in people whose laboratory test results indicate kidney dysfunction or blood in the urine and in people who develop symptoms of the disorder. Laboratory tests show variable amounts of protein and blood cells in the urine and often kidney dysfunction, as shown by a high concentration of urea and creatinine (waste products) in the blood.
In people with rapidly progressive glomerulonephritis, casts (clumps of red blood cells or white blood cells) are often visible in a urine sample that is examined under a microscope. Blood tests usually detect anemia.
When doctors suspect glomerulonephritis, a biopsy of a kidney is usually done to confirm the diagnosis, help determine the cause, and determine the amount of scarring and potential for reversibility. Kidney biopsy is done by inserting a needle in one of the kidneys under ultrasound or computed tomography (CT) guidance to obtain a small amount of kidney tissue. Although kidney biopsy is an invasive procedure and occasionally can become complicated, it is usually safe.
Additional tests are sometimes helpful for identifying the cause. For example, in the diagnosis of postinfectious glomerulonephritis, a throat culture may provide evidence of streptococcal infection. Blood levels of antibodies against streptococci may be higher than normal or progressively increase over several weeks. Acute glomerulonephritis that follows an infection other than strep throat is usually easier to diagnose because its symptoms often begin while the infection is still obvious. Cultures and blood tests that help identify the organisms that cause these other types of infections are sometimes needed to confirm the diagnosis.
When doctors suspect an autoimmune cause for glomerulonephritis, they do blood tests for antibodies directed against some of the body's own tissues (called autoantibodies) and tests that assess the complement system, a system of proteins involved in the body's immune system.
Chronic glomerulonephritis develops gradually, and therefore, a doctor may not be able to tell exactly when it began. It may be discovered when a urine test, done as part of a medical examination, reveals the presence of protein and blood cells in the urine in a person who is feeling well, has normal kidney function, and has no symptoms. Doctors usually do an imaging test of the kidneys, such as ultrasonography or CT. A kidney biopsy is the most reliable way to distinguish chronic glomerulonephritis from other kidney disorders. A biopsy, however, is rarely done in advanced stages. In these cases, the kidneys are shrunken and scarred, and the chance of obtaining specific information about the cause is small. Doctors suspect that the kidneys are shrunken and scarred if kidney function has been poor for a long time and the kidneys appear abnormally small on an imaging test.
Acute poststreptococcal glomerulonephritis resolves completely in most cases, especially in children. About 1% of children and 10% of adults develop chronic kidney disease.
The prognosis for people with rapidly progressive glomerulonephritis depends on the severity of glomerular scarring and whether the underlying disease, such as infection, can be cured. In some people who are treated early (within days to weeks), kidney function is preserved and dialysis is not needed. However, because the early symptoms can be subtle and vague, most people who have rapidly progressive glomerulonephritis are not aware of the underlying disease and do not seek medical care until kidney failure develops. If treatment occurs late, the person is more likely to develop chronic kidney disease with kidney failure. Because kidney failure tends to develop before people notice it, 80 to 90% of people who have rapidly progressive glomerulonephritis become dependent upon dialysis. The prognosis also depends on the cause, the person's age, and any other diseases the person might have. When the cause is unknown or the person is older, the prognosis is worse.
In some children and adults who do not recover completely from acute glomerulonephritis, other types of kidney disorders develop, such as asymptomatic proteinuria and hematuria syndrome or nephrotic syndrome. Other people with acute glomerulonephritis, especially older adults, often develop chronic glomerulonephritis.
Primary Glomerular Disorders That Can Cause Glomerulonephritis
No specific treatment is available in most cases of acute glomerulonephritis. The disorder causing glomerulonephritis is treated when possible. Following a diet that is low in protein and sodium may be necessary until kidney function recovers. Diuretics may be prescribed to help the kidneys excrete excess sodium and water. High blood pressure needs to be treated.
When a bacterial infection is suspected as the cause of acute glomerulonephritis, antibiotics are usually ineffective because the nephritis begins 1 to 6 weeks (average, 2 weeks) after the infection, which has, by then, usually resolved. However, if a bacterial infection is still present when acute glomerulonephritis is discovered, antibiotic therapy is started. Antimalarial drugs may be beneficial if glomerulonephritis is caused by malaria. Some autoimmune disorders that cause glomerulonephritis are treated with corticosteroids, drugs that suppress the immune system, or both.
For rapidly progressive glomerulonephritis, drugs to suppress the immune system are started promptly. High doses of corticosteroids are usually given intravenously for about a week, followed by a variable period of time when they are taken by mouth. Cyclophosphamide, an immunosuppressant, may also be given. In addition, plasma exchange is sometimes used to remove antibodies from the blood. The sooner treatment occurs, the less likely are kidney failure and the need for dialysis. Kidney transplantation is sometimes considered for people who develop chronic kidney disease with kidney failure, but rapidly progressive glomerulonephritis may recur in the transplanted kidney.
Taking either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) often slows progression of chronic glomerulonephritis and tends to reduce blood pressure and the excretion of protein in the urine. Reducing blood pressure and sodium intake are considered beneficial. Restricting the amount of protein in the diet is modestly helpful in reducing the rate of kidney deterioration. End-stage kidney failure can be treated with dialysis or a kidney transplant.
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